IOWA CHRONIC WASTING DISEASE CWD TSE PRION TOTAL TO DATE 304 CASES WILD AND CAPTIVE REPORT UPDATE JULY 2016
IOWA CHRONIC WASTING DISEASE CWD TSE PRION TOTAL TO DATE 304 CASES WILD AND
CAPTIVE REPORT UPDATE JULY 2016
WILD 6 CWD POSITIVE TO DATE
CAPTIVE 298 CWD POSITIVE TO DATE
personal communications...tss
IOWA
CWD Program Report:
57,792 wild white-tailed deer since surveillance began in 2002. First
positive in the wild was found from surveillance in 2013/14 deer season in
Allamakee County in NE Iowa. To date 6 total positives found - all in Allamakee
County.
Iowa’s Chronic Wasting Disease (CWD) Voluntary Program:
As of July 29, 2016 the Iowa Department of Agriculture & Land
Stewardship has 100 farm deer herds enrolled in Iowa’s Chronic Wasting Disease
Program. They are as follows:
71 Whitetail (only) Deer Producers
20 Elk Producers
1 Fallow Deer Producer
8 County Conservation Boards
There are a total of 4,249 Cervidae in Iowa’s CWD Program:
3,232 = Whitetail Deer
863 = Elk
154 = Fallow Deer
In 2015, Iowa permitted in from out-of-state 314 cervidae: 165 whitetail
deer (112 went to Hunting Preserves), 18 reindeer, 2 muntjack, 5 fallow deer and
12 elk from out of state.
Since 2002, the Iowa Department of Agriculture & Land Stewardship with
the Chronic Wasting Disease Program has submitted 6,222 CWD laboratory
submissions for testing.
PERSONAL COMMUNICATIONS END...TSS
Chronic Wasting Disease (CWD) Iowa has tested more than 57,000 wild deer
and more than 3,500 captive deer and elk as part of the surveillance efforts
since 2002 when CWD was found in Wisconsin. Samples are collected from all 99
counties; however the majority are taken in the counties nearest to areas where
CWD has been detected in Iowa and other states. Samples are collected
voluntarily from hunter-harvested deer in the field, at check stations and meat
lockers.
Chronic Wasting Disease Response Plan
(Iowa DNR and Iowa Department of Agriculture and Land Stewardship)
Surveillance Plan for Allamakee County
The Iowa DNR is asking for assistance from landowners and hunters in
dealing with what it hopes is an isolated case of Chronic Wasting Disease (CWD)
found in a wild deer harvested in Allamakee County. The deer, harvested south of
Harpers Ferry in Yellow River State Forest during the 2013 regular gun season,
is the first known case of CWD in a wild deer in the State of Iowa. The DNR has
collected and tested more than 51,000 samples statewide since 2002.
The DNR’s action plan is to increase surveillance efforts in a 5‐mile
radius from where the positive deer was harvested. This additional surveillance
along with the over 1,100 deer sampled in the past 12 years in this immediate
area will help determine if CWD has spread to other deer. If no further cases
are found in the next three years, the DNR will go back to routine testing. If
additional cases are found, the DNR will work with the public to decide how to
proceed.
The DNR is encouraging the public to report all roadkill deer and sick or
severely emaciated deer found in the targeted area (see map) to the Iowa DNR at
any of the following numbers:
Unit Headquarters 563.546.7962
Biologist Terry Haindfield 563.380.3422
Conservation Officer Bill Collins 563.380.0801
Conservation Officer Jerry Farmer 563.880.0422
Conservation Officer Burt Walters 563.880.0108
The goal for this fall will be to test 500 deer in Allamakee County,
including 300 from the targeted area around where the infected deer was killed.
Local DNR staff will work with hunters to obtain samples for testing during the
2014‐15 deer hunting seasons.
The DNR is especially interested in testing deer harvested from islands in
the Mississippi River or from land adjoining the river near Harpers Ferry.
Hunters are asked to refrain from shooting the deer in the head because it makes
testing more difficult.
Hunters can help reduce the risk of spreading CWD by not leaving bones on
the landscape after processing their deer. A better option is to bury them or
take them to a clay‐lined landfill.
Lastly, everyone should also refrain from feeding and baiting deer in the
targeted area. The risk of spreading any disease is greater when animals are
concentrated in a very small area.
CWD Cases in Iowa: Allamakee and Davis Counties
In April 2014, the DNR was notified that a deer harvested south of Harpers
Ferry in Yellow River State Forest during the 2013 regular gun season tested
positive for CWD. This was the first known case of CWD in a wild deer in the
state. In January 2015 three more CWD positives were reported for deer harvested
in 2014 from Allamakee County. The DNR is implementing a special CWD
surveillance plan in Allamakee County while continuing to implement its existing
CWD testing protocols statewide.
As a result of public meetings on February 17, 2015 in Harper’s Ferry and
Waukon, the DNR and local constituents agreed to begin an intensive sample
collection effort in the surveillance area, defined as the sections adjacent to,
and including, the sections where the four positive animals were found. The goal
of this intensive surveillance is to provide more information on the extent and
prevalence of CWD in this area. This information will then be used to guide
decisions for future surveillance efforts and hunting seasons. Additional deer
will be collected beginning on February 21 until March 15th OR when an
additional 200 samples are obtained. The samples will bring the total number
collected in the intensive surveillance area to 300, which will provide a better
understanding of the extent and prevalence of CWD in this area. Only adult deer
will be sampled. Cooperators will be issued permits to collect deer in the
intensive surveillance area only through local DNR wildlife staff.
Allamakee CWD Surveillance Area Map
In 2012, three deer tested positive for CWD on a shooting preserve among
captive deer in Davis County. This was the first time CWD was discovered in the
state. These positives were confirmed by the National Veterinary Services Lab in
Ames, Iowa. Below are the Emergency Order, the Emergency Consent Order, and the
Final Decision of the Natural Resource Commission related to the discovery of
CWD-positive deer at the preserve. On Feb. 13th, an Iowa District Court Judge
ruled that the Natural Resources Commission and Department of Natural Resources
do not have authority under current Iowa law to impose a quarantine on the land
and compel the owners to maintain fencing around the former hunting preserve.
That ruling is available on a link below. The Natural Resources Commission has
voted unanimously to appeal the district court ruling and the Iowa Attorney
General’s Office has filed a motion to stay the ruling until the requested
judicial review can take place.
DNR Emergency Order, issued June 6, 2013
DNR Emergency Consent Order, agreed upon July 3, 2013
Final Decision of the Natural Resource Commission, issued May 28, 2014
Iowa District Court Ruling February 13, 2015
Animal Industry Bureau Chronic Wasting Disease Elk Deer What is Chronic
Wasting Disease? Chronic wasting disease (CWD) is a fatal, neurological disease
of farmed and wild deer and elk. The disease has been identified in wild and
captive mule deer, white-tailed deer and North American elk, and in captive
black-tailed deer. CWD belongs to the family of diseases known as transmissible
spongiform encephalopathies (TSEs). TSEs include a number of different diseases
affecting animals or humans including bovine spongiform encephalopathy (BSE) in
cattle, scrapie in sheep and goats, and Creutzfeldt-Jacob disease (CJD) in
humans. Although CWD shares certain features with other TSEs, it is a distinct
disease affecting only deer and elk. CWD is a progressive, fatal, degenerative
disease. Clinical signs in affected animals include loss of body condition,
behavioral changes, excessive salivation, increased drinking and urination,
depression, and eventual death. CWD is always fatal. There is no known
treatment, vaccine, or live animal test for CWD.
CWD Fact Sheet & Frequently Asked Questions
Iowa’s Voluntary CWD Surveillance Program
Cervidae Import Requirements
Cervidae Intrastate Requirements
Chronic Wasting Disease Alliance
For information on the CWD Voluntary Surveillance Program, contact Dee
Clausen, at 515-281-8236, Iowa Department of Agriculture & Land Stewardship,
Bureau of Animal Industry, Wallace Building, 2nd Floor, 502 East 9th Street, Des
Moines, IA 50319, or e-mail: Delores.clausen@iowaagriculture.gov
Animal Industry Bureau Iowa's Voluntary Chronic Wasting Disease
Surveillance Program
What Is The Iowa Department of Agriculture and Land Stewardship, Bureau of
Animal Industry Doing About CWD?
The Iowa Department of Agriculture has initiated the voluntary CWD
Surveillance Inventory Program which requires CWD surveillance, reporting, and
testing of those farmed cervidae 12 months of age and older that dies Elk
from any cause. Before any cervidae is imported into the state it must have
a Certificate of Veterinary Inspection (CVI - health certificate), permit issued
by our Department, meet Iowa’s import requirements (http://www.iowaagriculture.gov/animalIndustry/animalAdmissionRegs.asp),
and a review of the herd history. Since the start of the CWD surveillance
program in 2000, the farmed cervid producers have submitted over 5,556 brain
samples for CWD testing. If CWD is diagnosed in a farmed cervid, the farm would
be quarantined and the disease eradicated using recommended disease control
strategies. The threat of CWD is a serious concern to Iowa and the cervidae
industry. All practical steps to minimize the spreading of the disease are
taken. Requirements for the Iowa CWD Program include annual inventory
reconciliation recorded by a State District Veterinarian within 90 days of the
CWD anniversary date. Inventory requirements are:
1) Records shall be kept to document the history/accountability of all
animals in the herd. This includes identification, date of birth and sex of all
animals born or received on the premise. 2) All animals must have two forms of
official identification which are outlined in the Rules under 64.104 Definitions
“Official Cervid Identification”. 3) A copy of a health certificate (CVI)
properly filled out and signed by an accredited veterinarian shall be kept to
document movement in or out of the herd. Owners need to retain their health
certificates for at least five years. 4) Surveillance will be maintained by
collecting and submitting appropriate samples from all cases of mortality,
including slaughter, in animals 12 months of age and older, keeping copies of
the laboratory reports.
The CWD Program herd producers upon satisfactory completion of their annual
inventories will receive a letter of status verification, and a billfold size
certificate card with their herd’s status, CWD herd number, anniversary date,
and expiration date. Triennial Physical Herd Inventory Inspections: Physical
Inventories can be performed as part of an official herd test for tuberculosis
or brucellosis. Physical Herd Inventories are separate and different from Annual
Inventories conducted by our State District Veterinarians and the Physical Herd
Inventories are to be conducted triennially. Physical Herd Inventories will be
required for advancement in the program. Physical Herd Inventory completions are
allowed during the 90 days before or the 90 days after your herd’s expiration
date. A complete Physical Herd Inventory must provide verification to reconcile
all deer and verification of two approved individual identifications (one must
be a USDA official identification tag) with the records maintained by the owner.
All Cervid animals must have official identification tags before 12 months of
age. The owner must present the entire herd for the Physical Herd Inventory
inspection where the department, a state authorized veterinarian (accredited
veterinarian – their herd veterinarian) or authorized federal personnel can
safely read all identifications on the animals and be able to record all
identification devices. Attached Instructions for the CWD HCP Physical Herd
Inventory/Inspection and Chronic Wasting Disease Herd Certification Program
Agreement to be reviewed and completed by an accredited veterinarian and a
farmed cervid producer. A complete physical herd inventory must be performed at
the time a herd enrolls in the Chronic Wasting Disease Herd Certification
Program. Official Cervid Identification: All Cervid 12 months of age or older
(All Animals under 12 months of age leaving the premises), shall have a minimum
of two forms of animal identification.
USDA Approved with USDA shield - Information on official animal
identification devices can be found on the APHIS Traceability website at the
following address:
The second form of identification must be one that is approved by IDALS:
Unique material tag which provides unique animal identification and CWD herd
number.
DNR News Releases
Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee County
Hunting 2/4/2016 4:26:00 PM Return DES MOINES – Two wild deer harvested in
Allamakee County during the recent hunting season have been confirmed positive
for chronic wasting disease (CWD), marking the third year in a row the disease
has been confirmed in a wild Iowa deer, all in Allamakee County.
“This is disappointing but not altogether surprising,” said Dr. Dale
Garner, chief of Wildlife for the Iowa Department of Natural Resources. “This
region was a focal point for increased surveillance and thanks to hunters in the
area we exceeded our goal of 400 samples. Our next step is to host another
public meeting up there, listen to their concerns and discuss options available
going forward.”
The surveillance zone covered a 140 square mile area in eastern Allamakee
and northeast Clayton County, including the area near Harper’s Ferry. The two
recent CWD positive deer were harvested within two miles of where the previous
positive deer were taken.
Last year, local residents partnered with the Iowa Department of Natural
Resources to collect 85 additional samples after the regular deer seasons. None
of those deer collected tested positive for the disease.
The Iowa Department of Natural Resources is currently working to obtain as
much information as possible about the infected deer to implement its CWD
response plan.
CWD is a neurological disease affecting primarily deer and elk. It is
caused by an abnormal protein, called a prion that attacks the brains of
infected animals, causing them to lose weight, display abnormal behavior and
lose bodily functions. Signs include excessive salivation, thirst and urination,
loss of appetite, progressive weight loss, listlessness and drooping ears and
head. The only reliable test for CWD requires testing of lymph nodes or brain
material after the animal is dead.
There is currently no evidence that humans contract CWD by eating venison.
However, the World Health Organization and the Center for Disease Control and
Prevention recommend that hunters do not eat the brain, eyeballs or spinal cord
of deer and that hunters wear protective gloves while field dressing game and
boning out meat for consumption.
Prior to the positive detection in Iowa, CWD had been previously detected
in every bordering state.
Since 2002, nearly 60,000 wild deer from across the state have been
tested.
Tags Chronic Wasting Disease , CWD , Allamakee County , Iowa
CWD Cases in Iowa: Allamakee and Davis Counties In April 2014, the DNR was
notified that a deer harvested south of Harpers Ferry in Yellow River State
Forest during the 2013 regular gun season tested positive for CWD. This was the
first known case of CWD in a wild deer in the state. In January 2015 three more
CWD positives were reported for deer harvested in 2014 from Allamakee County.
The DNR is implementing a special CWD surveillance plan in Allamakee County
while continuing to implement its existing CWD testing protocols statewide.
As a result of public meetings on February 17, 2015 in Harper’s Ferry and
Waukon, the DNR and local constituents agreed to begin an intensive sample
collection effort in the surveillance area, defined as the sections adjacent to,
and including, the sections where the four positive animals were found. The goal
of this intensive surveillance is to provide more information on the extent and
prevalence of CWD in this area. This information will then be used to guide
decisions for future surveillance efforts and hunting seasons. Additional deer
will be collected beginning on February 21 until March 15th OR when an
additional 200 samples are obtained. The samples will bring the total number
collected in the intensive surveillance area to 300, which will provide a better
understanding of the extent and prevalence of CWD in this area. Only adult deer
will be sampled. Cooperators will be issued permits to collect deer in the
intensive surveillance area only through local DNR wildlife staff.
CWD Frequently Asked Questions General Chronic Wasting Disease (CWD)
information
Allamakee CWD Surveillance Area Map
*** In 2012, three deer tested positive for CWD on a shooting preserve
among captive deer in Davis County. This was the first time CWD was discovered
in the state. These positives were confirmed by the National Veterinary Services
Lab in Ames, Iowa. Below are the Emergency Order, the Emergency Consent Order,
and the Final Decision of the Natural Resource Commission related to the
discovery of CWD-positive deer at the preserve. On Feb. 13th, an Iowa District
Court Judge ruled that the Natural Resources Commission and Department of
Natural Resources do not have authority under current Iowa law to impose a
quarantine on the land and compel the owners to maintain fencing around the
former hunting preserve. That ruling is available on a link below. The Natural
Resources Commission has voted unanimously to appeal the district court ruling
and the Iowa Attorney General’s Office has filed a motion to stay the ruling
until the requested judicial review can take place.
From: Terry S. Singeltary Sr.
Sent: Sunday, January 24, 2016 8:51 PM
Subject: [BSE-L] IOWA CHRONIC WASTING TSE PRION DISEASE UPDATE
we have not heard much from IOWA lately on CWD from 2015 final hunt
results, to date, but here is the latest on their site on CWD TSE PRION...
IOWA CHRONIC WASTING TSE PRION DISEASE UPDATE
DNR To Continue Surveillance for Chronic Wasting Disease Hunting
11/17/2015 4:13:00 PM
The Iowa DNR’s wildlife staff will be collecting tissue samples during
Iowa’s shotgun deer seasons to test for the presence of Chronic Wasting Disease
(CWD) in Iowa’s wild deer herd.
The effort will concentrate in Allamakee County after four wild deer tested
positive for CWD, and on portions of northeast and eastern Iowa near Wisconsin
and Illinois, south-central Iowa near Missouri, as well as in Pottawattamie,
Cerro Gordo and Buchanan counties, following positive tests in the past from
captive facilities and wild deer in or near those counties.
Most of the 4,500 samples the DNR hopes to collect will be taken during the
first half of December, as more than 120,000 hunters take part in Iowa’s shotgun
deer seasons. Sampling involves removing and testing the brain stem and lymph
nodes of mature deer.
Many hunters voluntarily contribute samples of their harvested deer for
these testing efforts. Most samples are obtained by wildlife staff, checking
with hunters in the field or at home processing points.
Hunters willing to provide samples may contact the DNR regionally to
arrange collection. In Allamakee, Clayton and Winneshiek counties, call
563-380-3422; in Dubuque, Jackson, Clinton, Scott and Delaware counties, call
563-357-2035; in Davis, Wapello, Van Buren and Jefferson counties, call
641-799-0793; in Wayne, Appanoose and Monroe counties, call 641-203-6185; in
Pottawattamie County, call 712-350-0147; in Cerro Gordo County, call
641-425-2814; and in Buchanan County, call 319-213-2815.
Since 2002, more than 51,000 wild deer in Iowa have been tested, with four
positive CWD results in the wild herd detected in Allamakee County, the first in
2013.
Iowa DNR’s website provides information about CWD and other information on
infectious disease at: http://www.iowadnr.gov/Hunting/DeerHunting/CWDEHDInformation.aspx
CWD Cases in Iowa: Allamakee and Davis Counties
In April 2014, the DNR was notified that a deer harvested south of Harpers
Ferry in Yellow River State Forest during the 2013 regular gun season tested
positive for CWD. This was the first known case of CWD in a wild deer in the
state.
In January 2015 three more CWD positives were reported for deer harvested
in 2014 from Allamakee County. The DNR is implementing a special CWD
surveillance plan in Allamakee County while continuing to implement its existing
CWD testing protocols statewide.
As a result of public meetings on February 17, 2015 in Harper’s Ferry and
Waukon, the DNR and local constituents agreed to begin an intensive sample
collection effort in the surveillance area, defined as the sections adjacent to,
and including, the sections where the four positive animals were found. The goal
of this intensive surveillance is to provide more information on the extent and
prevalence of CWD in this area. This information will then be used to guide
decisions for future surveillance efforts and hunting seasons. Additional deer
will be collected beginning on February 21 until March 15th OR when an
additional 200 samples are obtained. The samples will bring the total number
collected in the intensive surveillance area to 300, which will provide a better
understanding of the extent and prevalence of CWD in this area. Only adult deer
will be sampled. Cooperators will be issued permits to collect deer in the
intensive surveillance area only through local DNR wildlife staff.
Allamakee CWD Surveillance Area Map
In 2012, three deer tested positive for CWD on a shooting preserve among
captive deer in Davis County. This was the first time CWD was discovered in the
state. These positives were confirmed by the National Veterinary Services Lab in
Ames, Iowa. Below are the Emergency Order, the Emergency Consent Order, and the
Final Decision of the Natural Resource Commission related to the discovery of
CWD-positive deer at the preserve.
On Feb. 13th, an Iowa District Court Judge ruled that the Natural Resources
Commission and Department of Natural Resources do not have authority under
current Iowa law to impose a quarantine on the land and compel the owners to
maintain fencing around the former hunting preserve.
That ruling is available on a link below.
The Natural Resources Commission has voted unanimously to appeal the
district court ruling and the Iowa Attorney General’s Office has filed a motion
to stay the ruling until the requested judicial review can take place.
◾ DNR Emergency Order, issued June 6, 2013
◾ DNR Emergency Consent Order, agreed upon July 3, 2013
◾Final Decision of the Natural Resource Commission, issued May 28, 2014
◾Iowa District Court Ruling February 13, 2015
Chronic Wasting Disease
In 2013– 2014 Iowa Department of Natural Resources (IDNR) staff collected
brainstems and medial retropharyngeal lymph nodes from 4,040 (62 targeted, 10%
road kills, 38% adult males) wild (Fig. 2) and 304 captive whitetail deer, 4
free-ranging elk, 1 red deer and 1 fallow deer for Chronic Wasting Disease (CWD)
testing. Twenty samples from wild deer, 3 from elk and the red and fallow deer
were submitted to the National Veterinary Services Laboratory in Ames, Iowa and
4,325 (4,020 wild and 304 captive deer and 1 free-ranging elk) samples were
submitted to Texas Veterinary Medical Diagnostic Laboratory. Although the
majority of samples (38%) from wild deer were collected from eleven counties in
northeast Iowa, the area closest to the Wisconsin and Illinois CWD endemic areas
and Minnesota’s southeast containment area, sampling effort also concentrated on
3 areas surrounding captive facilities that had animals test positive in Iowa in
2012. Twenty two percent were from south-central Iowa. This area is north of the
area where Missouri’s positive CWD deer have been found. Since 2002, Iowa has
tested 50,998 wild deer and 3,429 captive deer and elk. Three captive deer
collected by IDNR staff in 2012 tested positive for presence of PrP protein. On
April 8, 2014, notification was received from NVSL confirming CWD in a sample
collected from an adult wild male white-tailed deer harvested during the fall
firearms season in Allamakee County in northeast Iowa. This is the first
positive from wild deer to date. Efforts are currently underway to gather
additional information on the deer herd in the vacitinity where the positive
animal was harvested.
Iowa CWD sample location sites for wild deer, 2013-14.
Genetic Analysis of White-tailed Deer Population Structure in Iowa:
Identifying Potential Patterns and Rates of Disease Spread
Principal Investigator:
Julie Blanchong
Student Investigator: Lynne Gardner (Ph.D.)
Collaborators: Duration: June 2011 to December 2015 Funding
Source(s):
Iowa Department of Natural Resources (IDNR)
Goals and Objectives:
o Conduct a statewide assessment of deer population genetic structure in
Iowa to determine the scale of spatial autocorrelation and dispersal rates among
sampled areas across the state.
o Determine the degree of genetic connectivity between free-ranging deer
populations in Iowa and free-ranging deer populations in states bordering Iowa
where CWD has been detected in free-ranging and/or captive deer.
Progress:
White-tailed deer (Odocoileus virginianus) are a valued resource for
hunters, for viewing, and for state revenue. Knowledge of deer population
structure can provide insight into aspects of deer ecology (e.g., dispersal)
that are important for managing populations and understanding potential for
disease spread. The goal of this project is to use genetic techniques to
characterize deer population genetic structure in Iowa.
Lynne Gardner, a PhD student, began work on this project in August 2011. We
received several thousand deer tissue samples collected for the Iowa Department
of Natural Resource’s 2010-2011, 2011-2012, 2012-2013, and 2013-2014 CWD
surveillance efforts. In addition, we obtained deer tissue samples from captive
cervid facilities in Iowa. We received deer samples from deer harvests in two
urban communities and from surrounding rural populations. Deer tissue samples
have been received from Illinois, Indiana, Kansas, Minnesota, Nebraska, Ohio,
North Dakota, South Dakota, and Wisconsin, and Missouri. Some of these samples
may be used to characterize deer genetic structure beyond the state of
Iowa.
Genotyping of deer harvested in areas of low, medium, and high density in
Iowa at 10 microsatellite loci has been completed and mitochondrial DNA (mtDNA)
sequencing is nearly complete. We also completed genotyping deer samples from
two urban areas and samples from surrounding rural areas to document the degree
of connectivity between urban and rural deer. Preliminary results of this
urban-rural comparison were presented at the at the Iowa chapter of the Wildlife
Society annual meeting and the national Wildlife Society meeting.
Future Plans:
We have requested a no-cost extension of this project through December
2015. During this time, we will complete genetic data collection to identify
factors shaping deer genetic structure across the state of Iowa. Samples from
surrounding states may also be included. We will also complete data analyses for
all components of the project. Specifically, we will use the genetic data to a)
characterize the relationship between genetic structure and deer density, b)
characterize genetic connectivity between captive and free-ranging deer, c)
determine genetic connectivity between urban and rural deer in Iowa, and d)
identify factors shaping deer population genetic structure across the state of
Iowa. A final report will be completed by December 2015.
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease ***
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after gaining approval
from surrounding landowners, and confirmed that the fenced had been cut or
removed in at least four separate locations; that the fence had degraded and was
failing to maintain the enclosure around the Quarantined Premises in at least
one area; that at least three gates had been opened;and that deer tracks were
visible in and around one of the open areas in the sand on both sides of the
fence, evidencing movement of deer into the Quarantined Premises.
***79.8 percent of the deer tested positive for the disease ***
***test results from the depopulation of a quarantined captive deer herd in
north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested
positive for Chronic Wasting Disease (CWD). ***
For Immediate Release
Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov Share on facebook Share on twitter Share on
email Share on print More Sharing Services 1
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED
79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD). The owners of the
quarantined herd have entered into a fence maintenance agreement with the Iowa
Department of Agriculture and Land Stewardship, which requires the owners to
maintain the 8’ foot perimeter fence around the herd premises for five years
after the depopulation was complete and the premises had been cleaned and
disinfected
CWD is a progressive, fatal, degenerative neurological disease of farmed
and free-ranging deer, elk, and moose. There is no known treatment or vaccine
for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS)
National Veterinary Services Lab in Ames, IA confirmed that a male white tail
deer harvested from a hunting preserve in southeast IA was positive for CWD. An
investigation revealed that this animal had just been introduced into the
hunting preserve from the above-referenced captive deer herd in north-central
Iowa.
The captive deer herd was immediately quarantined to prevent the spread of
CWD. The herd has remained in quarantine until its depopulation on August 25 to
27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a
joint operation to depopulate the infected herd with USDA Veterinary Services,
which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised
the captive deer herd of 376 animals at that time, which was before depopulation
and testing, at $1,354,250. At that time a herd plan was developed with the
owners and officials from USDA and the Iowa Department of Agriculture and Land
Stewardship.
Once the depopulation was complete and the premises had been cleaned and
disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to
the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a
voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms
participate in the voluntary program. The above-referenced captive deer facility
left the voluntary CWD program prior to the discovery of the disease as they had
stopped selling live animals. All deer harvested in a hunting preserve must be
tested for CWD.
-30-
Elk Shot In Monona County Sunday Hunting, TIP and Poaching, Wildlife,
Nongame 11/9/2015 9:25:00 AM Return An elk of unknown origin in west central
Iowa was shot at the request of the Iowa Department of Natural Resources (DNR)
Sunday morning to protect the Iowa deer herd and domestic livestock from the
potential impacts of chronic wasting disease and other diseases.
Elk sightings in Iowa are fairly common and when an elk is spotted, the DNR
works with the Iowa Department of Agriculture and Land Stewardship to determine
status of elk and the best available options. If the elk can be returned to the
proper owners, then they are. If not, they then pose a risk to spreading CWD
and/or other diseases and are dispatched.
The bull elk, estimated at 3-4 years old, was killed Sunday morning by a
Monona County deputy sheriff as directed by the DNR after it appeared in front
of a farmer combining his field. The animal was examined for identification
markings without success and was buried according to Iowa livestock burial
regulations in Monona County Monday morning. The brain stem and lymph nodes were
removed for testing.
While the risk that escapees are introducing CWD or TB to Iowa’s wild deer
may be small, the consequence to the resource is enormous and it is a risk that
should be avoided.
Removing a wandering elk is the responsibility of the Iowa DNR working in
conjunction with the IDALS, and is not allowed by the public.
Iowa CWD sample location sites for wild deer, 2013-14.
Chronic Wasting Disease
In 2013– 2014 Iowa Department of Natural Resources (IDNR) staff collected
brainstems and medial retropharyngeal lymph nodes from 4,040 (62 targeted, 10%
road kills, 38% adult males) wild (Fig. 2) and 304 captive whitetail deer, 4
free-ranging elk, 1 red deer and 1 fallow deer for Chronic Wasting Disease (CWD)
testing. Twenty samples from wild deer, 3 from elk and the red and fallow deer
were submitted to the National Veterinary Services Laboratory in Ames, Iowa and
4,325 (4,020 wild and 304 captive deer and 1 free-ranging elk) samples were
submitted to Texas Veterinary Medical Diagnostic Laboratory. Although the
majority of samples (38%) from wild deer were collected from eleven counties in
northeast Iowa, the area closest to the Wisconsin and Illinois CWD endemic areas
and Minnesota’s southeast containment area, sampling effort also concentrated on
3 areas surrounding captive facilities that had animals test positive in Iowa in
2012. Twenty two percent were from south-central Iowa. This area is north of the
area where Missouri’s positive CWD deer have been found. Since 2002, Iowa has
tested 50,998 wild deer and 3,429 captive deer and elk. Three captive deer
collected by IDNR staff in 2012 tested positive for presence of PrP protein. On
April 8, 2014, notification was received from NVSL confirming CWD in a sample
collected from an adult wild male white-tailed deer harvested during the fall
firearms season in Allamakee County in northeast Iowa. This is the first
positive from wild deer to date. Efforts are currently underway to gather
additional information on the deer herd in the vacitinity where the positive
animal was harvested.
Iowa CWD sample location sites for wild deer, 2013-14.
Friday, February 05, 2016
IOWA Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee
County
Sunday, January 24, 2016
IOWA CHRONIC WASTING TSE PRION DISEASE UPDATE
Wednesday, October 07, 2015
Iowa DNR Meeting to Discuss Chronic Wasting Disease in Deer Set for Oct
13th in Bloomfield
Tuesday, January 20, 2015
Iowa Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee
County
Thursday, October 02, 2014
IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
Wednesday, April 09, 2014
Iowa : Chronic Wasting Disease Detected for First Time in Wild Iowa Deer
Sunday, December 08, 2013
IOWA DNR to Continue Surveillance for Chronic Wasting Disease CWD TSE PRION
DISEASE
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
*** Federal indemnity funding became available in 2014. USDA APHIS
appraised the captive deer herd of 376 animals at that time, which was before
depopulation and testing, at $1,354,250.
*** At that time a herd plan was developed with the owners and officials
from USDA and the Iowa Department of Agriculture and Land Stewardship.
*** Once the depopulation was complete and the premises had been cleaned
and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid
to the owners as compensation for the 356 captive deer depopulated.
SEE A FEW OF WISCONSIN CWD ENTITLEMENT PAYOUTS TO CAPTIVE OWNERS ;
$298,770 + $465,000
Sunday, January 17, 2016
Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of $298,770
for 228 white-tailed deer killed on farm
this does not look good ;
Tuesday, January 19, 2016
Wisconsin Second CWD-positive deer found in Oneida County 5-year-old buck
shot at Three Lakes Trophy Ranch LLC agency received the CWD-positive report on
the animal Dec. 29
Sunday, July 17, 2016
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
***
Tuesday, April 12, 2016
The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging
reindeer from the Nordfjella population in South-Norway.
Tuesday, June 14, 2016
*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag
Norway ***
Thursday, July 07, 2016
Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd
Norwegian moose
14/06/2016 - Norway reports a third case
Saturday, July 16, 2016
Chronic wasting Disease in Deer (CWD or Spongiform Encephalopathy) The
British Deer Society 07/04/2016
*** IOWA CREUTZFELDT JAKOB DISEASE CJD SURVEILLANCE AND REPORTING
2016
*** CJD TSE PRION IN HUMANS IS STILL NOT REPORTABLE IN IOWA. ...TSS
*** IOWA HUMAN TSE PRION CJD NOT REPORTABLE 2016 ***
PERSONAL COMMUNICATIONS WITH THE STATE OF IOWA HEALTH DEPARTMENT INFECTIOUS
DISEASE ...TSS
I did just a quick search of cjd victims in Iowa, and there were so many, I
stopped counting...this was just first few pages...terry
2015
Mary Jo HansellDes MoinesMary Jo Hansell, 63, passed away September 7,
2015.
Mary Jo LOVED spending time with family and friends, traveling and
shopping. She spent her 43 year career at UnityPoint where she touched countless
lives as a nurse and educator.
In lieu of flowers, memorials may be directed to Creutzfeldt Jakob's
Disease research www.cjdfoundation.org.
David Lee Bearman, age 68 of Nashua, IA, died Sunday, August 9, 2015, at
his home due to complications from the Creutzfeldt-Jakob disease.
2013
John Raymond "Doc" Sievert, the son of Johnnie and Jean (Welch) Sievert,
was born November 16, 1945, in Heron Lake, Minnesota. He passed away Saturday,
May 25, 2013, at his home in Estherville, Iowa, from Creutzfeldt-Jakob disease
(CJD), at the age of 67.
Charles Bruce Belknap, age 75, of Wilton, IA, died on Wednesday, November
6, 2013 at Carrington Place, Muscatine, IA, following a battle with Creutzfeldt
- Jakob Disease (CJD).
2012
Kock passed away early Tuesday morning, September 25, 2012, at the Carroll
Health Center due to Creutzfeldt - Jakob disease, which he had been fighting
since June but which had been diagnosed just 12 days earlier.
He worked in the pork industry his entire career, first with DeKalb Swine
Breeders and then in the Livestock Production division of Farmland Industries.
In 2000, he was hired by Allied Producers Cooperative to raise funds and solicit
members, and the group eventually invested into the newest packing plant in the
country, Triumph Foods in St. Joseph, Mo. As general manager, he has been
instrumental in the co-op’s success, and he enjoyed the friendship of the people
he met all over the Midwest because of his work.
Kathryn E. ReicksWaukeeKathryn E. (Vagher) Reicks passed away at 12:50 a.m.
on Friday, February 17, 2012 -
Kathy was born in Bristol, CO on May 8, 1950 to John P. and Kathryn Vagher.
She was raised in Gary, IN by her sister and brother-in-law (Louis and Georgia
Robinette). Kathy met Tom when he was on leave from the navy. They married and
moved to Iowa, they raised their family in Des Moines -
Donations are being accepted in lieu of flowers. The family would like to
use these donations to help researchers find a cure for Creutzfeldt-Jakob
Disease (CJD).
2010
SIOUX CITY -- James Lee Lofgren, 60, of Omaha, formerly of Sioux City,
passed away Oct. 21, 2010, in McKinney, Texas, after a long battle with
Creutzfeldt-Jakob Disease. http://siouxcityjournal.com/news/local/obituaries/james-l-lofgren/article_adeeb496-284b-5992-91ed-e836c541a981.html
2009
2009 IDPH: CJD cases rare, but do occur in Iowa
Posted: Jan 02, 2009 1:24 PM CST Friday, January
2, 2009 2:24 PM EST
DES MOINES (KWWL) -- The Iowa Department of Public Health says it sees
about 3 cases of Sporadic Creutzfeldt-Jakob Disease (CJD) a year.
Relatives of a Charles City man told KWWL Thomas Squier, 60, died of
sporadic CJD at his home Wednesday. Creutzfeldt-Jakob disease (CJD) is a rare,
degenerative, invariably fatal brain disorder. Typically, onset of symptoms
occurs at about age 60.
"This is a genetic disease, it is not a virus, it is not a bacteria.
Sporadic CJD has nothing to do with the Mad Cow disease that surfaced in
England, it's just a different prion disease," said IDPH Medical Director
Patricia Quinslik.
Quinslik says the department can't comment on specific cases or people but
tells KWWL people who get sporadic CJD seem to have a gene that codes this prion
protein that naturally develops into an abnormal form later in life which leads
to the disease. The IDPH says right now there are no risks or threats to the
general public.
"Anyone diagnosed with sporadic CJD can not spread the disease. The only
way to spread it would be through some sort of transplant to another human. New
health regulations in the United States state prevent doctors from transplanting
any organs from someone diagnosed with sporadic CJD," Quinslik said.
Quinslik also adds "All the cases of CJD ever reported in Iowa have been
the "Classic" form, not the "Variant" form which is related to Mad Cow. We've
never had a case of Variant CJD in Iowa. There have only been 3 cases of variant
CJD in the US, but those people contracted the disease overseas."
CJD is referred to as the human form of mad cow. However, The Centers for
Disease Control and Prevention says Classic CJD is not related to "mad cow"
disease. "Variant CJD", another prion disease is related to bovine spongiform
encephalopathy (BSE) or Mad Cow Disease. Squier's family told KWWL doctors gave
Thomas a 90% diagnosis of Classic CJD.
The IDPH says all the cases of CJD ever reported in Iowa have been the
"Classic" form, not the "Variant" form which is related to Mad Cow.
"We've never had a case of Variant CJD in Iowa. There have only been 3
cases of variant CJD in the US, but those people contracted the disease
overseas," Quinslik said.
KWWL has taken a few calls and emails from local cattle farmers concerned
about the TV station showing video of animals infected with mad cow
disease.
"The only reason we used the video on Thursday was to show people how CJD
symptoms in humans mirror those of mad cow disease in animals. There was video
available of humans suffering from the disease, but we did not air that video
out of respect for the family," said KWWL News Director JJ Murray.
KWWL chose to run the story because we received numerous calls and e-mails
from people in Floyd County who were worried about mad cow disease rumors
spreading through the community.
"We are not trying to create a panic by any means. As far as we know, there
is no threat to humans, there is no proof this person contracted the disease by
any other means than a naturally developing disease. Our goal is to simply
educate the public about this disease," Murray said.
The Iowa Department of Public Health says there is no threat of mad cow
disease in Iowa or the United States.
"In this country we feed our cows vegetable protein, not animal protein.
Therefore mad cow can not spread from cow to cow in this country as it did in
Europe and thus can not get into the human food chain," said Quinslik.
Laura Jean Fletcher August 6, 1946 July 26, 2007 Laura passed peacefully at
her home in San Carlos surrounded by family and friends after a short battle
with Creutzfeldt-Jakob Disease.
Vicki Yoder, 59, of 79 Heron Circle, Iowa City, died Thursday, June 30,
2005, after a graceful battle with Creutzfeldt-Jakob Disease.
NEUFELD, Lisa Marie...lived a wonderful life, and died March 22, 2010, in
Tehachapi of a rate brain disease known as Creutzfeldt-Jakob’s Disease (CJD).
She was 43 years old...
2016
CHRONIC WASTING DISEASE TSE PRION ZOONOSIS
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
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
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.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
===========================================================
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.
============================================================
Key Molecular Mechanisms of TSEs
Zabel, Mark D.
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs),
are fatal neurodegenerative diseases affecting humans, cervids, bovids, and
ovids. The absolute requirement of PrPC expression to generate prion diseases
and the lack of instructional nucleic acid define prions as unique infectious
agents. Prions exhibit species-specific tropism, inferring that unique prion
strains exist that preferentially infct certain host species and confront
transmission barriers to heterologous host species. However, transmission
barriers are not absolute. Scientific consensus agrees that the sheep TSE
scrapie probably breached the transmission barrier to cattle causing bovine
spongiform encephalopathy that subsequently breached the human transmission
barrier and likely caused several hundred deaths by a new-variant form of the
human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human
health, emotion and economies can still be felt in areas like farming, blood and
organ donations and the threat of a latent TSE epidemic. This precedent raises
the real possibility of other TSEs, like chronic wasting disease of cervids,
overcoming similar human transmission barriers. A groundbreaking discovery made
last year revealed that mice infected with heterologous prion strains facing
significant transmission barriers replicated prions far more readily in spleens
than brains6. Furthermore, these splenic prions exhibited weakened transmission
barriers and expanded host ranges compared to neurogenic prions. These data
question conventional wisdom of avoiding neural tissue to avoid prion
xenotransmission, when more promiscuous prions may lurk in extraneural tissues.
Data derived from work previously funded by NIH demonstrate that Complement
receptors CD21/35 bind prions and high density PrPC and differentially impact
prion disease depending on the prion isolate or strain used. Recent advances in
live animal and whole organ imaging have led us to generate preliminary data to
support novel, innovative approaches to assessing prion capture and transport.
We plan to test our unifying hypothesis for this proposal that CD21/35 control
the processes of peripheral prion capture, transport, strain selection and
xenotransmission in the following specific aims.
1. Assess the role of CD21/35 in splenic prion strain selection and host
range expansion.
2. Determine whether CD21/35 and C1q differentially bind distinct prion
strains
3. Monitor the effects of CD21/35 on prion trafficking in real time and
space
4. Assess the role of CD21/35 in incunabular prion trafficking
Public Health Relevance Transmissible spongiform encephalopathies, or prion
diseases, are devastating illnesses that greatly impact public health,
agriculture and wildlife in North America and around the world. The impact to
human health, emotion and economies can still be felt in areas like farming,
blood and organ donations and the threat of a latent TSE epidemic. This
precedent raises the real possibility of other TSEs, like chronic wasting
disease (CWD) of cervids, overcoming similar human transmission barriers. Early
this year Canada reported its first case of BSE in over a decade audits first
case of CWD in farmed elk in three years, underscoring the need for continued
vigilance and research. Identifying mechanisms of transmission and zoonoses
remains an extremely important and intense area of research that will benefit
human and other animal populations.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Allergy and Infectious Diseases (NIAID)
Type High Priority, Short Term Project Award (R56)
Project # 1R56AI122273-01A1
Application # 9211114
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Beisel, Christopher E
Project Start 2016-02-16
Project End 2017-01-31
Budget Start 2016-02-16
Budget End 2017-01-31
Support Year 1
Fiscal Year 2016
Total Cost
Indirect Cost Institution Name Colorado State University-Fort Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
PMCA Detection of CWD Infection in Cervid and Non-Cervid Species
Hoover, Edward Arthur
Colorado State University-Fort Collins, Fort Collins, CO, United States
Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly
transmissible prion disease now recognized in 18 States, 2 Canadian provinces,
and Korea. We have shown that Infected deer harbor and shed high levels of
infectious prions in saliva, blood, urine, and feces, and in the tissues
generating those body fluids and excreta, thereby leading to facile transmission
by direct contact and environmental contamination. We have also shown that CWD
can infect some non-cervid species, thus the potential risk CWD represents to
domestic animal species and to humans remains unknown. Whether prions borne in
blood, saliva, nasal fluids, milk, or excreta are generated or modified in the
proximate peripheral tissue sites, may differ in subtle ways from those
generated in brain, or may be adapted for mucosal infection remain open
questions. The increasing parallels in the pathogenesis between prion diseases
and human neurodegenerative conditions, such as Alzheimer's and Parkinson's
diseases, add relevance to CWD as a transmissible protein misfolding disease.
The overall goal of this work is to elucidate the process of CWD prion
transmission from mucosal secretory and excretory tissue sites by addressing
these questions: (a) What are the kinetics and magnitude of CWD prion shedding
post-exposure? (b) Are excreted prions biochemically distinct, or not, from
those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the
source of excreted prions? and (d) Are excreted prions adapted for horizontal
transmission via natural/trans-mucosal routes? The specific aims of this
proposal are: (1) To determine the onset and consistency of CWD prion shedding
in deer and cervidized mice; (2); To compare the biochemical and biophysical
properties of excretory vs. CNS prions; (3) To determine the capacity of
peripheral tissues to support replication of CWD prions; (4) To determine the
protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To
compare the mucosal infectivity of excretory vs. CNS prions. Understanding the
mechanisms that enable efficient prion dissemination and shedding will help
elucidate how horizontally transmissible prions evolve and succeed, and is the
basis of this proposal. Understanding how infectious misfolded proteins (prions)
are generated, trafficked, shed, and transmitted will aid in preventing,
treating, and managing the risks associated with these agents and the diseases
they cause.
Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an
emergent highly transmissible prion disease now recognized throughout the USA as
well as in Canada and Korea. We have shown that infected deer harbor and shed
high levels of infectious prions in saliva, blood, urine, and feces thereby
leading to transmission by direct contact and environmental contamination. In
that our studies have also shown that CWD can infect some non-cervid species,
the potential risk CWD may represents to domestic animal species and humans
remains unknown. The increasing parallels in the development of major human
neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and
prion diseases add relevance to CWD as a model of a transmissible protein
misfolding disease. Understanding how infectious misfolded proteins (prions) are
generated and transmitted will aid in interrupting, treating, and managing the
risks associated with these agents and the diseases they cause.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 4R01NS061902-07
Application # 9010980
Study Section Cellular and Molecular Biology of Neurodegeneration Study
Section (CMND)
Program Officer Wong, May Project Start 2009-09-30
Project End 2018-02-28
Budget Start 2016-03-01
Budget End 2017-02-28
Support Year 7
Fiscal Year 2016
Total Cost $409,868
Indirect Cost $134,234 Institution Name Colorado State University-Fort
Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
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.
*** now, let’s see what the authors said about this casual link, personal
communications years ago, and then the latest on the zoonotic potential from CWD
to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS
casual evidence ???? “Our conclusion stating that we found no strong evidence of
CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
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
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
SCRAPIE AND CWD ZOONOSIS
PRION 2016 CONFERENCE TOKYO
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Transmission of scrapie prions to primate after an extended silent
incubation period
***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.***
Wednesday, June 29, 2016
CWD, SCRAPIE, ZOONOSIS, it’s for real folks, the risk factors have
increased greatly, and science has spoken, cwd and scrapie to humans as sporadic
cjd may have already happened.
Transmission of scrapie prions to primate after an extended silent
incubation period
Emmanuel E. Comoy , Jacqueline Mikol , Sophie Luccantoni-Freire , Evelyne
Correia , Nathalie Lescoutra-Etchegaray , Valérie Durand , Capucine Dehen ,
Olivier Andreoletti , Cristina Casalone , Juergen A. Richt , Justin J. Greenlee
, Thierry Baron , Sylvie L. Benestad , Paul Brown & Jean-Philippe Deslys
Abstract
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion
disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD)
in humans and having guided protective measures for animal and human health
against animal prion diseases. Recently, partial transmissions to humanized mice
showed that the zoonotic potential of scrapie might be similar to c-BSE. We here
report the direct transmission of a natural classical scrapie isolate to
cynomolgus macaque, a highly relevant model for human prion diseases, after a
10-year silent incubation period, with features similar to those reported for
human cases of sporadic CJD. Scrapie is thus actually transmissible to primates
with incubation periods compatible with their life expectancy, although fourfold
longer than BSE. Long-term experimental transmission studies are necessary to
better assess the zoonotic potential of other prion diseases with high
prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98
scrapie.
snip...
In addition to previous studies on scrapie transmission to primate1,8,9 and
the recently published study on transgenic humanized mice13, our results
constitute new evidence for recommending that the potential risk of scrapie for
human health should not be dismissed. Indeed, human PrP transgenic mice and
primates are the most relevant models for investigating the human transmission
barrier. To what extent such models are informative for measuring the zoonotic
potential of an animal TSE under field exposure conditions is unknown. During
the past decades, many protective measures have been successfully implemented to
protect cattle from the spread of c-BSE, and some of these measures have been
extended to sheep and goats to protect from scrapie according to the principle
of precaution. Since cases of c-BSE have greatly reduced in number, those
protective measures are currently being challenged and relaxed in the absence of
other known zoonotic animal prion disease. We recommend that risk managers
should be aware of the long term potential risk to human health of at least
certain scrapie isolates, notably for lymphotropic strains like the classical
scrapie strain used in the current study. Relatively high amounts of infectivity
in peripheral lymphoid organs in animals infected with these strains could lead
to contamination of food products produced for human consumption. Efforts should
also be maintained to further assess the zoonotic potential of other animal
prion strains in long-term studies, notably lymphotropic strains with high
prevalence like CWD, which is spreading across North America, and atypical/Nor98
scrapie (Nor98)50 that was first detected in the past two decades and now
represents approximately half of all reported cases of prion diseases in small
ruminants worldwide, including territories previously considered as scrapie
free. Even if the prevailing view is that sporadic CJD is due to the spontaneous
formation of CJD prions, it remains possible that its apparent sporadic nature
may, at least in part, result from our limited capacity to identify an
environmental origin.
***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.***
2015
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==============
*** 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
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
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.***
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
Monday, April 04, 2016
Limited amplification of chronic wasting disease prions in the peripheral
tissues of intracerebrally inoculated cattle
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
J Vet Diagn Invest 20:698–703 (2008)
Chronic wasting disease in a Wisconsin white-tailed deer farm
Delwyn P. Keane,1 Daniel J. Barr, Philip N. Bochsler, S. Mark Hall, Thomas
Gidlewski, Katherine I. O’Rourke, Terry R. Spraker, Michael D. Samuel
Abstract.
In September 2002, chronic wasting disease (CWD), a prion disorder of
captive and wild cervids, was diagnosed in a white-tailed deer (Odocoileus
virginianus) from a captive farm in Wisconsin. The facility was subsequently
quarantined, and in January 2006 the remaining 76 deer were depopulated. Sixty
animals (79%) were found to be positive by immunohistochemical staining for the
abnormal prion protein (PrPCWD) in at least one tissue; the prevalence of
positive staining was high even in young deer. Although none of the deer
displayed clinical signs suggestive of CWD at depopulation, 49 deer had
considerable accumulation of the abnormal prion in the medulla at the level of
the obex. Extraneural accumulation of the abnormal protein was observed in 59
deer, with accumulation in the retropharyngeal lymph node in 58 of 59 (98%), in
the tonsil in 56 of 59 (95%), and in the rectal mucosal lymphoid tissue in 48 of
58 (83%). The retina was positive in 4 deer, all with marked accumulation of
prion in the obex. One deer was considered positive for PrPCWD in the brain but
not in the extraneural tissue, a novel observation in white-tailed deer. The
infection rate in captive deer was 20- fold higher than in wild deer. Although
weakly related to infection rates in extraneural tissues, prion genotype was
strongly linked to progression of prion accumulation in the obex. Antemortem
testing by biopsy of recto– anal mucosal-associated lymphoid tissue (or other
peripheral lymphoid tissue) may be a useful adjunct to tonsil biopsy for
surveillance in captive herds at risk for CWD infection.
Key words: Cervids; chronic wasting disease; prion; transmissible
spongiform encephalopathy.
State pays farmer $298,000 for infected deer herd
Jan. 16, 2016 8:05 p.m.
The State of Wisconsin paid nearly $300,000 to the Eau Claire County farmer
whose deer herd was depopulated after it was found to be infected with chronic
wasting disease.
Rick Vojtik, owner of Fairchild Whitetails in Fairchild, received an
indemnity payment of $298,770 for 228 white-tailed deer killed on his farm,
according to officials with the Department of Agriculture, Trade and Consumer
Protection.
The money was taken from the agency's general program revenue funded by
Wisconsin taxpayers.
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after gaining approval
from surrounding landowners, and confirmed that the fenced had been cut or
removed in at least four separate locations; that the fence had degraded and was
failing to maintain the enclosure around the Quarantined Premises in at least
one area; that at least three gates had been opened;and that deer tracks were
visible in and around one of the open areas in the sand on both sides of the
fence, evidencing movement of deer into the Quarantined Premises.
The overall incidence of clinical CWD in white-tailed deer was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base
Scrapie TSE Prion Experiment 1964
*** 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...
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards
Singeltary Comment Submission
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
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
Sunday, July 17, 2016
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild
http://chronic-wasting-disease.blogspot.com/2016/02/report-of-committee-on-wildlife.html
P.S. PLEASE NOTE ;
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.
Wednesday, May 25, 2016
*** USDA APHIS National Scrapie TSE Prion Eradication Program April 2016
Monthly Report Prion 2016 Tokyo Update
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND
SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
Saturday, July 16, 2016
Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS,
are working to further legalize the trading of Transmissible Spongiform
Encephalopathy TSE Pion disease around the globe.
THIS is absolutely insane. it’s USDA INC.
NEEDLESS CONFLICT
http://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Terry S. Singeltary Sr.
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