Report of the Committee on Wildlife Diseases Chronic Wasting Disease CWD
TSE Prion
Report of the Committee on Wildlife Diseases
Chair: Colin Gillin, OR
Vice Chair: Peregrine Wolff, NV
Gary Anderson, KS; Paul Anderson, MN; Karen Beck, NC; Scott Bender, AZ;
Warren Bluntzer, TX; Tom Bragg, NE; Rhonda Brakke, IA; Dwight Bruno, NY; Beth
Carlson, ND; Matt Cochran, TX; Walter Cook, TX; Joseph Corn, GA; Susan Culp, TX;
Thomas DeLiberto, CO; Barbara Determan, IA; Mark Drew, ID; James Evermann, WA;
Anna Claire Fagre, CO; John Fischer, GA; Richard French, NH; Francis Galey, WY;
Tam Garland, TX; Donna Gatewood, IA; Robert Gerlach, AK; Paul Gibbs, FL; Linda
Glaser, MN; Paul Grosdidier, KS; Greg Hawkins, TX; Kristi Henderson, IL; Terry
Hensley, TX; Linda Hickam, MO; Robert Hilsenroth, FL; Donald Hoenig, ME; Dennis
Hughes, NE; David Hunter, MT; Susan Keller, ND; Diane Kitchen, FL; Patrice
Klein, MD; Todd Landt, IA; T.R. Lansford, TX; Charles Lewis, IA; Tsang Long Lin,
IN; Jim Logan, WY; Linda Logan, TX; Travis Lowe, MN; Mark Luedtke, MN; Margie
Lyness, GA; David Marshall, NC; Chuck Massengill, MO; Daniel Mead, GA; Robert
Meyer, CO; Myrna Miller, WY; Eric Mohlman, NE; Yvonne Nadler, IL; Julie Napier,
NE; Cheryl Nelson, KY; Mitchell Palmer, IA; William Parker, GA; William
Pittenger, MO; Jewell Plumley, WV; Kate Purple, TN; Jennifer Ramsey, MT; Jack
Rhyan, CO; Justin Roach, OK; Jonathan Roberts, LA; Shawn Schafer, OH; David
Schmitt, IA; Dennis Schmitt, MO; Brant Schumaker, WY; Marc Schwabenlander, MN;
Andy Schwartz, TX; Charly Seale, TX; Laurie Seale, WI; Daryl Simon, MN; Jonathan
Sleeman, WI; Robert Temple, OH; Lee Ann Thomas, MD; Brad Thurston, IN; Curt
Waldvogel, OH; Michele Walsh, ME; Skip West, OK; Ellen Wiedner, FL; Margaret
Wild, CO; Richard Willer, HI; Michelle Willette, MN; Ellen Mary Wilson, NM;
William Wilson, KS; David Winters, TX; Richard Winters, Jr., TX; Cindy Wolf, MN;
Mary Wood, WY; Marty Zaluski, MT; Glen Zebarth, MN.
The Committee met on October 25, 2015 at the Rhode Island Convention Center
in Providence, Rhode Island from 1230-5PM. There were 43 members and 59 guests
present. Chairperson Colin Gillin welcomed the membership and guests to the 2015
Committee meeting on Wildlife Diseases and read the committee purpose and
discussed committee membership and how to become a member. He also discussed the
process of submitting recommendations and resolutions and asked for any new
business, of which, there was none forwarded. There were no resolutions from
this committee from 2014 and one proposed resolution submitted by a committee
member for 2015. This resolution was emailed to the listed membership 10 days
prior to the committee meeting for review.
snip...
Summary of Recent Chronic Wasting Disease events in Texas
Mitch Lockwood, Texas Parks and Wildlife Department
Bob Ditmar (TPWD), Andy Schwartz, Texas Animal Health Commission
Introduction:
• 3.9 million free-ranging white-tailed deer
• 700K white-tailed deer hunters
• 600K white-tailed deer harvested annually
• $3.6 billion economic output for all hunting
• $2.1 billion for deer hunting
• 1,300 deer breeding facilities
• > 110,000 deer in breeding facilities
• > 2,200 free-ranging deer moved annually through various permits
Texas Parks and Wildlife Department (TPWD) has been conducting CWD
surveillance throughout the state since 2002. Biologists have collected more
than 26,000 samples from hunter-harvested deer, and others have collected more
than 21,000 samples in order to meet TPWD permitting requirements, totaling
almost 48,000 samples. Additionally, Texas Animal Health Commission (TAHC) has
maintained a Voluntary CWD Herd Certification Program since 1995.
In 2012, CWD was discovered in 2 mule deer samples from far West Texas
(Hueco Mountains) as a result of a targeted surveillance effort. This area is
directly adjacent to a region in New Mexico with documented CWD occurrence. To
date, five more positive samples have been obtained from this population through
hunter harvested mule deer, indicating a disease prevalence of 10%.
Mule deer and white-tailed deer are regulated by TPWD, while other
susceptible species (including elk) are regulated by the TAHC. This has
generated the need for enhanced coordination and communication between these two
agencies. The TPWD/TAHC CWD Management Plan was developed by both agencies in
consultation with the state’s CWD Task Force. The Task Force is comprised of
wildlife biologists, deer and elk breeders, veterinarians and other
animal-health experts from TPWD, TAHC, Texas Veterinary Medical Diagnostic
Laboratory, Texas Department of State Health Services, Texas A&M College of
Veterinary Medicine, and USDA. The plan includes mandatory check stations for
susceptible species taken inside the CWD Containment Zone, which covers portions
of Hudspeth, Culberson, and El Paso counties. Artificial movement of deer is
prohibited in the CWD Containment Zone.
On June 30, 2015 a sample from a Medina County (area on border of southern
Edwards Plateau and northern South Texas Plains ecoregions) deer breeding
facility was confirmed positive for CWD. The index breeding facility
participated in TAHC’s voluntary CWD Herd Certification Program, and had tested
62 of 65 mortalities prior to June 2015 (60 not detected, 2 location results)
since permitted in 2006. There were a total of 136 adult deer in the inventory
on June 30, 2015, and the herd was considered to be relatively young.
During the previous 5 years, 107 deer were transferred from 30 deer
breeding facilities into the index facility. During that same period, 835 were
transferred from the index facility to 147 different facilities including 96
deer breeding facilities, 46 release sites, 3 DMP sites, and 2 sites in
Mexico.
TPWD and TAHC immediately placed a temporary moratorium on movements of all
captive deer in the state, and TAHC placed a Hold Order on the 177 “Tier 1”
facilities. Since then, TPWD and TAHC worked with the CWD Task Force and
industry stakeholders to develop a plan to lift the moratorium on deer
transfers, which includes additional CWD testing requirements in deer breeding
facilities or on registered release sites. Additionally, TAHC has removed the
Hold Order for 120 facilities, leaving a total 57 facilities remaining under a
Hold Order as of October 16, 2015. Most deer breeding facilities were authorized
to transfer deer by August 24, 2015.
Depopulation at the index facility was initiated in July 28 and completed
on September 30, 2015. CWD was detected in a total of 4 (out of 136 adults)
white-tailed deer in the index facility, all of which were 2-year-old bucks that
were natural additions.
On September 15, 2015, CWD was confirmed in one of the trace-forward
facilities, from which 84 deer had transferred out to 9 different facilities (5
deer breeding facilities, 3 release sites, and 1 nursing facility) since it
received deer from the index herd. This resulted in 7 additional Hold Orders
being issued by TAHC, 4 of which have since been released. The CWD-positive at
the trace-forward facility was also a 2-year-old buck that was born in the index
facility.
In summary, CWD has been detected in a total of 5 captive white-tailed deer
in Texas, 4 of which were located in the index facility, and 1 was located in a
trace-forward facility. There are 36 deer from the 2-year-old cohort originating
in the index facility that are reported to be alive in 7 deer breeding
facilities, and possibly as many as 6 deer from that cohort still alive on
release sites. Additionally, there are 33 deer that traced through the index
facility that are still alive in 15 deer breeding facilities, and possibly as
many as 51 trace-through deer are still alive on 24 different release sites, and
2 trace-through deer may still be alive in Mexico.
TPWD has intensified the statewide CWD surveillance efforts, with a goal to
collect samples from more than 8,000 hunter-harvested deer, including 300
samples within a 5-mile radius of the index facility. TAHC will continue to
pursue indemnity on exposed deer located in trace-forward facilities in an
attempt to conduct a more thorough epidemiological investigation. TPWD and TAHC
have committed to reevaluate movement qualification standards that apply to deer
breeding facilities and release sites following the 2015-16 hunting season. Both
agencies are exploring ante-mortem testing protocols, and will continue to seek
guidance from experts in the field.
Epidemiology of Recent CWD Cases in Ohio
Susan Skorupski, Assistant Director, USDA-APHIS-VS
Background
Ohio has had a voluntary Chronic Wasting Disease (CWD) Herd Certification
Program for all cervidae for at least 12 years.
Ohio has 331 cervidae herds in the CWD monitoring program with 256 at
Certified level. In October 2012, Ohio White Tail Deer rule became effective. It
includes several categories of white tail deer operations. Monitored Herds
cannot sell or give away animals and includes hunting preserves. Under this
rule, hunting preserves cannot move live animals from the premises and must
annually sample 30 animals or 30% of harvested deer, based on the number of deer
harvested during the previous year. Herds with Status are herds enrolled in the
CWD Certification Program but not yet at certified level. Certified Status Herds
are enrolled in the CWD monitoring program and have reached certified status.
Ohio has 135 Monitored Herds, including 24 hunting preserves, 75 Herds with
Status, and 256 Certified Status herds.
Ohio’s approach to infected animals and associated animals and herds
Infected herd – herd where a CWD infected animal resided when the test
positive sample was collected. Herd quarantined.
Exposed herd – any herd where an animal that tested CWD positive has
resided within the 5 years before the CWD diagnosis. Whole herd
quarantined
Herd that contains an exposed animal – whole herd quarantined unless
epidemiology information suggests the animal is of lower risk of spreading
CWD.
Exposed animal – animal that was exposed to the CWD infected animal any
time during the five years prior to when the animal died or was euthanized and
sampled/tested positive for CWD.
Recent CWD history in Ohio
a.Pennsylvania traces
In the spring of 2014, Ohio received information on traces associated with
CWD positive cases in Pennsylvania. Three Ohio herds were designated as Exposed
herds because positive deer from infected herds in PA had been in the Ohio herd
s during the previous 5 years. Fifty Ohio herds received 256 exposed deer from
the 5 PA herds and 3 Ohio exposed herds. 85 of those animals were tested with
Not Detected results in Ohio herds. 66 animals were traced to Out of State
herds. That leaves 101 animals either standing in quarantined herds or not
tested when they died or were harvested. 18 herds/preserves remain under
quarantine.
b. First CWD positive found in Ohio
On October 22, 2014, National Veterinary Services Laboratory (NVSL)
confirmed a CWD positive result for a 2.5 year old buck killed at a hunting
preserve in Holmes County Ohio on October 2, 2014. The hunting preserve had been
under quarantine since April 1, 2014 because of PA traces and was required to do
100% sampling of harvested deer. The positive animal had official identification
tracing the animal to a CWD certified Pennsylvania herd. Records including a
Certificate of Veterinary Inspection indicate the animal moved to Ohio March 13,
2013. Genetic testing was conducted to support the accuracy of the trace to the
Pennsylvania herd. This herd was depopulated without indemnity April 27-29,
2015. 224 animals were depopulated at owner expense and sampled for CWD. All
tests had Not Detected results for CWD. The premises was evaluated as a
minimally contaminated facility. No cervidae have been added to the premises at
this time.
The owner of the hunting preserve business also owns or is associated with
breeding herds at other locations in Holmes County.
c. Second positive premises in Ohio
A white tail deer breeding herd owned by the same person who owned the CWD
positive hunting preserve was designated as a positive herd in the spring of
2015. A CWD positive animal was sampled on 3/12/2015 and reported on March 25,
2015. The animal was a 5 year old whitetail doe purchased from a Wisconsin herd
in February 2013. A second CWD positive animal was reported from this herd on
May 22, 2015. This animal was a 1.5 year old natural addition doe. This herd was
initially established in the fall of 2012 with the purchase of a CWD certified
herd from the estate of a deceased owner. In the spring and fall of 2013,
additional animals were added from at least 9 OH herds , 1 WI herd, 17 PA herds,
and 3 IN herds. This herd had been quarantined since April 1,2014 because of
traces from several CWD exposed or positive herds in Pennsylvania, including the
herd that was the source of the CWD positive deer in the Ohio hunting preserve.
It had received over 120 animals from these herds.
On June 15 and 16, this herd was depopulated with federal indemnity.
Samples were collected for research purposes. 241 animals including 44 fawns
were euthanized, sampled and tested. Sixteen additional positive were
identified. They originated from 5 Ohio CWD certified herds and 4 Pennsylvania
CWD certified herds. One of the Ohio herds was the herd that was used to
initially establish this herd. One positive animal was over 60 months of age so
that Ohio herd was not designated as an exposed herd. The other three Ohio herds
were quarantined as exposed herds.
Records reviews identified 334 exposed animals associated with Ohio exposed
herds. 42 Ohio herds containing these animals were quarantined. They have
remained under quarantine until the quarantined animal(s) are euthanized and
tested Not Detected for CWD or 60 months have passed since animals entered the
herd. From Ohio Exposed Herd 1, 56 animals moved to 21 Ohio herds and 83 animals
moved out of state. 27 animals were either already dead and tested with CWD Not
Detected results or have since been tested with CWD Not Detected results. From
Ohio Exposed Herd 2, 76 animals moved to 16 Ohio herds and 94 animals moved out
of state. 25 animals were either already dead and tested with CWD Not Detected
results or have since been tested with CWD Not Detected results. From Oho
Exposed Herd 3, 21 animals moved to 5 Ohio herds and 4 animals moved out of
state. 7 animals were either already dead and tested with CWD Not Detected
results or have since been tested with CWD Not Detected results. Ohio received 2
exposed animals from the exposed herd in Pennsylvania associated with this case.
In summary, 334 exposed animals were identified and traced to 40 Ohio herds. 59
of those in Ohio have been tested with Not Detected CWD results. 181 have been
traced out of state and 94 are still standing in 26 quarantined herds/hunting
preserves.
Ohio Exposed Herd 1 has been in the CWD Certification Program since
September 2003 and has an inventory as of 48 head over 1 year old. Ohio Exposed
Herd 2 has been in the CWD Certification Program since October 2003 and has an
inventory of 93 animals. Ohio Exposed Herd 3 has been in the CWD Certification
Program since February 2009 but started with a status date of May, 2001 and has
an inventory of 17 deer.
In addition Ohio received reports of 72 exposed deer form OOS Exposed herds
traced to 18 Ohio herds. 18 of those animals had moved to out of state herds. 30
animals were tested in Ohio with Not Detected results. 12 animals remain in 7
quarantined herds. The summary of all traces associated with positive cases in
Ohio and Pennsylvania in 2014 – 2015 are:
Total exposed animals traced to Ohio:661
Total tested Not Detected: 176
Total animals traced to Out of State Premises: 265
Total premises initially quarantined 87
Total premises remaining quarantined: 40
Total Hunting Preserves quarantined: 10
USDA Cervid Health Program Updates
Randy Pritchard, USDA, APHIS, Veterinary Services
Voluntary Chronic Wasting Disease (CWD) Herd Certification Program
The APHIS National CWD Herd Certification Program (HCP) was implemented in
2014. It is a voluntary Federal-State-industry cooperative program administered
by APHIS and implemented by participating States. The program provides uniform
national herd certification standards that minimize the risk of spreading CWD in
farmed cervid populations. Participating States and herd owners must comply with
requirements for animal identification, fencing, recordkeeping,
inspections/inventories, as well as animal mortality testing and response to any
CWD-exposed, suspect, and positive herds. APHIS monitors the Approved State HCPs
to ensure consistency with Federal standards through annual reporting by the
States. With each year of successful surveillance, participating herds will
advance in status until reaching five years with no evidence of CWD, at which
time herds are certified as being low-risk for CWD. Only captive cervids from
enrolled herds certified as low risk for CWD may move interstate. Currently, 30
States participate in the voluntary CWD Herd Certification Program; 29 have
Approved HCPs and one has Provisional Approved status. VS is working with the
remaining State to transition it to Approved status. FY2015 marks the second
year that Approved States have submitted their CWD HCP annual reports to APHIS.
APHIS is currently reviewing these reports.
Review of CWD Program Standards
The CWD Program Standards provide clarification and guidance on how to meet
CWD Herd Certification Program and interstate movement requirements. VS
committed to an annual review of the Program Standards by representatives of the
cervid industry and appropriate State and Federal agencies. VS planned to
perform a review in FY2015; however, this did not occur due to the response to
highly pathogenic avian influenza (HPAI). VS expects to conduct a review in
FY2016.
CWD in Farmed and Wild Cervids
Retrospective Epidemiology of CWD in Farmed Cervids: In response to a 2014
USAHA Resolution, VS asked States to include a retrospective summary of the
epidemiology of all positive herds with their annual HCP reports for FY2015.
Unfortunately, the response to HPAI delayed completion of this summary. Five
States reported information to date. A few States indicated that they did not
have the resources to devote to this request. VS will continue to gather this
data and to collect more comprehensive data in the future.
Summary of CWD detections. As of September 30, 2015, CWD has been confirmed
in wild deer and elk in 21 U.S. States, and in farmed cervids in 16 States. In
total, 23 States have identified CWD in wild and/or farmed cervids. CWD has been
reported in 70 farmed cervid herds in the United States. Confirmation of the
disease in 3 free-ranging, wild white-tailed deer in Michigan in 2015 marked the
first report of CWD in the wild cervid population in this State.
FY2015 CWD Detections in Farmed Cervids: In FY2015, CWD was identified in
eight farmed cervid herds: one white-tailed deer breeding herd in Pennsylvania,
one elk breeding herd in Utah (traced back from a hunting facility in Utah), one
white-tailed deer (WTD) breeding herd and one WTD hunting preserve in Ohio
(owned by the same producer), two WTD breeding herds in Wisconsin, one WTD and
elk herd in Texas, and a second WTD herd in Texas (traced from the first
positive herd in Texas). The positive animals in Utah, Ohio, and Texas
represented the first reported cases of CWD in captive cervids in all three of
these States.
White-Tailed Deer Breeding Herd, Pennsylvania: On October 6, 2014, the
National Veterinary Services Laboratories (NVSL) confirmed CWD in a 6-year-old
doe from a captive WTD breeding facility in Reynoldsville, Pennsylvania. The doe
was euthanized and tested because she was classified as a CWD-exposed animal
that had previously resided in two trace back exposed herds. This herd was
assembled in 2013 through the purchase of 16 animals from other HCP-certified
herds in Pennsylvania, and had been under quarantine for receiving exposed
animals from a trace back exposed herd. The remaining herd of eight WTD was
depopulated with Federal indemnity on February 18, 2015, and no additional
positive animals were detected. USDA collected samples for research
purposes.
Elk Breeding Herd, Utah: On December 23, 2014, NVSL confirmed CWD in
3-year-old captive elk. The elk had been at a hunting park located in northern
Utah, where he had resided for approximately 3 weeks prior to being hunter
killed. All hunter-killed animals at the hunt park are required to be tested for
CWD, and this animal was sampled through routine surveillance. The elk was
traced back to its herd of origin, and that facility was quarantined. The herd
was assembled in 1999 with bulls, and later elk cows, that originated from
Colorado. Historical testing records for the herd were unavailable. The
remaining 70 elk were depopulated using Federal indemnity funds on March 3,
2015, and an additional 25 elk were confirmed as CWD-positive. USDA collected
samples for research purposes.
White-Tailed Deer Hunting Preserve, Ohio: On October 22, 2014, NVSL
confirmed CWD in a buck taken from a captive WTD deer hunting preserve in Ohio.
This was the first time that CWD had been detected in Ohio. The preserve was
tested as part of Ohio’s CWD monitoring program. The herd had been under
quarantine since April 2014 because it was a trace-forward herd associated with
a CWD-exposed herd in Pennsylvania. The positive animal was traced to its herd
of origin, a captive WTD breeding herd in Pennsylvania, through DNA identity
testing. On November 26, 2014, the Ohio State Veterinarian issued an Order of
Destruction for animals on the hunting preserve. The State executed this Order
on April 27-30, 2015. The herd of 224 WTD was depopulated and no other positives
were detected. USDA did not provide Federal indemnity.
White-Tailed Deer Breeding Herd, Ohio: On March 31, 2015, NVSL confirmed
CWD infection in a 5-year-old WTD doe from a captive breeding herd in
Holmesville, Ohio. The index animal was received from a Wisconsin WTD farm in
January 2013. The CWD-positive herd was owned by the same individual as the Ohio
hunt preserve that was found to be CWD positive in October 2014. On May 22,
2015, NVSL confirmed a second positive case in the same herd -- a yearling WTD
doe that was a natural addition in the same breeding herd. The herd had been
under quarantine since April 1, 2014 due to epidemiological linkages with two
WTD herds in Pennsylvania – one a positive herd and the other a traceback
exposed herd. USDA provided Federal indemnity and depopulated this herd on June
15 and 16, 2015. USDA collected samples for research purposes. NVSL confirmed
CWD in 16 additional animals in the herd. Of the 16 positives, one was natural
addition and the rest were purchased additions. The positive animals were
purchased from February 26, 2013 through September 24, 2013, except for one
purchased in 2012. Eleven purchased additions traced-back to 3 herds in
Pennsylvania and four purchased additions traced to three other herds in
Ohio.
White-Tailed Deer Breeding Herd, Wisconsin: On October 6, 2014, NVSL
confirmed CWD in a 2-year-old doe born in June of 2012 that died on a Richland
County farm. The facility is within the CWD management zone in Wisconsin. The
remaining 51 deer were euthanized on November 20, 2014, and seven additional
positives (all males born in 2012) were found. Two of these 7 were purchased
additions with the last added to the herd in January 2013. All sales from this
herd were to shooting preserves. This premises was double fenced and had been
compliant in a herd certification program for over 10 years. White-Tailed Deer
Breeding Herd, Wisconsin: On June 19, 2015, NVSL confirmed CWD in a 7-year-old
female WTD from a breeding facility in Eau Claire County. The doe was a natural
addition to this breeding herd. This is the first positive CWD case, captive or
wild, in this county. The doe was found dead and was showing no clinical signs
of CWD at the time of death. Since 2003, this herd has tested 391 animals for
CWD and all had “not detected” results. In addition, 317 animals have tested
“not detected” from the associated hunting preserve over the same time period. A
second positive natural addition doe from this herd was confirmed positive by
NVSL on September 10, 2015. Several escape episodes have occurred from this
herd. The herd is currently under quarantine and plans are underway for
depopulation with State indemnity.
White-Tailed Deer and Elk Breeding Herd, Texas: On June 30, 2015, NVSL
confirmed CWD in a 2-year-old WTD buck from a captive WTD and elk breeding herd
in Medina County, Texas, approximately 500 miles from previously reported
positive free-ranging mule deer in far West Texas. This was the first time that
the disease had been detected in farmed cervids in the State. The index buck was
born on the premises and found dead on June 18, 2015. Over 40 high-risk deer
(i.e., pen mates, dam, others) were euthanized and tested after the index case
was found. The NVSL confirmed CWD infection in two of those deer. Interestingly,
all three of the positive deer identified to date on this premises have the same
AI sire. However, the significance of this finding is unclear. In the past 5
years, records indicate that 130 WTD from 33 facilities moved into the positive
herd and 838 WTD moved out of the positive herd to 147 different herds. One
positive WTD was found in one of these trace-out herds (see herd description
below). Additionally, 23 elk were also moved from this herd to another herd in
TX in 2014. All trace-outs have been intrastate except for movements to two
premises in Mexico. Premises that have received deer from the index herd are
under movement restrictions. VS is collaborating with animal health authorities
in Mexico. VS paid indemnity and depopulated this herd on September 30, 2015,
and no additional positive animals were detected. USDA collected samples for
research purposes.
White-Tailed Deer Herd, Texas: On September 14, 2015 NVSL confirmed CWD
from tissues from a WTD in Lavaca County, Texas. This animal was a traceout from
the first CWD positive herd from June 30, 2015. Additional epidemiology is
ongoing.
Cervid Health Program Budget
The Cervid Health Program includes the CWD herd certification program and
the cervid TB program. It is funded through the Equine, Cervid, and Small
Ruminant Line Item. In FY2015, the Cervid Health Program was appropriated $3.0
million by Congress for cervid health activities. This funding was allocated as
follows:
o Indemnity−$1.1 million for CWD and cervid TB. (An additional $230,000 was
provided to support herd depopulation activities in TX)
o CWD Research−$200,000 to support USDA Wildlife Services research for
development of CWD live animal diagnostic testing
o Cervid Health Program−$1.2 million for general program support (primarily
field activities).
APHIS anticipates the FY2016 Cervid Health Program funding will remain at
FY2015 levels.
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.
Chronic Wasting Disease Research and Updates in Colorado
Michael Miller, Colorado Division of Parks and Wildlife
Dr. Michael Miller, Colorado Division of Parks and Wildlife, led a brief
discussion on the implications of a recent study on chronic wasting disease
(CWD) host range. The Case Western study results, presented at an international
prion conference in May 2015, complement other efforts to assess human
susceptibility to chronic wasting disease that have been ongoing since the
mid-1990s. Findings from a variety of experimental & epidemiological studies
support messaging since the mid-1990s that human illness resulting from CWD
exposure appears unlikely. The new study’s results are consistent with other
previous & contemporary data suggesting a low probability of human prion
disease resulting from CWD exposure. Dr. Miller noted that even though human
illness seems unlikely, minimizing the occurrence of CWD and encouraging other
precautions for minimizing human exposure to CWD may be prudent. Trends observed
in Colorado since 2002 suggest increasing infection rates in affected mule deer
and elk herds, with the exception of one population unit intensively managed
through harvest in the early 2000s. Controlling CWD will likely need to rely on
hunting in order to remain politically, socially, and fiscally sustainable.
Consequently, early intervention -- while infection rates are still low -- may
offer the best opportunity to both suppress epidemics and minimize the
likelihood of hunters harvesting infected animals. Dr. Miller suggested that the
timing and approaches to CWD control may deserve more attention and
reconsideration than given in recent years.
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C.
Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡,
Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...
Abstract The emergence of chronic wasting disease (CWD) in deer and elk in
an increasingly wide geographic area, as well as the interspecies transmission
of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt
Jakob disease, have raised concerns about the zoonotic potential of CWD. Because
meat consumption is the most likely means of exposure, it is important to
determine whether skeletal muscle of diseased cervids contains prion
infectivity. Here bioassays in transgenic mice expressing cervid prion protein
revealed the presence of infectious prions in skeletal muscles of CWD-infected
deer, demonstrating that humans consuming or handling meat from CWD-infected
deer are at risk to prion exposure.
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
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.
==============
===============
game farms help spread cwd, simple fact. it’s been proven. game farms are
not the only risk factor though, however, they are a big part of the problem,
history shows this.
the quarantine of cwd tse prion infected game farms must be extended to 16
years now.
the CWD LOTTO ENTITLEMENT of captive game farms where the states pays game
farms for CWD MUST BE STOPPED. if the cwd infected farm does not buy insurance
for any and all loss from CWD for them and any party that does business with
them, and or any loss to the state, and or any products there from, that’s to
bad, they should never be allowed to be permitted. in fact, for any state that
does allow game farming, urine mills, sperm mills, antler mills, velvet mills,
big high fence ranch, little low fence farm, in my opinion, it’s that states
responsibility to protect that state, thus, any states that allow these farms
and business there from, it should be mandatory before any permit is allowed,
that game farm must have enough personal insurance that would cover that farm,
any farm that does business with them, and or any products there from, and the
state, before such permit is issued. personally, I am sick and tired of all the
big ag entitlement programs, and that’s all cwd indemnity is. in fact, the USDA
CWD INDEMNITY PROGRAM, should read, THE USDA CWD ENTITLEMENT PROGRAM.
we cannot, and must not, let the industry regulate itself, especially with
the junk science they try to use.
if they are not going to be science based, they must be banned.
science has told us for 3 decade or longer, that these are the things that
_might_ work, yet thanks to the industry, and government catering to industry,
regulations there from have failed, because of catering to the industry, and the
cwd tse prion agent has continued to spread during this time. a fine example is
Texas.
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
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:
$298,770 + $465,000
THE CWD ENTITLEMENT PROGRAM FOR GAME FARMS MUST BE STOPPED!
IOWA CWD
Friday, February 05, 2016
IOWA Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee
County
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after gaining approval
from surrounding landowners, and confirmed that the fenced had been cut or
removed in at least four separate locations; that the fence had degraded and was
failing to maintain the enclosure around the Quarantined Premises in at least
one area; that at least three gates had been opened;and that deer tracks were
visible in and around one of the open areas in the sand on both sides of the
fence, evidencing movement of deer into the Quarantined Premises.
The overall incidence of clinical CWD in white-tailed deer was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
***Title: Transmission of chronic wasting disease to sentinel reindeer
(Rangifer tarandus tarandus)
Authors
item Moore, S - item Kunkle, Robert item Nicholson, Eric item Richt,
Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A
Technical Abstract:
Chronic wasting disease (CWD) is a naturally-occurring, fatal
neurodegenerative disease of North American cervids. Reindeer (Rangifer tarandus
tarandus) are susceptible to CWD following oral challenge, but CWD has not been
reported in free-ranging caribou (Rangifer tarandus caribou) or farmed reindeer.
Potential contact between CWD-affected cervids and Rangifer species that are
free-ranging or co-housed on farms presents a potential risk of CWD
transmission. The aims of this study were to 1) investigate the transmission of
CWD from white-tailed deer (Odocoileus virginianus; CWD-wtd), mule deer
(Odocoileus hemionus; CWD-md), or elk (Cervus elaphus nelsoni; CWD-elk) to
reindeer via the intracranial route, and 2) to assess for direct and indirect
horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer
fawns were challenged intracranially with CWD-wtd, CWD-md, or CWD-elk. Two years
after challenge of inoculated reindeer, non-inoculated control reindeer were
introduced into the same pen as the CWD-wtd inoculated reindeer (n=4) or into a
pen adjacent to the CWD-md inoculated reindeer (n=2). Reindeer were allowed to
develop clinical disease. At death/euthanasia a complete necropsy examination
was performed, including immunohistochemical testing of tissues for
disease-associated CWD prion protein (PrP-CWD). Intracranially challenged
reindeer developed clinical disease from 21 months post-inoculation (MPI).
PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed
clinical disease during the study period (<57 div="" mpi="">
***We have shown that reindeer are susceptible to CWD from various cervid
sources and can transmit CWD to naive reindeer both directly and indirectly.
Last Modified: 12/3/2015
***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6
developed clinical disease during the study period (<57 div="" mpi="">
***We have shown that reindeer are susceptible to CWD from various cervid
sources and can transmit CWD to naive reindeer both directly and indirectly.
Tuesday, September 29, 2015
*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer
tarandus tarandus) can transmit CWD to naive reindeer both directly and
indirectly
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
CHRONIC WASTING DISEASE CWD TSE PRION AKA MAD COW TYPE DISEASE
Friday, January 01, 2016
Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population
Monitoring and Capture-Recapture Data
Chris Geremia, Michael W. Miller, Jennifer A. Hoeting, Michael F. Antolin,
N. Thompson Hobbs PLOS x Published: October 28, 2015 DOI:
10.1371/journal.pone.0140687
Abstract
Epidemics of chronic wasting disease (CWD) of North American Cervidae have
potential to harm ecosystems and economies. We studied a migratory population of
mule deer (Odocoileus hemionus) affected by CWD for at least three decades using
a Bayesian framework to integrate matrix population and disease models with
long-term monitoring data and detailed process-level studies. We hypothesized
CWD prevalence would be stable or increase between two observation periods
during the late 1990s and after 2010, with higher CWD prevalence making deer
population decline more likely. The weight of evidence suggested a reduction in
the CWD outbreak over time, perhaps in response to intervening harvest-mediated
population reductions. Disease effects on deer population growth under current
conditions were subtle with a 72% chance that CWD depressed population growth.
With CWD, we forecasted a growth rate near one and largely stable deer
population. Disease effects appear to be moderated by timing of infection,
prolonged disease course, and locally variable infection. Long-term outcomes
will depend heavily on whether current conditions hold and high prevalence
remains a localized phenomenon.
Discussion
The protracted time-scale of the CWD outbreak is much longer than the
timespan of our research, which limits our ability to identify the true
explanation of our findings. Nonetheless, our research suggests that, at least
for the foreseeable future (e.g., decades), mule deer populations sharing the
overall survival and infection probabilities estimated from our analyses may
persist but likely will not thrive where CWD becomes established as an endemic
infectious disease.
‘’Nonetheless, our research suggests that, at least for the foreseeable
future (e.g., decades), mule deer populations sharing the overall survival and
infection probabilities estimated from our analyses may persist but likely will
not thrive where CWD becomes established as an endemic infectious disease. ‘’
*** Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using
Population Monitoring and Capture-Recapture Data
‘’Mountain lions prey selectively on CWD infected deer [33] and CWD could
result in an abundance of vulnerable prey, thereby enhancing mountain lion
survival and reproduction [20].’’
please see ;
‘’preliminary results suggesting that bobcats (Lynx rufus) may be
susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting
disease agent.’’
references on Feline Spongiform Encephalopathy FSE toward the bottom, see ;
Assessing Transmissible Spongiform Encephalopathy Species Barriers with an
In Vitro Prion Protein Conversion Assay
Tuesday, December 15, 2015
Chronic Wasting Disease will cause a Wyoming deer herd to go virtually
extinct in 41 years, a five-year study predicts
Study: Chronic Wasting Disease kills 19% of deer herd annually
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al.,
2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
PPo3-22:
Detection of Environmentally Associated PrPSc on a Farm with Endemic
Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh
Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of
Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories
Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University
of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes of
transmission and specifically the role of fomites in transmission remain poorly
defined. Here we present biochemical data demonstrating that on a
scrapie-affected sheep farm, scrapie prion contamination is widespread. It was
anticipated at the outset that if prions contaminate the environment that they
would be there at extremely low levels, as such the most sensitive method
available for the detection of PrPSc, serial Protein Misfolding Cyclic
Amplification (sPMCA), was used in this study. We investigated the distribution
of environmental scrapie prions by applying ovine sPMCA to samples taken from a
range of surfaces that were accessible to animals and could be collected by use
of a wetted foam swab. Prion was amplified by sPMCA from a number of these
environmental swab samples including those taken from metal, plastic and wooden
surfaces, both in the indoor and outdoor environment. At the time of sampling
there had been no sheep contact with these areas for at least 20 days prior to
sampling indicating that prions persist for at least this duration in the
environment. These data implicate inanimate objects as environmental reservoirs
of prion infectivity which are likely to contribute to disease transmission.
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after gaining approval
from surrounding landowners, and confirmed that the fenced had been cut or
removed in at least four separate locations; that the fence had degraded and was
failing to maintain the enclosure around the Quarantined Premises in at least
one area; that at least three gates had been opened;and that deer tracks were
visible in and around one of the open areas in the sand on both sides of the
fence, evidencing movement of deer into the Quarantined Premises.
The overall incidence of clinical CWD in white-tailed deer was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
WISCONSIN CWD
Friday, January 29, 2016
Wisconsin CWD-positive white-tailed deer found on Iowa County farm January
29, 2016
$298,770 + $465,000
Friday, December 04, 2015
Wisconsin CWD-positive white-tailed deer found on Oneida County hunting
preserve December 3, 2015
Thursday, November 19, 2015
Wisconsin Eau Claire Co. deer herd two day round of depopulation CWD
testing shows 23 positive
Wednesday, December 16, 2015
Wisconsin Chronic wasting disease confirmed in Crawford County buck
harvested on private land
Tuesday, February 11, 2014
Wisconsin tracks 81 deer from game farm with CWD buck to seven other states
Tuesday, December 17, 2013
Wisconsin Second CWD positive deer found in Grant County
Monday, December 02, 2013
WISCONSIN CHRONIC WASTING DISEASE CWD DISCOVERED MARATHON COUNTY HUNTING
PRESERVE
Sunday, November 03, 2013
Wisconsin Second CWD deer found in Portage County
Wisconsin : 436 Deer Have Escaped From Farms to Wild
Date: March 18, 2003 Source: Milwaukee Journal Sentinel snip...
Sunday, November 03, 2013
Wisconsin Second CWD deer found in Portage County
Second CWD deer found in Portage County
News Release
Published: November 1, 2013 by the Northwest Region Contact(s): Kris
Johansen, DNR area wildlife supervisor, 715-284-1430; Ed Culhane,
DNR communications, 715-781-1683 WISCONSIN RAPIDS – A deer harvested by a
bow hunter in southeast Portage County has tested positive for chronic wasting
disease, the state Department of Natural Resources reports. This is the second
CWD-positive wild deer found in the county. Wildlife biologists in central
Wisconsin now are asking bow hunters to assist with increased surveillance for
the disease in four separate areas where positives have been confirmed outside
the CWD management zone.
CWD is contagious and fatal for deer, elk and moose. “Last fall CWD was
discovered for the first time in three wild, white-tailed deer in Adams, Juneau
and Portage counties” said DNR area wildlife supervisor Kris Johansen. “Now we
have a second positive in a different area of Portage County. To better define
the geographic extent of CWD in central Wisconsin, we are focusing additional
surveillance around each of these four locations.”
The latest CWD positive deer was harvested Oct. 6 just northwest of Almond
in Portage County.
To view where the surveillance focus areas are located, hunters can go to
the DNR website and enter “CWD registration” in the key word search, then click
on “CWD registration and sampling.” On this page – http://dnr.wi.gov/topic/wildlifehabitat/registersample.html
– detailed maps show the precise location of these surveillance circles for the
first three positives, the ones in Adams and Juneau counties and the first find
in Portage County, located in the northwest corner of the county.
There is also a map showing the two Portage County locations. A new map,
showing the precise surveillance area for the fourth positive, in southeast
Portage County, will be added to the web page as soon as it is prepared. This
page also links to a list of cooperating taxidermists and meat processors where
samples can be collected.
The DNR is asking hunters to work with these cooperators to have head and
lymph node samples from adult deer – harvested within the four focus areas –
removed for testing. To have the sample removed, the hunter can bring the whole
deer to one of the listed cooperators or just remove the head with at least
three inches of neck attached and bring that in for sampling.
“Please call ahead to set up an appointment,” Johansen said. “These are
private business operators who are helping us out, and we want to respect their
time and their schedules.” This list will be updated online as new cooperators
join the surveillance effort:
• Wisconsin River Meats, N5340 County HH, Mauston 608-847-7413
• A&B Butchering, 6971 Hwy 34, Rudolph 715-435-3893
• Strickly Wild Processing, 140 Buffalo St, Wisconsin Rapids 715-421-0587
• Hartnell's Wild Game Processing, 1925 Cypress Ave., Arkdale 608-339-7288
• Trevor Athens Taxidermy, 982 15th Ave., Arkdale 608-547-6117
• Tall Tines Taxidermy, N2621 Cassidy Road, Mauston 608-547-0818
• Todd's Wildlife Taxidermy, N2148 State 58, Mauston 608-847-7693
• Vollmer Taxidermy, 3631 Plover Road, Plover 715-345-1934
• Field and Stream Taxidermy, 217 S. Front St., Coloma 608-547-1565
• DNR Service Center, 473 Griffith Ave., Wisconsin Rapids 715-421-7813
• Mead Wildlife Area, S2148 County S, Milladore 715-457-6771
• Adams Ranger Station, 532 N. Adams St., Adams 608-339-4819
• Almond Market, 111 Main St., Almond 715-366-2002
Hunters may also have deer from any of the four focus areas tested for CWD
by contacting one of these DNR offices:
• Mead Wildlife Area headquarters, S2148 County S, Milladore – 715-457-6771
• WI Rapids Service Center, 473 Griffith Avenue, Wisconsin Rapids –
715-421-7813
• Adams-Friendship Ranger Station, 532 N. Main Street, Adams – 608-339-4819
On the weekends or during warm periods, hunters should remove the deer head
with at least three inches of neck attached, freeze the head and then contact
the DNR to arrange a drop off. DNR staff will also collect samples from
hunter-harvested deer on the opening weekend of the gun deer season. Collection
stations and hours will be published prior to the gun deer season. The CWD tests
are free to hunters. Each person who submits a head for testing will receive lab
results within three or four weeks.
Friday, February 03, 2012
*** Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report
Singeltary et al
IOWA CWD
Friday, February 05, 2016
IOWA Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee
County
ILLINOIS CWD
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
Monday, August 31, 2015
Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with
71 confirmed in 2015 and 538 confirmed cases to date
NEBRASKA CWD
Friday, January 29, 2016
NEBRASKA Three Positives for CWD Found in Recent Testing of Deer
OHIO CWD
Monday, August 24, 2015
Ohio wildlife officials ramp up fight against fatal deer brain disease
after 17 more positive tests CWD
Wednesday, August 05, 2015
*** Ohio confirms to me Chronic Wasting Disease CWD Spreads 19 confirmed
cases to date ***
Just got off the phone with Christy Clevenger of Ohio
Ohio Department of Agriculture March 2012 – Present (3 years 6
months)Reynoldsburg, Ohio CWD program
Ms. Clevenger confirmed, to date, from the Yoder debacle, 1 confirmed case
of CWD from the Hunting Preserve, 2 confirmed cases from the Breeding Farm, and
16 confirmed cases of CWD from the Breeder Depopulation, with a total to date of
19 cases of CWD in Ohio...
Terry
Thursday, April 02, 2015
OHIO CONFIRMS SECOND POSTIVE CHRONIC WASTING DISEASE CWD on Yoder's
properties near Millersburg
Second Ohio white-tailed deer tests positive for deadly brain disease
Print Email D'Arcy Egan, The Plain Dealer By D'Arcy Egan, The Plain Dealer
Email the author | Follow on Twitter on April 01, 2015 at 2:10 PM, updated April
01, 2015 at 3:09 PM
Ohio Dept. of Agriculture.jpg CLEVELAND, Ohio -- As state officials try to
legally force Holmes County deer farmer Daniel Yoder to euthanize a herd of
expensive white-tailed deer, a second deer has tested positive for chronic
wasting disease (CWD) on Yoder's properties near Millersburg.
The first positive test ever for CWD in Ohio was from a deer killed Oct. 22
at Yoder's hunting preserve, World Class Whitetails. The second positive result
came a few days ago while testing another Yoder deer that had died.
The National Veterinary Services Laboratories in Ames, Iowa confirmed the
results.
"It has always been a case of not if, but when another deer would test
positive on those properties," said Communications Director Erica Hawkins of the
Ohio Department of Agriculture. "This wasn't unexpected. We expected to find
positives at his facilities and, with de-population, we expect to find more."
Yoder's two breeding farms and hunting preserve were quarantined a year ago
after it was discovered an infected Pennsylvania deer had been shipped there. It
has become common for the breeding and hunting operations to ship deer to other
states.
In Ohio, the ODA manages captive deer herds. The Ohio Division of Wildlife
manages the wild deer herd.
Breeding large-antlered deer to supply the fenced deer-hunting operations
has become a booming business. The price for a deer sporting trophy antlers can
range from a few thousands dollars to more than $50,000.
Because the disease is highly contagious and almost impossible to
eradicate, Yoder's breeding farms and fenced deer hunting operation was shut
down and all deer 12 months and older that die on the properties were required
to be tested for CWD, regardless of the circumstances, said Hawkins.
While CWD has become a major problem in Wisconsin and many western states,
Yoder's captive deer have been the only Ohio animals to test positive for the
always-fatal brain disease. CWD is found in the wild, but spreads far more
quickly among crowded herds of captive deer or elk.
The ODOW constantly tests road-killed deer and deer killed by hunters for
the disease. Because of the positive test in Holmes County, wildlife officials
focused on deer harvested from that area during the recent hunting seasons.
The disease is related to mad cow disease, but has never been contracted by
humans, according to the Centers for Disease Control and Prevention.
The ODOW reported last fall at least two deer had escaped from Yoder's
farms and were killed by sport hunters. There have also been other instances of
deer escaping from fenced hunting operations around state.
Hawkins said discussions are still underway to determine the best way to
eliminate the herd because of the high cost of destruction and disposal of the
deer.
"A lot of questions still need to be answered," Hawkins said. "This is the
first situation like this in Ohio."
Yoder was charged in Holmes County Common Pleas Court on Feb. 25 with two
counts of tampering with evidence, reported the Wooster Daily Record. Yoder had
given a customer packages of venison obtained from a doe after the trophy buck
he had killed appeared to be ill. The customer received the antlers, but Yoder
disposed of the buck's head and carcass without performing the required tests,
charged ODA enforcement agent William Lesho.
Three West Virginia hunters had paid to kill three deer on the preserve on
another date and the required samples of the deer were not collected. In order
to determine if a deer has CWD, the brain or brain stem must be tested
First Case of Chronic Wasting Disease Confirmed in Ohio on Private Preserve
10/23/2014 Ohio DNR in Wildlife
Active steps taken to control further spread; no evidence the disease
affects humans
REYNOLDSBURG, OHIO – The Ohio Department of Agriculture (ODA) and the Ohio
Department of Natural Resources (ODNR) today confirmed the first positive case
of Chronic Wasting Disease (CWD) in the state in a captive deer herd in Holmes
County. The state continues to take quarantine action to control the further
spread of the disease. There is no evidence that CWD has affected the wild deer
population in the state.
The positive sample was taken from a single buck on a hunting preserve in
Millersburg and tested as part of Ohio’s CWD monitoring program for captive
white-tailed deer operations. The preserve had been under quarantine since April
24, 2014, and was subject to intensive monitoring and sampling protocols because
of a known connection to a captive deer operation in Pennsylvania that tested
positive for CWD earlier this year. The quarantine will remain enforced until
the state is satisfied that disease transference can no longer occur.
“Ohio’s captive white-tail deer licensing program was enacted two years ago
for the purpose of continuously monitoring the heath of the captive deer
populations in the state to manage the spread of and exposure to diseases such
as CWD. We have worked closely with the Pennsylvania Department of Agriculture
to identify and trace back positive cases,” said State Veterinarian Dr. Tony
Forshey. “We will continue to take aggressive steps to ensure that CWD does not
pose a threat to the state’s wild deer population.”
The state has quarantined 43 captive deer operations in Ohio since April
15, 2014, for receiving approximately 125 deer from operations in Pennsylvania
that later tested positive for CWD. Twenty-two of those quarantines were lifted
after negative CWD test results were confirmed in 53 of the suspect animals from
Pennsylvania. ODA will continue to enforce quarantine restrictions on 21
operations, including five hunting preserves, until the department is satisfied
that the threat of disease transference has passed.
The disease is fatal in deer, elk and moose, but there is no evidence CWD
can be transmitted to humans, according to the Centers for Disease Control and
Prevention (CDC) and The World Health Organization. Though no human disease has
been associated with CWD, the CDC recommends, as a precaution, that people or
other animals do not eat any part of an animal diagnosed with or showing signs
of CWD.
“We have no reason to believe that there has been transference to the
state’s wild deer population,” said Scott Zody, chief of the ODNR Division of
Wildlife. “With hunting season in progress, there are no CWD concerns that
should prevent anyone from enjoying wild deer hunting in Ohio or from consuming
meat from healthy animals.”
The ODNR Division of Wildlife is recommending that hunters continue to take
standard precautions such as shooting only animals that appear healthy, wearing
rubber gloves when field-dressing their deer and washing thoroughly when
finished. If hunters should observe a deer that appears unhealthy, they are
encouraged to contact their local wildlife office or officer.
Since 2002, the state has conducted surveillance throughout Ohio for the
disease. State and federal officials will continue this regular sampling and
testing throughout the hunting season to continue to monitor the health of the
state’s wild deer population. Tissue samples from 753 deer killed on Ohio’s
roads were collected from September 2013 through March 2014 and were tested for
CWD. An additional 88 hunter-harvested mature white-tailed deer and nine deer
displaying symptoms consistent with CWD were tested as well and were all
negative.
In response to this positive finding, the ODNR Division of Wildlife will
increase sampling efforts in the wild deer population within six miles of the
hunting preserve from which the CWD-positive deer came as well as near the other
captive operations that are under quarantine. Those samples will include
high-risk animals such as those killed on roads or exhibiting neurological
symptoms as well as hunter-harvested deer in the area.
CWD, first discovered in captive mule deer in Colorado in 1967, attacks the
brains of infected deer, elk and moose, producing small lesions that eventually
result in death. It is transmitted by direct animal-to-animal contact through
saliva, feces and urine. Signs of the disease include weight loss, excessive
salivation, increased drinking and urination, and abnormal behavior like
stumbling, trembling and depression. Infected deer and elk may also allow
unusually close approach by humans or natural predators. The disease is fatal in
deer, and there is no known treatment or vaccine.
FOR IMMEDIATE RELEASE
Media Contacts:
Erica Hawkins, ODA, (614) 752‐9817, erica.hawkins@agri.ohio.gov
Susie Vance, ODNR, (614) 265‐6335, susie.vance@dnr.state.oh.us
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE
PRESERVE
Active steps taken to control further spread; no evidence the disease
affects humans
REYNOLDSBURG, Ohio (Oct. 23, 2014) – The Ohio Department of Agriculture and
the Ohio Department of Natural Resources today confirmed the first positive case
of Chronic Wasting Disease (CWD) in the state in a captive deer operation in
Holmes County. The state continues to take quarantine action to control the
further spread of the disease. There is no evidence that CWD has affected the
wild deer population in the state.
The positive sample was taken from a single buck on a hunting preserve in
Millersburg and tested as part of Ohio’s CWD monitoring program for captive
white‐tailed deer operations. The preserve had been under quarantine since April
24, 2014, and was subject to intensive monitoring and sampling protocols because
of a known connection to a captive deer operation in Pennsylvania that tested
positive for CWD earlier this year. The quarantine will remain enforced until
the state is satisfied that disease transference can no longer occur.
“Ohio’s captive white‐tail deer licensing program was enacted two years ago
for the purpose of continuously monitoring the heath of the captive deer
populations in the state to manage the spread of and exposure to diseases such
as CWD. We have worked closely with the Pennsylvania Department of Agriculture
to identify and trace back positive cases,” said State Veterinarian Dr. Tony
Forshey. “We will continue to take aggressive steps to ensure that CWD does not
pose a threat to the state’s wild deer population.”
The state has quarantined 43 captive deer operations in Ohio since April
15, 2014 for receiving approximately 125 deer from operations in Pennsylvania
that later tested positive for CWD. Twenty‐two of those quarantines were lifted
after negative CWD test results were confirmed in 53 of the suspect animals from
Pennsylvania. ODA will continue to enforce quarantine restrictions on 21
operations, including five hunting preserves, until the department is satisfied
that the threat of disease transference has passed.
The disease is fatal in deer, elk and moose, but there is no evidence CWD
can be transmitted to humans, according to the Centers for Disease Control and
Prevention (CDC) and The World Health Organization. Though no human disease has
been associated with CWD, the CDC recommends, as a precaution, that people or
other animals do not eat any part of an animal diagnosed with or showing signs
of CWD. “We have no reason to believe that there has been transference to the
state’s wild deer population,” said Scott Zody, Chief of the Ohio Department of
Natural Resources’ Division of Wildlife. “With hunting season in progress, there
are no CWD concerns that should prevent anyone from enjoying wild deer hunting
in Ohio or from consuming meat from healthy animals.”
The Division of Wildlife is recommending that hunters continue to take
standard precautions such as shooting only animals that appear healthy, wearing
rubber gloves when field‐dressing their deer, and washing thoroughly when
finished. If hunters should observe a deer that appears unhealthy, they are
encouraged to contact their local wildlife office or officer.
Since 2002, the state has conducted surveillance throughout Ohio for the
disease. State and federal officials will continue this regular sampling and
testing throughout the hunting season to continue to monitor the health of the
state’s wild deer population. Tissue samples from 753 deer killed on Ohio’s
roads were collected from September 2013 through March 2014 and were tested for
CWD. An additional 88 hunter‐harvested mature white‐tailed deer and nine deer
displaying symptoms consistent with CWD were tested as well and were all
negative.
In response to this positive finding, the Division of Wildlife will
increase sampling efforts in the wild deer population within six miles of the
hunting preserve from which the CWD‐positive deer came as well as near the other
captive operations that are under quarantine. Those samples will include
high‐risk animals such as those killed on roads or exhibiting neurological
symptoms as well as hunter‐harvested deer in the area.
CWD, first discovered in captive mule deer in Colorado in 1967, attacks the
brains of infected deer, elk and moose, producing small lesions that eventually
result in death. It is transmitted by direct animal‐toanimal contact through
saliva, feces and urine. Signs of the disease include weight loss, excessive
salivation, increased drinking and urination, and abnormal behavior like
stumbling, trembling and depression. Infected deer and elk may also allow
unusually close approach by humans or natural predators. The disease is fatal in
deer and there is no known treatment or vaccine.
‐‐ 30 ‐‐
Thursday, October 23, 2014
*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE
PRESERVE
Wednesday, February 11, 2015
World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with
two counts of tampering with evidence
PENNSYLVANIA CWD
Sunday, October 18, 2015
*** Pennsylvania Game Commission Law and Law Makers CWD TSE PRION Bans
Singeltary 2002 from speaking A smelly situation UPDATED 2015
Saturday, November 07, 2015
PENNSYLVANIA CHRONIC WASTING DISEASE CWD TSE PRION RULES EXPAND
Saturday, November 07, 2015
Pennsylvania 2015 September Minutes CWD Urine Scents
Tuesday, May 05, 2015
Pennsylvania CWD DETECTED IN SIX MORE FREE-RANGING DEER Disease Management
Area 2 again expanded due to new cases Release #030-15
Sunday, July 13, 2014
Louisiana deer mystery unleashes litigation 6 does still missing from CWD
index herd in Pennsylvania Great Escape
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN
INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Tuesday, June 11, 2013
*** CWD GONE WILD, More cervid escapees from more shooting pens on the
loose in Pennsylvania
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd
Pennsylvania Update May 28, 2013
*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana,
quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
”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.
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO
LOUISIANA and INDIANA
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Thursday, October 11, 2012
Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests
Positive
Thursday, January 21, 2016
*** INDIANA With end of long legal challenge last year, high-fence hunting
operations currently unregulated
MICHIGAN CWD
Wednesday, December 30, 2015
Michigan Deer suspected positive for CWD found in Watertown Township; Jan.
12 public meeting set ‘confirmed’
WYOMING CWD
Wednesday, December 16, 2015
Wyoming Game and Fish finds CWD in new elk hunt area in southeast
UTAH CWD
Chronic Wasting Disease has been found in three different geographic areas
within Utah (see CWD positive map). The disease was first discovered in Utah in
2002 in a buck taken during the rifle hunt near Vernal. A second positive was
discovered in Utah in early 2003, when a mule deer doe that died in an
agricultural field near Moab, Utah, also tested positive. A third area of Utah
was found with CWD in late 2003 when a mule deer doe taken in a depredation
situation near Fountain Green tested positive. To date, 56 mule deer and one elk
have tested positive for CWD in Utah. The highest prevalence rate (two percent
in the buck population) in Utah is found on Wildlife Management Unit (WMU) 13,
the La Sal Mountains, where 38 of the 56 cases have been found. Prevalence rates
are less than one percent in the other two areas of Utah, near Vernal (WMU 9)
and Fountain Green (WMU 16).
There is considerable concern that CWD will spread into additional Utah
deer, elk or moose populations. The Utah Division of Wildlife Resources is
conducting random sampling of deer and elk to check for the disease.
UTAH 2014-2015 CWD COLLECTION UPDATE REPORT PERIOD 07/01-2014 -
6/30/2015
TOTAL POSITIVES 2002-2014 = 59
TOTAL POSITIVES 2014-2015 = 3
TOTAL POSITIVES ALL YEARS = 62
Saturday, January 31, 2015
*** Chronic wasting disease found in bull elk killed on private Utah
ranch
TEXAS CWD TSE PRION
Sunday, January 17, 2016
Texas 10,000 deer in Texas tested for deadly disease CWD TSE, but not
tested much in the most logical place, the five-mile radius around the Medina
County captive-deer facility where it was discovered
Friday, January 15, 2016
TEXAS PARKS & WILDLIFE CWD Ante-Mortem Testing Symposium Texas Disposal
Systems Events Pavilion January 12, 2016
Sunday, January 10, 2016
TEXAS MEDIA REPORTING A BIT OF GOOD NEWS ON CWD TESTING SO FAR INSTEAD OF
TAHC which is still mum, still refusing timely updates to the public TSE PRION
DISEASE
Tuesday, December 29, 2015
*** TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS
STILL DON'T GET IT $
Chronic Wasting Unease
*** The emergence of a deadly disease has wildlife officials and deer
breeders eyeing each other suspiciously. ***
TEXAS CWD FIGURES ???
actually, if these two new captive suspect CWD cases are confirmed, that
would be a total of 7 cases of CWD in Captive in Texas, PLUS the 8 other
confirmed cases of CWD up in the Texas Trans Pecos region to date in the mule
deer. So the total would be 15 cases of the CWD TSE Prion aka mad cow type
disease in Cervid in Texas, to date. just to put everything in perspective. BUT,
that would only be IF and WHEN, the TAHC or the TPWD ever confirm these two new
recent suspect CWD cases.
I am only reminded of another great article Shannon Tompkins wrote years
ago, when the CWD TSE Prion shoe was on the other foot...
March 14, 2002
"Ten years ago, elk and deer (imported into Texas) were not regulated at
all," said Dr. Ken Waldrup, an epidemiologist with the Texas Animal Health
Commission and one of the agency's point men on CWD. "If Texas doesn't already
have CWD, then I say that proves that God is a Texan. "For everyone's sake, I
sure hope He is."
========================
*** Tompkins: There are a lot of reasons to be concerned about CWD
Houston Chronicle Published 5:30 a.m., Thursday, March 14, 2002
where are any statements from the TAHC or TPWD either confirming this, or
refuting this???
Saturday, November 14, 2015 TEXAS CAPTIVE BREEDER CHRONIC WASTING DISEASE
CWD 2 MORE SUSPECTS DECTECTED
Monday, November 16, 2015
*** TEXAS PARKS AND WILDLIFE DEPARTMENT EXECUTIVE DIRECTOR ORDER NO.
015-006
*** Chronic Wasting Disease (CWD) immediate danger to the white-tailed deer
and mule deer resources of Texas
Saturday, November 14, 2015
TEXAS CAPTIVE BREEDER CHRONIC WASTING DISEASE CWD 2 MORE SUSPECTS DECTECTED
BRINGING NUMBER TO 7 DETECTED IN CAPTIVE BREEDER (if/when the last two are
confirmed).
Thursday, November 05, 2015
*** TPW Commission Adopts Interim Deer Breeder Movement Rules
Friday, October 09, 2015
Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October
2015
Saturday, October 03, 2015
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO
2015
Thursday, September 24, 2015
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE
Prion Testing
*** I cannot stress enough to all of you, for the sake of your family and
mine, before putting anything in the freezer, have those deer tested for CWD.
...terry
***raw and uncut
Sunday, August 23, 2015
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig
and take her to the dance in Texas
Friday, August 07, 2015
*** Texas CWD Captive, and then there were 4 ?
Thursday, August 06, 2015
*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Thursday, July 09, 2015
TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed
Herd with Testing of Exposed Animals
Wednesday, July 01, 2015
TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Wednesday, March 18, 2015
*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18,
2015
Wednesday, March 25, 2015
*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Thursday, May 02, 2013
*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY
TEXTING
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West
Texas
***CWD TEXAS TAHC OLD FILE HISTORY
updated from some of my old files. ...
Subject: CWD SURVEILLANCE STATISTICS TEXAS (total testing figures less than
50 in two years)
Date: Sun, 25 Aug 2002 21:06:49 –0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
greetings list members,
here are some figures on CWD testing in TEXAS...TSS
Dear Dr. Singletary,
In Fiscal Year 2001, seven deer from Texas were tested by the National
Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed
deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer).
During these two years, an additional six elk and one white-tailed deer were
tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal
Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least
eight other white-tailed deer have been tested at TVMDL. One elk has been tested
at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke
of the Texas Parks and Wildlife Department also has records of 601 clinically
ill white-tailed deer which were necropsied at Texas A&M during the late
1960's and early 1970's, and no spongiform encepalopathies were noted. Thank you
for your consideration.
xxxxxxx
Texas Animal Health Commission
(personal communication...TSS)
Austin 8 news
snip...
"There's about 4 million deer in the state of Texas, and as a resource I
think we need to be doing as much as we can to look for these diseases," said
Doug Humphreys with Texas Parks and Wildlife. "Right now Texas is clear. We
haven't found any, but that doesn't mean we don't look."
With approximately 4 million animals, Texas has the largest population of
white-tailed deer in the nation. In addition, about 19,000 white-tailed deer and
17,000 elk are being held in private facilities. To know if CWD is present in
captive herds, TPWD and Texas Animal Health Commission are working with breeders
to monitor their herds.
How is it spread?
It is not known exactly how CWD is spread. It is believed that the agent
responsible for the disease may be spread both directly (animal to animal
contact) and indirectly (soil or other surface to animal). It is thought that
the most common mode of transmission from an infected animal is via saliva,
feces, and urine.
some surveillance?
beyond the _potential_ methods of transmissions above, why, not a single
word of SRM of various TSE species in feed as a source?
it's a known fact they have been feeding the deer/elk the same stuff as
cows here in USA.
and the oral route has been documented of CWD to mule deer fawns in lab
studies.
not to say that other _potential_ transmission mechanisms are possible, but
why over look the obvious?
TSS
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From: Ken Waldrup, DVM, PhD (host25-207.tahc.state.tx.us)
Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border)
Date: December 15, 2003 at 3:43 pm PST
In Reply to: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border) posted by TSS on December 12, 2003 at 2:15 pm:
Dear sirs:
With regard to your comment about Texas NOT looking for CWD along the New
Mexico border, it is painfully obvious that you do not know or understand the
natural distribution of mule deer out there or the rights of the land owners in
this state. As of 15 December 2003, a total of 42 deer had been sampled from
what we call "Trans-Pecos", beyond the Pecos River. Mule deer are very widely
dispersed through this area, sometimes at densities of one animal per 6 square
miles. The Texas Parks and Wildlife Department does not have the legal authority
to trepass on private property to collect deer. Some landowners are cooperative.
Some are not. Franklin State Park is at the very tip of Texas, and deer from the
park have been tested (all negative). One of the single largest land owners
along the border is the National Park Service. Deer and elk from the Guadalupe
Peak National Park cannot be collected with federal permission. The sampling
throughout the state is based on the deer populations by eco-region and is
dictated by the availability of funds. I am concerned about your insinuation
that CWD is a human health risk. We are at a stand-off - you have no proof that
it is and I have no definitive proof that it isn't. However I would say that the
inferred evidence from Colorado, Wyoming and Wisconsin suggests that CWD is not
a human health concern (i.e. no evidence of an increased incidence of human
brain disorders within the CWD "endemic" areas of these states). From my
professional interactions with the Texas Parks and Wildlife Department, I can
definitely say that they want to do a thorough and sound survey throughout the
state, not willy-nilly "look here, look there". There are limitations of
manpower, finances and, in some places, deer populations. I would congratulate
TPWD for doing the best job with the limitations at hand rather than trying to
browbeat them when you obviously do not understand the ecology of West Texas.
Thank you for your consideration.
======================
From: TSS (216-119-139-126.ipset19.wt.net)
Subject: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border)
Date: December 16, 2003 at 11:03 am PST
In Reply to: Re: CWD SAMPLING TEXAS (but NOT in the obvious place, the NM,
TEXAS border) posted by Ken Waldrup, DVM, PhD on December 15, 2003 at 3:43 pm:
HEllo Dr. Waldrup,
thank you for your comments and time to come to this board.
Ken Waldrup, DVM, PhD states;
> it is painfully obvious that you do not know or understand the natural
distribution of mule deer out there or the rights of the land owners in this
state...
TSS states;
I am concerned about all deer/elk not just mule deer, and the rights of
land owners (in the case with human/animal TSEs) well i am not sure of the
correct terminology, but when the States deer/elk/cattle/sheep/humans are at
risk, there should be no rights for land owners in this case. the state should
have the right to test those animals. there are too many folks out there that
are just plain ignorant about this agent. with an agent such as this, you cannot
let landowners (and i am one) dictate human/animal health, especially when you
cannot regulate the movement of such animals...
Ken Waldrup, DVM, PhD states;
> Deer and elk from the Guadalupe Peak National Park cannot be collected
with federal permission.
TSS states;
I do not understand this? so there is no recourse of action even if every
deer/elk was contaminated with CWD in this area (hypothetical)?
Ken Waldrup, DVM, PhD states;
> I am concerned about your insinuation that CWD is a human health risk.
We are at a stand-off - you have no proof that it is and I have no definitive
proof that it isn't. However I would say that the inferred evidence from
Colorado, Wyoming and Wisconsin suggests that CWD is not a human health concern
(i.e. no evidence of an increased incidence of human brain disorders within the
CWD "endemic" areas of these states)...
TSS states;
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging
Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
Ecoregions of TEXAS
IF you look at the area around the NM WSMR where the CWD cluster was and
where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my
Geography and my Ciphering is correct ;-) that region only tested 55% of it's
goal. THE most important area on the MAP and they only test some 96 samples,
this in an area that has found some 7 positive animals? NOW if we look at the
only other border where these deer from NM could cross the border into TEXAS,
this area is called the High Plains ecoregion, and again, we find that the
sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD
sampling was met, only 16 samples were tested from some 175 that were suppose to
be sampled.
AS i said before;
> SADLY, they have not tested enough from the total population to
> know if CWD is in Texas or not.
BUT now, I will go one step further and state categorically that they are
not trying to find it. just the opposite it seems, they are waiting for CWD to
find them, as with BSE/TSE in cattle, and it will eventually...
snip...end...TSS
===============================
2005
SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;
NO update on CWD testing in Texas, New Mexico that i could find. I have
inquired about it though, no reply yet...
-------- Original Message --------
Subject: CWD testing to date TEXAS ?
Date: Mon, 09 May 2005 12:26:20 –0500
From: "Terry S. Singeltary Sr."
To: kristen.everett@tpwd.state.tx.us
Hello Mrs. Everett,
I am most curious about the current status on CWD testing in Texas. could
you please tell me what the current and past testing figures are to date and
what geographical locations these tests have been in. good bust on the illegal
deer trapping case. keep up the good work there.........
thank you, with kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
-------- Original Message --------
Subject: CWD testing in New Mexico
Date: Mon, 09 May 2005 14:39:18 –0500
From: "Terry S. Singeltary Sr."
To: ispa@state.nm.us
Greetings,
I am most curious of the current and past CWD testing in New Mexico, and
there geographical locations...
thank you,
Terry S. Singeltary SR. CJD Watch
#################### https://lists.aegee.org/bse-l.html
####################
2006
----- Original Message -----
From: "Terry S. Singeltary Sr." flounder9@VERIZON.NET
To: BSE-L@aegee.org
Sent: Saturday, December 23, 2006 1:47 PM
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???
Date: December 23, 2006 at 11:25 am PST
Greetings BSE-L members,
i never know if i am going crazy or just more of the same BSe. several
years ago i brought up the fact to the TAHC that CWD was literally at the Texas
borders and that the sample size for cwd testing was no where near enough in the
location of that zone bordering NM. well, i just wrote them another letter
questioning this again on Dec. 14, 2006 (see below) and showed them two
different pdf maps, one referencing this url, which both worked just fine then.
since then, i have NOT received a letter from them answering my question, and
the url for the map i used as reference is no longer working? i had reference
this map several times from the hunter-kill cwd sampling as of 31 August 2005
pdf which NO longer works now??? but here are those figures for that zone
bordering NM, for those that were questioning the url. the testing samples
elsewhere across Texas where much much more than that figure in the zone
bordering NM where CWD has been documented bordering TEXAS, near the White Sands
Missile Range. SO, why was the Texas hunter-kill cwd sampling as of 31 August
2005 document removed from the internet??? you know, this reminds me of the
infamous TEXAS MAD COW that i documented some 7 or 8 months before USDA et al
documented it, when the TAHC accidentally started ramping up for the
announcement on there web site, then removed it (see history at bottom). i am
not screaming conspiracy here, but confusious is confused again on the ciphering
there using for geographical distribution of cwd tissue sample size survey, IF
they are serious about finding CWD in TEXAS. common sense would tell you if cwd
is 35 miles from the border, you would not run across state and have your larger
samples there, and least samples 35 miles from where is what
found..........daaa..........TSS
THEN NOTICE CWD sample along that border in TEXAS, Three Year Summary of
Hunter-Kill CWD sampling as of 31 August 2005 of only 191 samples, then compare
to the other sample locations ;
TPWD has been conducting surveys of hunter-kill animals since 2002 and has
collected more than 7300 samples (as of 31 August 2005). In total, there have
been over 9400 samples, both hunter-kill and private samples, tested in Texas to
date, and no positives have been found.
SO, out of a total of 9,400 samples taken for CWD surveillance in TEXAS
since 2002 of both hunter-kill and private kill, ONLY 191 samples have been
taken in the most likely place one would find CWD i.e. the border where CWD has
been documented at TEXAS and New Mexico
latest map NM cwd old data
CWD in New Mexico ;
What is the Department doing to prevent the spread of CWD?
Chronic wasting disease (CWD) was recently detected in a mule deer from
Unit 34. Until 2005, CWD had only been found in Unit 19. With this discovery,
the Department will increase its surveillance of deer and elk harvested in Units
29, 30 and 34.
Lymph nodes and/or brain stems from every harvested deer and brain stems
from all elk taken in Unit 34 will be sampled.
snip...
CWD SURVEILLANCE TEXAS
SNIP...SEE FULL TEXT ;
2011 – 2012
Friday, October 28, 2011
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
Greetings TAHC et al,
A kind greetings from Bacliff, Texas.
In reply to ;
Texas Animal Health Commission (TAHC) Announcement October 27, 2011
I kindly submit the following ;
***for anyone interested, here is some history of CWD along the Texas, New
Mexico border, and my attempt to keep up with it...terry
snip...
see history CWD Texas, New Mexico Border ;
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
Sunday, October 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009 2009 Summary of Chronic
Wasting Disease in New Mexico New Mexico Department of Game and Fish
Saturday, January 23, 2016
Texas new interim rule governing Deer Management Permit (DMP) activities as
part of the state’s response to the detection of chronic wasting disease (CWD)
in captive deer populations
Saturday, January 23, 2016
Texas Chronic Wasting Disease Response Update and Interim Deer Management
Permit Rules Recommended Adoption of Proposed Rules
CANADA CWD
Friday, January 29, 2016
Survey finds more CWD in Western Canada 200 animal heads submitted for
testing, 18 or about 10 percent tested positive for CWD TSE PRION
P.153: An independent and blinded confirmation of real-time quakinginduced
conversion (RT-QuIC) analysis of cervid rectal biopsies for detection of chronic
wasting disease
Sireesha Manne1,*, Naveen Kondru1, Nicholas Haley2, Tracy Nichols3, Bruce
Thomsen4, Roger Main5, Patrick Halbur5, Arthi Kanthasamy1, and Anumantha
Kanthasamy1 1Biomedical Sciences; Iowa State University; Ames, IA USA; 2Kansas
State University; Manhattan, KS USA; 3United States Department of Agriculture;
Fort Collins, CO USA; 4National Veterinary Service Laboratories; Ames, IA USA;
5VDPAM; Iowa State University; Ames, IA USA
Prion diseases are transmissible spongiform encephalopathies (TSEs)
characterized by an always fatal, progressive neuronal degeneration in the brain
due to infectious misfolded prion proteins whose prolonged incubation periods
often make ante-mortem diagnosis difficult. Chronic wasting disease (CWD) is a
TSE affecting both wild and captive populations of mule deer, whitetailed deer,
elk and moose. CWD in cervids was first identified in Rocky Mountain States and
has recently spread to several other states including Iowa. In this current
study, we attempted to independently confirm the results of a Real-Time
Quaking-Induced Conversion (RT-QuIC) assay to diagnose CWD using rectal biopsy
sections from farmed white-tailed deer. First, we generated recombinant prion
protein substrate and then validated the quality of protein for RT-QuIC using a
reference prion protein kindly provided by Dr. Caughey’s lab. After validating
the assay, we blindly evaluated approximately 350 rectal biopsy samples analyzed
previously by another institution. All assay plates included positive and
negative controls and were analyzed in triplicate. Samples were analyzed using
the Biotek Cytation-3 multimode plate reader for 24-hrs duration. Our RT-QuIC
assays showed 55% positivity for 356 rectal samples analyzed. Comparison of
RT-QuIC results with the immunohistochemical results of obex revealed 93%
sensitivity (95% confidence limits: 88.05–95.78%) and 96% specificity (95% CL:
91–99%), confirming that the RT-QuIC assay may be one of the most promising
rapid assays for detecting CWD prions. We are currently working on applying the
RT-QuIC assay to other test samples (ISU Presidential Wildlife initiative,
ISU-CVM Diagnostic lab and ES10586).
Saturday, May 30, 2015
PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS
Article Citation: (2015)
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER
(ODOCOILEUS HEMIONUS) IN COLORADO, USA.
Journal of Wildlife Diseases In-Press. doi: http://dx.doi.org/10.7589/2014-12-284
Ahead of Print
AGE AND REPEATED BIOPSY INFLUENCE ANTEMORTEM PRPCWD TESTING IN MULE DEER
(ODOCOILEUS HEMIONUS) IN COLORADO, USA
Chris Geremia1,6,7 Jennifer A. Hoeting2, Lisa L. Wolfe3, Nathan L.
Galloway4, Michael F. Antolin4, Terry R. Spraker5, Michael W. Miller3, and N.
Thompson Hobbs1
1 Natural Resource Ecology Laboratory, Graduate Degree Program in Ecology,
Colorado State University, Fort Collins, Colorado, 80523-1499, USA
2 Department of Statistics, Colorado State University, Fort Collins,
Colorado 80523, USA
3 Colorado Division of Parks and Wildlife, Wildlife Health Program, 4330
Laporte Avenue, Fort Collins, Colorado 80521, USA
4 Department of Biology, Colorado State University, Fort Collins, Colorado
80523-1878, USA
5 Colorado State University Diagnostics Laboratory, Colorado State
University, Fort Collins, Colorado 80523, USA
Key words: Bayesian, capture–mark–recapture, chronic wasting disease, mule
deer, prion, test sensitivity
Abstract
Biopsy of rectal-mucosa associated lymphoid tissue provides a useful, but
imperfect, live-animal test for chronic wasting disease (CWD) in mule deer
(Odocoileus hemionus). It is difficult and expensive to complete these tests on
free-ranging animals, and wildlife health managers will benefit from methods
that can accommodate test results of varying quality. To this end, we developed
a hierarchical Bayesian model to estimate the probability that an individual is
infected based on test results. Our model was estimated with the use of data on
210 adult female mule deer repeatedly tested during 2010−2014. The ability to
identify infected individuals correctly declined with age and may have been
influenced by repeated biopsy. Fewer isolated lymphoid follicles (where PrPCWD
accumulates) were obtained in biopsies of older deer and the proportion of
follicles showing PrPCWD was reduced. A deer’s genotype in the prion gene (PRNP)
also influenced detection. At least five follicles were needed in a biopsy to
assure a 95% accurate test in PRNP genotype 225SS deer.
Received: December 15, 2014; Accepted: April 23, 2015
6 Current address: Yellowstone Center for Resources, P.O. Box 168,
Yellowstone National Park, Mammoth Hot Springs, Wyoming 82190, USA
7 Corresponding author (email: chris_geremia@nps.gov)
CWD DIAGNOSTICS
Article | Open
Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of
Prion Infection
A. Christy Wyckoff , Nathan Galloway , Crystal Meyerett-Reid , Jenny Powers
, Terry Spraker , Ryan J. Monello , Bruce Pulford , Margaret Wild , Michael
Antolin , Kurt VerCauteren
& Mark Zabel
Scientific Reports 5, Article number: 8358 (2015) doi:10.1038/srep08358
Download Citation Molecular ecology | Proteins | Statistics
Received:27 June 2014Accepted:19 January 2015Published online:10 February
2015 Article Tools
Abstract
Prions are unique infectious agents that replicate without a genome and
cause neurodegenerative diseases that include chronic wasting disease (CWD) of
cervids. Immunohistochemistry (IHC) is currently considered the gold standard
for diagnosis of a prion infection but may be insensitive to early or
sub-clinical CWD that are important to understanding CWD transmission and
ecology. We assessed the potential of serial protein misfolding cyclic
amplification (sPMCA) to improve detection of CWD prior to the onset of clinical
signs. We analyzed tissue samples from free-ranging Rocky Mountain elk (Cervus
elaphus nelsoni) and used hierarchical Bayesian analysis to estimate the
specificity and sensitivity of IHC and sPMCA conditional on simultaneously
estimated disease states. Sensitivity estimates were higher for sPMCA (99.51%,
credible interval (CI) 97.15–100%) than IHC of obex (brain stem, 76.56%, CI
57.00–91.46%) or retropharyngeal lymph node (90.06%, CI 74.13–98.70%) tissues,
or both (98.99%, CI 90.01–100%). Our hierarchical Bayesian model predicts the
prevalence of prion infection in this elk population to be 18.90% (CI
15.50–32.72%), compared to previous estimates of 12.90%. Our data reveal a
previously unidentified sub-clinical prion-positive portion of the elk
population that could represent silent carriers capable of significantly
impacting CWD ecology.
snip...
Our data demonstrate that previous IHC-based studies are possibly missing
early stage or sub-clinical cases in sampled populations. It is widely accepted
that IHC is sensitive enough to detect pre-clinical cases, but we propose that
sPMCA can detect additional cases even earlier, possibly soon after infection.
In previous work we found sPMCA had a detection limit of 10−9 35,46 which is
much more sensitive than the sensitivity of a mouse bioassay at 10−4. This
suggests that animals found positive by sPMCA have much lower levels of PrPCWD
than animals with clinical disease, but are indeed infected. The detection of
very early sub-clinical cases raises the question of biological relevance at the
population level. We propose that this sub-clinical subset of the population may
be ecologically important to the disease transmission cycle because of potential
preclinical vertical transmission from mother to offspring47, horizontal
transmission through direct contact, or indirect transmission through
environmental deposits of prions.
It remains unclear when animals begin shedding prions into the environment.
Through the use of a mouse bioassay Tamguney et al.22,24,44,45 showed
asymptomatic deer were capable of shedding infectious levels of CWD as early as
10 months prior to clinical disease. Bioassays, both in mice and deer, have
limited sensitivity so shedding could be occurring much earlier than 10 months
post-infection but at levels insufficient to cause clinical disease in the
infected host. It is also unclear if genotype plays a role in prion shedding, as
well as disease course. Our data suggest that having at least one L allele at
codon 132 does not alter the disease prevalence within the ML genotype,
supporting data reported by Perucchini et al.27. The slow disease course and the
potential existence of a carrier state facilitate a high prevalence and frequent
opportunity for transmission between animals with the MM and ML genotypes.
It is commonly stated in the literature that CWD is an invariably fatal
disease, but it may be more accurate to state that once animals begin to show
clinical signs they are certain to succumb to CWD or other associated causes of
death such as predation4,24,48. Perhaps other carrier states exist within the
population, which may or may not contribute to the transmission and deposition
of prions in the population and the environment. Further research is required to
address the role of a carrier state in the ecology of CWD transmission.
The application of sPMCA will be important both to research and for
diagnostic investigation, and may improve state and federal surveillance
programs for CWD in both naïve and endemic host populations. Increased
sensitivity, and the need for only obex tissue, may lead to detection of new
focal points prior to clinical disease emerging in otherwise CWD-free
populations. Additionally, in the economically and politically difficult
scenario of culling captive herds that tested positive for CWD, extremely
sensitive assays such as sPMCA of prions from tissue and excreta are essential
to verify that more animals besides the index case were infected, and if any
sub-clinical carriers may have been shedding into the environment.
Overall, our data contribute to the increasing evidence that a portion of a
herd may be infected, but die from other causes while infected with PrPCWD
because of age, genetic susceptibility or other unknown factors. However, the
contribution of prions shed into the environment from this sub-clinical
population may be important and requires further investigation. The existence of
an infectious PrPCWD carrier state aligns with disease ecology theory, which
proposes balance between transmissibility and pathogenesis of a pathogen. As
such, through selection pressures from the host and external environment the
pathogen will tend towards the greatest transmissibility strategy. CWD
transmission may be more complicated than disease ecology might predict, since
prolonged persistence and indirect transmission of prions in the environment may
potentiate spread without affecting pathogenesis.
Despite the fact that prions are only protein, studies continue to point at
evolutionary behavior and selection pressures of prions which indicate that like
other pathogens, prions are capable of evolving and adapting to their
environment4,27,48,49. With increasing prevalence at the population level, as is
reported in this study, sPMCA will continue to be an important tool to
investigate CWD in wildlife.
P170
Clinical Stage of Infection is Critical in the Antemortem Diagnosis of
Chronic Wasting Disease in Deer and Elk
Chris Siepker1, Nicholas Haley1, W. David Walter2, Matteo Manca3, Laura
Hoon-Hanks4, Ryan Monello5, Jenny Powers5, Justin Greenlee6 , Bruce Thomsen7 ,
Aaron Lehmkuhl7, Gordon Mitchell8, Tracy Nichols9,Byron Caughey3, Edward
Hoover4, and Juergen Richt1.
1. Department of Diagnostic Medicine and Pathobiology, Kansas State
University, Manhattan KS USA 2. United States G e o l o g i c a l Survey, P e n
n s y l v a n i a Cooperative Fish and Wildlife Research Unit, University Park
PA USA 3. TSE/Prion Biochemistry Section, Rocky Mountain Laboratories, National
Institutes of Health, Hamilton, MT USA 3. Department of MIP, Colorado State
University, Fort Collins CO USA 4. National Park Service, Wildlife Health
Branch, Fort Collins CO USA 5. Virus and Prion Research Unit, National Animal
Disease Center, ARS, USDA, Ames IA USA 6. USDA, APHIS, VS, STAS, National
Veterinary Service Laboratories, Ames IA USA 7. National and OIE Reference
Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa ON
Canada 8. National Wildlife Research Center Wildlife Services, APHIS, USDA, Fort
Collins CO USA
Chronic wasting disease (CWD) is an e f f i c i e n t l y t r a n s mi t t
e d s p o n g i f o r m encephalopathy of cervids (e.g. deer, elk, and moose),
and is the only known prion disease affecting both free-ranging wildlife and
captive animals. The antemortem detection of CWD and other prion diseases has
proven difficult, due in part to difficulties in identifying an appropriate
peripheral tissue specimen and complications with conventional test sensitivity.
At present, biopsies of the recto-
Prion2015 Program Guide 22
anal mucosal-associated lymphoid tissues (RAMALT) have shown promising
sensitivity and are not impractical to collect in live animals. Nasal brush
collections have likewise proven both sensitive and practical for identification
of prion infections in humans. In this study, we evaluated both RAMALT and nasal
brush collections by real time quaking-induced conversion (RT-QuIC), and
compared our findings to RAMALT immu n o h i s t o c h emi s t r y a s we l l a
s conventional postmortem evaluation of obex and retropharyngeal lymph node
tissues from over 700 captive and free-ranging deer and elk in areas with
endemic CWD. We correlated our results with various clinical findings, including
pathological stage of infection as determined by obex scoring, PrP genotype,
age, and sex. While the sensitivity of RAMALT RT-QuIC analyses exceeded that of
RAMALT IHC (69-80% vs. >44%) and nasal brush collections (15-30%), the
sensitivity of both biopsy and nasal brush analyses were dependent primarily on
clinical stage of disease, although PrP genotype was also an important predictor
of sample positivity. Our findings further demonstrate the potential and
limitations of antemortem sample analyses by RT-QuIC in the identification and
management of prion diseases.
J Vet Sci. 2015 Jun; 16(2): 179–186.
Published online 2015 Jun 17. doi: 10.4142/jvs.2015.16.2.179
PMCID: PMC4483501
Classical natural ovine scrapie prions detected in practical volumes of
blood by lamb and transgenic mouse bioassays
Rohana P. Dassanayake,corresponding author1 Thomas C. Truscott,2 Dongyue
Zhuang,2 David A. Schneider,2 Sally A. Madsen-Bouterse,1 Alan J. Young,3 James
B. Stanton,1 William C. Davis,1 Katherine I. O'Rourke1
J Virol. 2013 May; 87(10): 5895–5903. doi: 10.1128/JVI.03469-12 PMCID:
PMC3648199 Dissociation between Transmissible Spongiform Encephalopathy (TSE)
Infectivity and Proteinase K-Resistant PrPSc Levels in Peripheral Tissue from a
Murine Transgenic Model of TSE Disease Karen Dobie and Rona Barroncorresponding
author Neurobiology Division, The Roslin Institute & R(D)SVS, Easter Bush,
Midlothian, United Kingdom corresponding authorCorresponding author. Address
correspondence to Rona Barron, Email: ku.ca.de.nilsor@norrab.anor. Author
information ► Article notes ► Copyright and License information ► Received 2012
Dec 19; Accepted 2013 Mar 7. Copyright © 2013, American Society for
Microbiology. All Rights Reserved. This article has been cited by other articles
in PMC. Go to: Abstract Most current diagnostic tests for transmissible
spongiform encephalopathies (TSE) rely on the presence of proteinase K
(PK)-resistant PrPSc (PrP-res) in postmortem tissues as an indication of TSE
disease. However, a number of studies have highlighted a discrepancy between TSE
infectivity and PrP-res levels in both natural and experimental cases of TSE
disease. Previously, we have shown high TSE infectivity levels in the brain
tissue of mice that have a clinical TSE disease with associated vacuolar
pathology but little or no detectable PrP-res. Here, the levels of TSE
infectivity and PrP-res within a peripheral tissue of this mouse model were
investigated. Biochemical analysis showed that low levels of PrP-res were
present in the spleen tissue in comparison to the levels observed in the spleen
of mice infected with ME7 or 79A. However, upon subpassage of brain and spleen
tissue from clinically ill mice with little or no PrP-res detectable, similar
short incubation periods to disease were observed, indicating that infectivity
levels were similarly high in both tissues. Thus, the discrepancy between
PrP-res and TSE infectivity was also present in the peripheral tissues of this
disease model. This result indicates that peripheral tissues can contain higher
levels of infectivity given the correct combination of host species, PrP
genotype, and TSE agent. Therefore, the assumption that the levels of peripheral
infectivity are lower than those in the central nervous system is not always
correct, and this could have implications for current food safety regulations.
SNIP...
Several recent studies have identified the presence of quasispecies within
individual cases of TSE disease in humans (23, 24) and animals (25) and in
cell-culture models (26). Indeed, it has been hypothesized that subvariants of
disease-associated PrP replicate preferentially in specific tissue types, with a
dependence on tissue-specific host factors (25, 27). The biochemical and
immunohistochemical analyses of the recipient mice from the 101LL/GSS subpassage
demonstrated that PrP-res deposition was lower in the brain tissue of mice that
received the spleen homogenate inocula than in those that received the brain
homogenate inocula (Fig. 6), while in contrast, the vacuolation score in mice
was greater in those that received the spleen homogenate than in those that
received the brain homogenate (Fig. 4). These results indicate that a
potentially heterogeneous population of PrP-res was present. It is hypothesized
that tissue-specific conditions supported the replication of different
subvariants that showed different replication efficiencies upon subpassage. If
heterogeneous populations of PrP-res exist that include variants that have
different replication capabilities, a variant present in peripheral tissues may
have a higher level of infectivity than the corresponding brain-derived variant.
Therefore, assessment of the peripheral infectivity levels from novel and
emerging isolates is urgently required to ensure that an accurate titer is
established to maintain food safety.
Together, these results indicate that a form of the infectious agent may be
present in this disease model that remains undetectable by current standard
analysis. Given the increasing costs of bioassay to identify the presence of TSE
infectivity, the majority of disease cases are being confirmed by biochemical
techniques specific for the presence of PrP-res, without confirmation of the
presence of infectivity. This current reliance on PrP-res as indicative of TSE
disease may not detect all cases of TSE disease, with the possible emergence of
cases with high infectivity levels associated with low levels or an absence of
PrP-res. Indeed, the discovery of significant levels of TSE infectivity despite
the absence of PrP-res in spleens from sheep infected with atypical scrapie (13)
indicates that this disease phenomenon can occur in natural cases of TSE disease
present in the environment. Furthermore, a recent study by Gonzalez and
colleagues highlighted the discrepancy between levels of PrP-res and TSE
infectivity in sheep scrapie and sheep BSE and indicated that quantitative
laboratory tests to detect disease-associated PrP could not be used to
accurately predict infectious titers (28). While TSEs remain in the environment,
the emergence of novel isolates or the possibility that a known isolate could
infect a different host species remains. Our data show that a combination of
host species, PrP genotype, and TSE isolate that could produce a novel disease
phenotype with high levels of TSE infectivity in the absence of PrP-res has the
potential to occur. Therefore, if the infectivity levels in the peripheral
tissues of disease cases with low levels of PrP-res are higher than originally
hypothesized from previous research into classical isolates and current
biochemical tests, the emergence of a novel isolate could pose a major risk to
food safety if tissues were able to enter the food chain. Together with the
discrepancy between PrP-res and TSE infectivity levels presented here, the
estimation of infectious titer should not rely on the detection of PrP-res as
the sole indicator of TSE disease.
cwd diagnostics
Wednesday, September 17, 2014
Cost benefit analysis of the development and use of ante-mortem tests for
transmissible spongiform encephalopathies
Terry S. Singeltary SR.
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