Friday, July 29, 2016

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.
 
 
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
 
 
 
 
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.