Friday, August 31, 2012
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK and CWD 2009-2012 a
review
COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK 2011
The Committee met on October 2, 2011 at the Adams Mark Hotel in Buffalo,
New York from 12:30-5:3 0p.m. There were 25 members and 31 guests present. Dr.
John Fischer presided as acting chair for the Committee due to unavoidable
conflicts of Drs. Miller and Hilsenroth. Bovine TB
snip...
USDA-APHIS-VS Chronic Wasting Disease National Program
Patrice N. Klein of USDA APHIS VS – National Center for Animal Health
Programs provided an update on the agency’s CWD–related activities:
CWD Rule Update: The amended final rule on chronic wasting disease (CWD) is
currently in departmental clearance. The rule will set minimum standards for
interstate movement and establish the national
___voluntary___
Herd Certification Program (HCP). Farmed/captive cervid surveillance
testing: Through FY2010, VS conducted surveillance testing on approximately
20,000 farmed /captive cervids by the immunohistochemistry (IHC) standard
protocol. As of September 15, 2011, approximately 19,000 farmed /captive cervids
were tested by IHC for CWD with funding to cover lab costs provided through
NVSL.
Farmed/captive cervid CWD status: The CWD positive captive white-tailed
deer (WTD) herd reported in Missouri (February 2010) was indemnified and
depopulation activities were completed in June 2011. All depopulated animals
were tested for CWD and no additional CWD positive animals were found.
In FY 2011, CWD was reported in two captive elk herds in Nebraska
(December, 2010 and April 2011, respectively). To date, 52 farmed/captive cervid
herds have been identified in 11 states: CO, KS, MI, MN, MO, MT, NE, NY, OK, SD,
WI. Thirty-nine were elk herds and 13 were WTD herds. At this time, eight CWD
positive herds remain – six elk herds in Colorado and the two elk herds in
Nebraska.
Wild Cervid surveillance: In FY 2009 funding supported surveillance in
approximately 74,330 wild cervids in 47 cooperating States. Wild cervid CWD
surveillance totals are pending for fiscal year 2010 (2010 – 2011 calendar year)
due to seasonal surveillance activities and completion of final cooperative
agreement reporting to APHIS.
In fiscal year 2011, there are 15 ‘tier 1’ States, 20 ‘tier 2’ States, and
15 ‘tier 3’ States. Two new ‘tier 1’ States, Minnesota and Maryland, were added
in fiscal year 2011 based on the new CWD detections in a free-ranging
white-tailed deer in southeastern Minnesota and in western Maryland.
Consequently, Delaware was upgraded to ‘tier 2’ status as an adjacent State to
Maryland. For FY 2011, 45 States and 32 Tribes will receive cooperative
agreement funds to complete wild cervid surveillance and other approved work
plan activities. Based on FY 2012 projected budget reductions, future
cooperative agreement funds will be eliminated.
APHIS CWD Funding: In FY2011, APHIS received approximately $15.8 million in
appropriated funding for the CWD Program. The President’s FY 2012 budget
proposes to reduce program funding for CWD by $13.9 million, leaving the program
with a request of $1.925 million to provide some level of Federal coordination
for the national herd certification program (HCP).
Consequently, APHIS is planning to amend its role in the program to one of
Federal coordination. Based on the projected FY 2012 budget, funding for CWD
cooperative agreements and indemnity funding for States and Tribes will be
eliminated. Under this scenario, the States or cervid industry producers will
likely be responsible for the costs of surveillance testing and indemnity for
appraisal, depopulation, and disposal of CWD-positive animals.
Commodity Health Line Structure: In the FY 2012 budget, livestock
commodities regulated by USDA have been organized into ‘Commodity Health Line’
structures or groupings. APHIS’ Equine, Cervid and Small Ruminant (ECSR) Health
line supports efforts to protect the health and thereby improve the quality and
productivity of the equine, cervid and small ruminant industries. Activities
supported by the ECSR Health line range from monitoring and surveillance to
investigation and response actions undertaken when health issues relevant to the
industry are identified. APHIS also maintains regulations and program standards
which guide ECSR activities at both the Federal and State/Tribal level.
The ECSR Health line funds essential activities necessary to maintain
current ECSR surveillance and program operations while providing the flexibility
to respond to new and emerging industry-specific health concerns. APHIS’ current
activities include Scrapie, Chronic Wasting Disease (CWD), Slaughter Horse
Transport, and Brucellosis/Tuberculosis in cervids. Overall, APHIS will use
funding from the ECSR Health Line Item to support Agency efforts in the
following mission areas: prevention, preparedness and communication; monitoring,
surveillance and detection; response and containment; and continuity of
business, mitigation and recovery
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National
Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie
and CWD in inoculated deer. Interspecies transmission studies afford the
opportunity to better understand the potential host range and origins of prion
diseases. We inoculated white-tailed deer intracranially (IC) and by a natural
route of exposure (concurrent oral and intranasal inoculation) with a US scrapie
isolate. All deer inoculated by the intracranial route had evidence of PrPSc
accumulation and those necropsied after 20 months post-inoculation (PI) (3/5)
had clinical signs, spongiform encephalopathy, and widespread distribution of
PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6
months PI did not have clinical signs, but had widespread distribution of PrPSc.
This highlights the facts that 1) prior to the onset of clinical signs PrPSc is
widely distributed in the CNS and lymphoid tissues and 2) currently used
diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical
signs. The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in white-tailed deer 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 consistent with 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 white-tailed deer 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 scrapie by
IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil,
retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and
spleen. While two WB patterns have been detected in brain regions of deer
inoculated by the natural route, unlike the IC inoculated deer, the pattern
similar to the scrapie inoculum predominates.
Committee Business:
The Committee discussed and approved three resolutions regarding CWD. They
can be found in the report of the Reswolutions Committee. Essentially the
resolutions urged USDA-APHIS-VS to:
Continue to provide funding for CWD testing of captive cervids
• Finalize and publish the national CWD rule for Herd Certification and
Interstate Movement
• Evaluate live animal test, including rectal mucosal biopsy, for CWD in
cervids
BACKGROUND INFORMATION:
The proposed rule for Chronic Wasting Disease (CWD) Herd Certification and
Interstate Movement of Captive Cervids in farmed cervidae requires that all
farmed cervidae greater than 12 months of age that die or are slaughtered must
be tested for CWD. Farmed cervidae producers across the nation have complied
with testing requirements, in large part because laboratory costs for CWD
testing have traditionally been paid with United States Department of
Agriculture (USDA) funds.
The CWD testing protocol that is recommended for farmed cervidae is the
immunohistochemistry (IHC) test using formalin fixed samples of brain stem and
retropharyngeal lymph node from each animal. It is the most sensitive and
specific test for detecting CWD. The test is expensive and costs at least $25.00
per slide to perform at USDA approved laboratories.
There is an urgency to maintain USDA funding to cover the costs of CWD
testing for farmed cervidae. If USDA funding for CWD tests ends and farmed
cervidae producers are forced to cover the cost of such tests, there is a real
possibility that producer compliance with CWD testing requirements will
decrease. Without producer cooperation, the national CWD control program for
farmed cervidae could collapse.
RESOLUTION:
The United States Animal Health Association urges the United States
Department of Agriculture, Animal and Plant Health Inspection Service,
Veterinary Services to continue to provide funding to cover the laboratory costs
of testing farmed cervidae for Chronic Wasting Disease by immunohistochemistry
at all approved laboratories.
INTERIM RESPONSE:
The U.S. Department of Agriculture (USDA), Animal and Plant Health
Inspection Service (APHIS), Veterinary Services (VS) recognizes the concerns of
the United States Animal Health Association (USAHA) and appreciates the
opportunity to respond.
Resolution 14 / pg 2
In fiscal year 2012, the congressional appropriation for the chronic
wasting disease (CWD) program was reduced by $13.9 million, to approximately
$1.9 million. Consequently, VS no longer has funds to cover testing costs for
farmed cervids. Laboratories and industry were informed that this funding ended
on December 31, 2011; all such costs must now be borne by the producers. VS will
continue to cover only confirmatory testing on any presumptive CWD positive
samples from farmed and wild cervidae at the National Veterinary Services
Laboratories.
VS will direct remaining program funds to the publication of the CWD final
rule and the administrative costs associated with implementation of the national
CWD herd certification program.
UNITED STATES ANIMAL HEALTH ASSOCIATION
115th Annual Meeting
September 29- October 5, 2011
Buffalo, New York
_________________________________________________________
RESOLUTION NUMBER: 15 APPROVED
SOURCE: COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK
SUBJECT MATTER: CHRONIC WASTING DISEASE HERD CERTIFICATION AND INTERSTATE
MOVEMENT FINAL RULE
BACKGROUND INFORMATION:
Implementation of rules for Chronic Wasting Disease (CWD) that define the
CWD herd certification program (9 CFR 55 Subpart B) and requirements for
interstate movement of farmed cervidae (9 CFR 81) has been delayed since 2006.
There is an urgency to finalize these rules to ensure that CWD certification
programs are uniformly administered in all states and that all farmed cervidae
that move from state to state meet the same requirements. These rules are
critically important to the survival of the farmed cervidae industry. These
rules are needed to preserve the ability of producers to move farmed cervidae
and their products interstate and internationally without unnecessary
restrictions.
RESOLUTION:
The United States Animal Health Association urges the United States
Department of Agriculture, Animal and Plant Health Inspection Service,
Veterinary Services to finalize rules for Chronic Wasting Disease herd
certification programs (9 CFR 55 Subpart B) and interstate movement of farmed
cervidae (9 CFR 81).
INTERIM RESPONSE:
The U.S. Department of Agriculture (USDA), Animal and Plant Health
Inspection Service, Veterinary Services appreciates your interest in the
rulemaking for chronic wasting disease (CWD).
The CWD amended final rule was cleared by USDA and is in clearance in the
Office of Management and Budget (OMB). Once OMB clearance is completed, the CWD
amended rule would become effective 60 days after its publication.
UNITED STATES ANIMAL HEALTH ASSOCIATION
115th Annual Meeting
September 29- October 5, 2011
Buffalo, New York
_________________________________________________________
RESOLUTION NUMBER: 16 APPROVED
SOURCE: COMMITTEE ON CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK
SUBJECT MATTER: LIVE ANIMAL TESTING FOR CHRONIC WASTING DISEASE
BACKGROUND INFORMATION:
Detection of Chronic Wasting Disease (CWD) in live animals is an important
component of CWD Prevention and Control Programs.
With the funding decrease for CWD indemnification, the need has increased
for additional diagnostic tools to monitor CWD positive herds and
epidemiologically linked herds that may be maintained in quarantine rather than
depopulated. The use of recto-anal mucosa associated lymphoid tissue (RAMALT)
has been approved as a live animal test for Scrapie. There have been numerous
studies evaluating the sensitivity and specificity of RAMALT in cervids. There
are several additional advantages to RAMALT sampling. There is a large amount of
suitable tissue to sample and multiple sites can be sampled allowing repeat
sampling over time.
RESOLUTION:
The United States Animal Health Association requests that the United States
Department of Agriculture, Animal and Plant Health Inspection Service,
Veterinary Services evaluate live animal tests, including the rectal biopsy
(RAMALT), as a live animal test for Chronic Wasting Disease.
INTERIM RESPONSE:
The U.S. Department of Agriculture, Animal and Plant Health Inspection
Service (APHIS), Veterinary Services appreciates your interest in live animal
tests for chronic wasting disease (CWD).
APHIS is completing analysis of a multi-year study evaluating recto-anal
mucosa associated lymphoid tissue (RAMALT) biopsy testing as a diagnostic tool
for CWD detection in captive white-tailed deer. This is a collaborative study
with APHIS Wildlife Services, Agricultural Research Service, Canadian Food
Inspection Agency, Colorado State University, and others to evaluate the
existing collective data on white-tailed deer relative to diagnostic testing and
interpretation of the immunohistochemistry test for CWD
Resolution 16 / pg 2
on rectal biopsy testing in the United States and Canada. Currently, there
is insufficient data available to evaluate this technique on other captive
Cervidae.
After this analysis is completed, APHIS will determine the applicability of
RAMALT for use in a CWD Herd Certification Program (HCP). We plan to complete
this determination by September 30, 2012. APHIS also will continue to evaluate
other live animal tests for CWD, as they are developed, to assess appropriate
use in a CWD HCP.
Friday, August 24, 2012
Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting
disease within white-tailed deer (Odocoileus virginianus) herds in North America
The overall diagnostic specificity was 99.8%. Selective use of antemortem
rectal biopsy sample testing would provide valuable information during disease
investigations of CWD-suspect deer herds.
(E) Beginning one hundred-eighty days after the effective date of this
rule,
(K) All monitored captive deer, three hundred sixty-five days of age or
older which die from injury, illness, slaughter, hunting, or any other cause,
shall be reported within twenty-four hours of discovery to an approved
accredited licensed veterinarian or if not available, the Chief, Division of
Animal Health or his representative. Monitored captive deer in hunting preserves
are exempt from the twenty-four hour requirement for notification.
Monitored captive deer shall be tested for chronic wasting disease
according to the following:
(1) Herds with ten head or less must test all deaths.
(2) Herds with eleven heads or more must annually test thirty percent or
thirty head of deaths, whichever is less.
(L) The owner of all captive whitetail deer being tested for chronic
wasting disease, is responsible for arranging for the submission of the required
brain tissue and any other tissues as directed by the Chief, Division of Animal
Health or his representative, to a department approved laboratory for chronic
wasting disease testing. The submission form for CWD shall be signed by an
approved accredited licensed veterinarian and shall accompany the sample. Owners
are responsible for the cost of collecting and submitting, and testing of
samples.
The animal’s official identification tag must accompany the sample; if the
animal does not have a tag at time of death, a tag must be issued and accompany
the sample.
Q. What does the 2012 amended CWD final rule entail?
A. The interim final rule responds to the concerns raised to APHIS in 2006
and finalizes the changes to the CWD program APHIS proposed in March, 2009.
It establishes a ___voluntary___ national CWD Herd Certification Program
(HCP), providing consistent minimum standards for participating states and
minimum requirements for the interstate movement of cervids.
States that participate in the HCP must establish programs that are
approved by APHIS.
snip...
Q. What are the requirements for a State to become a CWD HCP participant?
A. States interested in having their State CWD HCP approved should submit
the required application and supporting documents to APHIS for review and
approval. Application materials should be sent to the Area Veterinarian in
Charge (AVIC) in the APHIS Veterinary Service (VS) Area Office in the requesting
State. Information provided must describe the State’s CWD prevention and control
activities, and the deer, elk, and moose herd certification activities, and cite
relevant State statutes, regulations, and directives pertaining to animal health
activities and reports and publications of the State.
This must include:
• Movement restrictions,
• Surveillance and disease reporting capabilities,
• Herd/animal identification requirements
• Diagnostic testing capacities,
• Recordkeeping and data management,
• Ability to conduct epidemiologic investigations and trace-outs
• Education and outreach Details of requirements are described in 9 CFR
Part 55.23.
Q. What must a herd owner do to become a CWD HCP participant?
A. Herd owners seeking approval to participate in their Approved State CWD
HCP should contact their State agency for information on herd owner enrollment
United States Department of Agriculture
• Animal and Plant Health Inspection Service
• Safeguarding American Agriculture and State requirements. In general,
herd owners may be eligible to enroll in an Approved State CWD HCP if they:
• Add to their herds only animals that are from herds enrolled in the CWD
Herd Certification Program, to ensure that animals added to herds are of known
risk. Additions to the herd should be from other enrolled herds of equal or
greater status in the program.
• Maintain perimeter fencing adequate to prevent entry or exit of cervids,
and to minimize the possibility of CWD transmission by direct contact between
farmed and free-ranging wild cervid populations.
• Report to APHIS or the State all animals that escape or disappear, and
report to APHIS or the State all animals that die or are killed and make their
carcasses available for tissue sampling and testing. Minimum federal standards
for herd owner enrollment in their State CWD HCP are described in the 9 CFR Part
55.22.
snip...
Q. Do I have to be enrolled in an Approved State CWD HCP if the cervid
species I raise is not known to be susceptible to CWD?
A. No. The federal rule establishes federal standards for a voluntary
Approved State CWD HCP and includes cervids in the genera Cervus, Odocoileus,
and Alces and their hybrids. These genera represent cervids known to be
susceptible to CWD. Individual States may have additional requirements for other
cervid species not included in the federal rule.
never say never...tss
5. A positive result from a chimpanzee challenged severely would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
Monday, June 18, 2012
natural cases of CWD in eight Sika deer (Cervus nippon) and five Sika/red
deer crossbreeds captive Korea and Experimental oral transmission to red deer
(Cervus elaphus elaphus)
Tuesday, June 19, 2012
Experimental Oral Transmission of Chronic Wasting Disease to Reindeer
(Rangifer tarandus tarandus)
USAHA Committee on Captive Wildlife and Alternative Livestock
Tuesday October 23, 2012 8:00 AM–12:00 PM
Grandover West, Sheraton Greensboro
Greensboro, North Carolina
Chronic Wasting Disease
9:00-9:30AM Review and Updates of the USDA/APHIS Veterinary Services
National CWD Program
Patrice Klein
9:30-10:00AM CWD surveillance using the RAMALT (rectal biopsy) method Bruce
Thomsen
10:00-10:30AM Break
2010
Status: CWD was detected in one captive white-tailed deer (WTD) herd in
Missouri in February 2010. To date, 50 farmed/captive cervid herds have been
identified in 11 states: CO, KS, MI, MN, MO, MT, NE, NY, OK, SD, WI.
Thirty-seven were elk herds and 13 were WTD herds. At this time, six CWD
positive elk herds remain in Colorado and one WTD herd remains in MO. VS has
continued to offer indemnity for appraised value of the animals and to cover
costs of depopulation, disposal, and testing of CWD-positive and exposed herds.
Indemnity is provided based on availability of federal funding.
2009
Status: Five positive farmed cervid herds were detected in FY 2009: Two
white-tailed deer herds in Wisconsin, one elk herd in Minnesota, and two elk
herds in Colorado. The Wisconsin and Minnesota facilities have been depopulated.
This brings to 47 the number of positive herds that have been identified since
1997. At this time, six positive elk herds remain in Colorado. Also, CWD was
detected at slaughter for the first time in FY 2009. VS continues to offer
indemnity and cover depopulation, disposal and testing costs for CWD-positive
and exposed herds and trace animals.
Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease
in the United States
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B).
SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).
PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B).
Tuesday, June 05, 2012
Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012
Legislative Session
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol
Needs To Be Revised
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
Monday, November 14, 2011
WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Sunday, November 13, 2011
COLORADO CWD CJD TSE PRION REPORTING 2011
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
" although the infection rate was low (4 of 13 animals [Hamir et al.
2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly
as possible all updates/comments that contribute substantially to the topic
under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author
Affiliations
1Institute for Neurodegenerative Diseases, University of California, San
Francisco, San Francisco, California 94143 2Department of Neurology, University
of California, San Francisco, San Francisco, California 94143 Correspondence:
stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As
the only prion disease identified in free-ranging animals, CWD appears to be far
more communicable than other forms of prion disease. CWD was first described in
1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of
histopathology of the brain. Originally detected in the American West, CWD has
spread across much of North America and has been reported also in South Korea.
In captive populations, up to 90% of mule deer have been reported to be positive
for prions (Williams and Young 1980). The incidence of CWD in cervids living in
the wild has been estimated to be as high as 15% (Miller et al. 2000). The
development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible
to CWD, has enhanced detection of CWD and the estimation of prion titers
(Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces,
even in presymptomatic deer, has been identified as a likely source of infection
for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD
has been transmitted to cattle after intracerebral inoculation, although the
infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding
raised concerns that CWD prions might be transmitted to cattle grazing in
contaminated pastures.
snip...
----- Original Message -----
From: David Colby To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor
Department of Chemical Engineering University of Delaware
====================END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION
CONGRESS SEPTEMBER 8-11 2010
Sunday, August 19, 2012
Susceptibility of cattle to the agent of chronic wasting disease from elk
after intracranial inoculation 2012
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Wednesday, August 29, 2012
SUMNER COUNTY DEER DID NOT HAVE CHRONIC WASTING DISEASE
SUMNER COUNTY DEER DID NOT HAVE CHRONIC WASTING DISEASE Aug. 30, 2012
Initial test was false-positive
PRATT— In July, the Kansas Department of Wildlife, Parks and Tourism
(KDWPT) reported that nine deer had tested positive for chronic wasting disease
(CWD) during the 2011-12 testing period. The agency now reports that the
National Veterinary Services Laboratory in Ames, Iowa, after two different
tests, did not detect CWD prions in the Sumner County deer, so initial testing
in this case yielded a false-positive result. This reduces the total 2011-2012
positives to eight. Counties where CWD was detected during the 2011-2012
surveillance period include Wallace (one), Rawlins (one), Decatur (one), Norton
(two), Trego (one), Ford (one), and Stafford (one).
The white-tailed deer in question was taken from Sumner County last winter.
This result brings the total number of confirmed CWD cases in Kansas to 48 since
testing began in 1996. In total, 2,446 animals were tested for CWD during the
2011-2012 surveillance period, Aug. 1, 2011, through July 31, 2012.
Annual testing is part of an ongoing effort by KDWPT to monitor the
prevalence and spread of CWD. The fatal disease was first detected in the Kansas
free-ranging deer herd in 2005 in Cheyenne County.
More information on CWD can be found on KDWPT’s website, ksoutdoors.com, or
at the Chronic Wasting Disease Alliance website, www.cwd-info.org.
-30-
Thursday, July 19, 2012
NINE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE
TSS
Saturday, August 25, 2012
Missouri Suspends Issuing Permits for New Deer Breeders and Big-game Hunting Facilities
Commission approves suspension of issuing permits for new deer breeders and
big-game hunting facilities
Published on: Aug. 24, 2012
Posted by Joe Jerek
JEFFERSON CITY, Mo. – At its Aug. 24 meeting in Jefferson City, the
Missouri Conservation Commission approved changes to the Wildlife Code of
Missouri that indefinitely suspend issuing permits for new big-game hunting
facilities and new wildlife breeding facilities in Missouri that hold
white-tailed deer or mule deer.
The regulation changes to suspend the issuance of new permits do not apply
to wildlife breeders and game ranches with existing permits. The suspension of
issuing permits does not include wildlife-breeders or game ranches who wish to
hold approved wildlife species other than white-tailed deer or mule deer.
Renewal of existing permits for hunting and breeding facilities will be
considered under established requirements of the Wildlife Code.
“The Missouri Department of Conservation (MDC) is responsible for managing
and protecting the wildlife resources of the state and we take that
responsibility very seriously,” says MDC Deputy Director Tom Draper. “With
Chronic Wasting Disease now in Missouri, this suspension of issuing permits for
new deer breeders and hunting ranches is one of several actions we are taking to
help protect free-ranging deer from CWD, and to help ensure the health of
captive deer and other cervids.”
MDC permit records show there are 27 permitted big-game hunting preserves
in Missouri with white-tailed deer, and 277 permitted wildlife breeders with
white-tailed deer.
MDC has held numerous open houses to share information and get public
feedback on the issue of Chronic Wasting Disease (CWD) and Department actions to
contain the disease.
MDC provided current information on CWD and the proposed suspension of
issuing permits for new big-game ranches and wildlife breeders that hold
white-tailed deer or mule deer to members of the Missouri Whitetail Breeders and
Hunting Ranch Association at the Association’s annual conference on Aug.
4.
Draper adds that MDC continues to work with landowners, deer hunters,
members of the captive cervid industry and others on the issue of CWD and
welcomes related comments at mdc.mo.gov/node/17901.
Chronic Wasting Disease is a fatal disease that attacks the nervous systems
of cervids, such as white-tailed, mule and other types of deer. It is
transmitted by animal-to-animal contact or soil-to-animal contact. It can spread
through activities that unnaturally concentrate animals, the natural movement
and dispersal of infected free-ranging deer, the transportation of live captive
deer with CWD or the transportation and improper disposal of infected
carcasses.
According to the Missouri Department of Agriculture, there is no evidence
from existing research that CWD can spread to domestic livestock, such as sheep
or cattle. According to the Missouri Department of Health and Senior Services
(MDHSS), there is no evidence that CWD can infect people.
The first two cases of CWD in the state were found in 2010 and 2011 at two
private big-game hunting preserves in Linn and Macon counties. Following those
discoveries, the first two cases of CWD in free-ranging deer were confirmed in
2012 in Macon County. Missouri’s confirmed cases of CWD total 11 in captive deer
from the private hunting preserves and five in free-ranging deer harvested in
Macon County.
With the help of hunters, MDC has tested more than 35,000 free-ranging deer
for CWD from all parts of the state since 2002 and up to 2012. As a result of
that testing, MDC scientists have determined it is highly unlikely that CWD has
been present in the state prior to its recent discovery in northeast
Missouri.
Draper says that the Code changes allow time for MDC to further assess the
CWD situation, continue to engage stakeholders, plan for the future and identify
and utilize the best and most current science to manage the disease.
New federal regulations for the interstate movement and disease
certification of captive deer and other cervids were recently open for review
and comment through the Federal Register at www.federalregister.gov. Additional
information is pending publication. Draper says that the Code changes also give
MDC, deer breeders and others time to review these new regulations.
“Conservation efforts such as providing good habitat and progressive deer
management practices on both public and private land make Missouri a great place
to hunt deer,” Draper says. “The cultural, social and economic importance that
white-tailed deer provide the people of our state is, and will continue to be,
one of our top priorities.”
According to MDC, Missouri has more than 507,000 deer hunters who spend
about $690 million in the state each year on deer hunting and related
activities. This has an overall economic impact of $1.1 billion in Missouri each
year and supports almost 12,000 jobs. Many Missourians also enjoy viewing deer.
A 2009 Gallup survey found that about 91% of Missourians are somewhat or very
interested in observing deer in the outdoors.
Other actions the Conservation Commission and MDC have taken to limit the
spread of CWD in Missouri include regulation changes, recommendations and
continuing sampling of harvested deer to test for CWD.
The Conservation Commission approved a regulation change in May that
restricts activities that are likely to unnaturally concentrate white-tailed
deer and promote the spread of CWD. The regulation will become effective Oct.
30. It bans the placement of grain, salt products, minerals and other consumable
natural or manufactured products in the CWD Containment Zone, which consists of
Adair, Chariton, Linn, Macon, Randolph and Sullivan counties. The regulation
includes exceptions for backyard feeding of wildlife and normal agricultural,
forest management, crop and wildlife food production practices.
The Conservation Commission also approved a regulation change in May that
rescinds the antler-point restriction (four-point rule) in the CWD Containment
Zone, which became effective July 1. Yearling and adult male deer have been
found to exhibit CWD at higher rates than female deer so a reduction in the
number of male deer can help limit the spread of CWD. The dispersal of yearling
males from their natal or birth range in search of territory and mates is also
one of the primary means of expanding the distribution of CWD.
MDC also encourages hunters who harvest deer in the CWD Containment Zone
not to take whole deer carcasses or certain carcass parts out of the area.
MDC will also continue to work with hunters who harvest deer in the CWD
Containment Zone to collect samples for CWD testing.
Detailed information can be found in MDC’s “2012 Fall Deer & Turkey
Hunting Regulations and Information” booklet available at MDC offices, from
permit vendors and online at
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol
Needs To Be Revised
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Tuesday, June 05, 2012
Captive Deer Breeding Legislation Overwhelmingly Defeated During 2012
Legislative Session
Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease
in the United States
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis
M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason† Colorado State University; Fort Collins, CO USA†Presenting author;
Email: ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness. Two of these cats have
developed rear limb ataxia. Although the limited data from this ongoing study
must be considered preliminary, they raise the potential for cervid-to-feline
transmission in nature. www.landesbioscience.com Prion
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
----- Original Message -----
From: David Colby
To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter.
Warm Regards, David Colby
--
David Colby, PhDAssistant ProfessorDepartment of Chemical
EngineeringUniversity of Delaware
====================END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Tuesday, January 24, 2012
CWD found in two free-ranging deer from Macon County Missouri
Friday, October 21, 2011
Chronic Wasting Disease Found in Captive Deer Missouri
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B).
SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).
PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
Friday, August 24, 2012
Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting
disease within white-tailed deer (Odocoileus virginianus) herds in North America
TSS
Friday, August 24, 2012
Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America
Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting
disease within white-tailed deer (Odocoileus virginianus) herds in North America
Effects of age, sex, polymorphism at PRNP codon 96, and disease progression
Bruce... V. Thomsen1 David A. Schneider Katherine I. O’Rourke Thomas
Gidlewski James McLane Robert W. Allen Alex A. McIsaac Gordon B. Mitchell Delwyn
P. Keane Terry R. Spraker Aru Balachandran
U.S. Department of Agriculture, National Veterinary Services Laboratories,
Ames, IA (Thomsen)
U.S. Department of Agriculture, Agricultural Research Service, Pullman, WA
(Schneider, O’Rourke)
U.S. Department of Agriculture, Animal and Plant Health Inspection Service,
Wildlife Services, Fort Collins, CO (Gidlewski)
Canadian Food Inspection Agency, Battleford, Saskatchewan, Canada (McLane)
Canadian Food Inspection Agency, Prince Albert, Saskatchewan, Canada
(Allen)
Canadian Food Inspection Agency, Saskatoon, Saskatchewan, Canada (McIsaac)
National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food
Inspection Agency, Ottawa Laboratory–Fallowfield, Ottawa, Ontario, Canada
(Mitchell, Balachandran)
University of Wisconsin, Wisconsin Veterinary Diagnostic Laboratory,
Madison, WI (Keane)
Colorado State University Diagnostic Laboratory, Fort Collins, CO
(Spraker)
↵1 Bruce V. Thomsen, National Veterinary Services Laboratories, 1920 Dayton
Avenue, Ames, IA 50010. bruce.v.thomsen@aphis.usda.gov
Abstract
An effective live animal diagnostic test is needed to assist in the control
of chronic wasting disease (CWD), which has spread through captive and wild
herds of white-tailed deer (Odocoileus virginianus) in Canada and the United
States. In the present study, the diagnostic accuracy of rectal mucosa biopsy
sample testing was determined in white-tailed deer from 4 CWD-infected captive
herds. Specifically, the current study compared the immunohistochemical
detection of disease-associated prion protein in postmortem rectal mucosa biopsy
samples to the CWD status of each deer as determined by immunodiagnostic
evaluations of the brainstem at the obex, the medial retropharyngeal lymph node,
and the palatine tonsil. The effects of age, sex, genotype, and disease
progression were also evaluated. Diagnostic sensitivity on rectal biopsy samples
for CWD in white-tailed deer ranged from 63% to 100%; the pooled estimate of
sensitivity was 68% with 95% confidence limits (95% CLs) of 49% and 82%.
However, diagnostic sensitivity was dependent on genotype at prion protein gene
(PRNP) codon 96 and on disease progression as assessed by obex grade. Diagnostic
sensitivity was 76% (95% CLs: 49%, 91%) for 96GG deer but only 42% (95% CLs:
13%, 79%) for 96GS deer. Furthermore, diagnostic sensitivity was only 36% for
deer in the earliest stage of disease (obex grade 0) but was 100% for deer in
the last 2 stages of preclinical disease (obex grades 3 and 4). The overall
diagnostic specificity was 99.8%. Selective use of antemortem rectal biopsy
sample testing would provide valuable information during disease investigations
of CWD-suspect deer herds.
*** 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.
(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN,
AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY
PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF
FILE...TSS)
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
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
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
High-Fence 226-Inch Whitetail Escapes, Shot in Louisiana
by Dylan Polk•December 1, 2011
Volume 18, Number 3—March 2012
Synopsis
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
Samuel E. Saunders1, Shannon L. Bartelt-Hunt, and Jason C. Bartz Author
affiliations: University of Nebraska-Lincoln, Omaha, Nebraska, USA (S.E.
Saunders, S.L. Bartelt-Hunt); Creighton University, Omaha (J.C. Bartz)
snip...
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B). Except in South Korea, CWD has not been
detected outside North America. In most locations reporting CWD cases in
free-ranging animals, the disease continues to emerge in wider geographic areas,
and prevalence appears to be increasing in many disease-endemic areas. Areas of
Wyoming now have an apparent CWD prevalence of near 50% in mule deer, and
prevalence in areas of Colorado and Wisconsin is <15 0="0" 10="10" 5="5" according="according" adult="adult" age="age" agencies.="agencies." and="and" appear="appear" areas="areas" between="between" but="but" cwd="cwd" data="data" deer.="deer." deer="deer" div="div" elk="elk" factors="factors" for="for" from="from" gene="gene" genetic="genetic" highest="highest" however="however" in="in" include="include" influence="influence" influences="influences" is="is" known="known" less="less" lower="lower" male="male" many="many" obtained="obtained" of="of" parts="parts" polymorphisms="polymorphisms" prevalence="prevalence" provincial="provincial" prp="prp" reaches="reaches" remain="remain" remains="remains" reports="reports" risk="risk" scrapie.="scrapie." sex="sex" show="show" state="state" strong="strong" susceptibility="susceptibility" than="than" the="the" to="to" understood="understood" wildlife="wildlife" wyoming.="wyoming.">
snip...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5). In addition, CWD-infected deer are
selectively preyed upon by mountain lions (5), and may also be more vulnerable
to vehicle collisions (10).
snip...
Conclusions
Much remains unknown about prion diseases and CWD in particular, especially
about CWD strains (which may have varied zoonotic potentials) and the long-term
effects of CWD on cervid ecosystems. CWD prevalence and geographic range appear
likely to continue to increase. Moreover, the disease is inevitably fatal, and
no effective therapeutic measures are presently available. As such, it would
seem wise to continue research and surveillance of CWD to elucidate the details
of its transmission, pathogenesis, and continued emergence in cervid populations
in hopes that strategies for mitigating its negative effects on humans and
cervid ecosystems can be identified.
Tuesday, December 20, 2011
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.
Despite the five year premise plan and site decontamination, The WI DNR has
concerns over the bioavailability of infectious prions at this site to wild
white-tail deer should these fences be removed. Current research indicates that
prions can persist in soil for a minimum of 3 years.
However, Georgsson et al. (2006) concluded that prions that produced
scrapie disease in sheep remained bioavailable and infectious for at least 16
years in natural Icelandic environments, most likely in contaminated soil.
Additionally, the authors reported that from 1978-2004, scrapie recurred on
33 sheep farms, of which 9 recurrences occurred 14-21 years after initial
culling and subsequent restocking efforts; these findings further emphasize the
effect of environmental contamination on sustaining TSE infectivity and that
long-term persistence of prions in soils may be substantially greater than
previously thought. < < <
SNIP...SEE FULL TEXT ;
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE CWD
2012
Tuesday, December 20, 2011
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.
Despite the five year premise plan and site decontamination, The WI DNR has
concerns over the bioavailability of infectious prions at this site to wild
white-tail deer should these fences be removed. Current research indicates that
prions can persist in soil for a minimum of 3 years.
However, Georgsson et al. (2006) concluded that prions that produced
scrapie disease in sheep remained bioavailable and infectious for at least 16
years in natural Icelandic environments, most likely in contaminated soil.
Additionally, the authors reported that from 1978-2004, scrapie recurred on
33 sheep farms, of which 9 recurrences occurred 14-21 years after initial
culling and subsequent restocking efforts; these findings further emphasize the
effect of environmental contamination on sustaining TSE infectivity and that
long-term persistence of prions in soils may be substantially greater than
previously thought
SNIP...SEE FULL TEXT ;
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol
Needs To Be Revised
Monday, June 11, 2012
OHIO Captive deer escapees and non-reporting
Ohio's testing is spontaneous and voluntary, and is limited to 16 month old
only, and only after found dead. so, the flaws there are obvious. anything
voluntary is useless, and the voluntary mad cow feed ban proved just how useless
anything voluntary is. ...
Friday, July 20, 2012
CWD found for first time in Iowa at hunting preserve
TSS
15>Sunday, August 19, 2012
Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation 2012
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
Title: Susceptibility of cattle to the agent of chronic wasting disease
from elk after intracranial inoculation
Authors
Greenlee, Justin Nicholson, Eric Smith, Jodi Kunkle, Robert Hamir, Amirali
Submitted to: Journal of Veterinary Diagnostic Investigation Publication
Type: Peer Reviewed Journal Publication Acceptance Date: July 12, 2012
Publication Date: N/A
Interpretive Summary: Chronic Wasting Disease (CWD), a fatal
neurodegenerative disease that occurs in farmed and wild cervids (deer and elk)
of North America, is a transmissible spongiform encephalopathy (TSE). TSEs are
caused by infectious proteins called prions that are resistant to various
methods of decontamination and environmental degradation. Cattle could be
exposed to chronic wasting disease (CWD) by contact with infected farmed or
free-ranging cervids. The purpose of this study was to assess the potential
transmission of CWD from elk to cattle after intracranial inoculation, the most
direct route to test the potential of a host to replicate an isolate of the
prion agent. This study reports that only 2 of 14 calves inoculated with CWD
from elk had clinical signs or evidence of abnormal prion protein accumulation.
These results suggest that cattle are unlikely to be susceptible to CWD if
inoculated by a more natural route. This information could have an impact on
regulatory officials developing plans to reduce or eliminate TSEs and farmers
with concerns about ranging cattle on areas where CWD may be present.
Technical Abstract: Cattle could be exposed to the agent of chronic
wasting disease (CWD) through contact with infected farmed or free-ranging
cervids or exposure to contaminated premises. The purpose of this study was to
assess the potential for CWD derived from elk to transmit to cattle after
intracranial inoculation. Calves (n=14) were inoculated with brain homogenate
derived from elk with CWD to determine the potential for transmission and define
the clinicopathologic features of disease. Cattle were necropsied if clinical
signs occurred or at the termination of experiment (49 months post-inoculation
(MPI)). Clinical signs of poor appetite, weight loss, circling, and bruxism
occurred in two cattle (14%) at 16 and 17 MPI, respectively. Accumulation of
abnormal prion protein (PrP**Sc) in these cattle was confined to the central
nervous system with the most prominent immunoreactivity in midbrain, brainstem,
and hippocampus with lesser immunoreactivity in the cervical spinal cord. The
rate of transmission was lower than in cattle inoculated with CWD derived from
mule deer (38%) or white-tailed deer (86%). Additional studies are required to
fully assess the potential for cattle to develop CWD through a more natural
route of exposure, but a low rate of transmission after intracranial inoculation
suggests that risk of transmission through other routes is low. A critical
finding here is that if CWD did transmit to exposed cattle, currently used
diagnostic techniques would detect and differentiate it from other prion
diseases in cattle based on absence of spongiform change, distinct pattern of
PrP**Sc deposition, and unique molecular profile.
Last Modified: 08/16/2012
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
" although the infection rate was low (4 of 13 animals [Hamir et al.
2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly
as possible all updates/comments that contribute substantially to the topic
under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author
Affiliations
1Institute for Neurodegenerative Diseases, University of California, San
Francisco, San Francisco, California 94143 2Department of Neurology, University
of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As
the only prion disease identified in free-ranging animals, CWD appears to be far
more communicable than other forms of prion disease. CWD was first described in
1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of
histopathology of the brain. Originally detected in the American West, CWD has
spread across much of North America and has been reported also in South Korea.
In captive populations, up to 90% of mule deer have been reported to be positive
for prions (Williams and Young 1980). The incidence of CWD in cervids living in
the wild has been estimated to be as high as 15% (Miller et al. 2000). The
development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible
to CWD, has enhanced detection of CWD and the estimation of prion titers
(Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces,
even in presymptomatic deer, has been identified as a likely source of infection
for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD
has been transmitted to cattle after intracerebral inoculation, although the
infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding
raised concerns that CWD prions might be transmitted to cattle grazing in
contaminated pastures.
snip...
----- Original Message -----
From: David Colby
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter.
Warm Regards, David Colby
--
David Colby, PhDAssistant Professor
Department of Chemical Engineering
University of Delaware
====================END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈ 100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B). SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).
PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS
PLEASE READ THIS CDC 2012 UPDATE ON CWD RISK FACTORS ;
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
CWD has been identified in free-ranging cervids in 15 US states and 2
Canadian provinces and in ≈100 captive herds in 15 states and provinces and in
South Korea (Figure 1, panel B).
SNIP...
CWD Zoonotic Potential, Species Barriers, and Strains
Current Understanding of the CWD Species Barrier Strong evidence of
zoonotic transmission of BSE to humans has led to concerns about zoonotic
transmission of CWD (2,3). As noted above, CWD prions are present nearly
ubiquitously throughout diseased hosts, including in muscle, fat, various glands
and organs, antler velvet, and peripheral and CNS tissue (2,14,15). Thus, the
potential for human exposure to CWD by handling and consumption of infectious
cervid material is substantial and increases with increased disease prevalence.
Interspecies transmission of prion diseases often yields a species-barrier
effect, in which transmission is less efficient compared with intraspecies
transmission, as shown by lower attack rates and extended incubation periods
(3,28). The species barrier effect is associated with minor differences in PrPc
sequence and structure between the host and target species (3). Prion strain
(discussed below) and route of inoculation also affect the species barrier
(3,28). For instance, interspecies transmission by intracerebral inoculation is
often possible but oral challenge is completely ineffective (29). Most
epidemiologic studies and experimental work have suggested that the potential
for CWD transmission to humans is low, and such transmission has not been
documented through ongoing surveillance (2,3). In vitro prion replication assays
report a relatively low efficiency of CWD PrPSc-directed conversion of human
PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are resistant
to CWD infection (31); these findings indicate low zoonotic potential. However,
squirrel monkeys are susceptible to CWD by intracerebral and oral inoculation
(32). Cynomolgus macaques, which are evolutionarily closer to humans than
squirrel monkeys, are resistant to CWD infection (32). Regardless, the finding
that a primate is orally susceptible to CWD is of concern. Interspecies
transmission of CWD to noncervids has not been observed under natural
conditions. CWD infection of carcass scavengers such as raccoons, opossums, and
coyotes was not observed in a recent study in Wisconsin (22). In addition,
natural transmission of CWD to cattle has not been observed in experimentally
controlled natural exposure studies or targeted surveillance (2). However, CWD
has been experimentally transmitted to cattle, sheep, goats, mink, ferrets,
voles, and mice by intracerebral inoculation (2,29,33). CWD is likely
transmitted among mule, white-tailed deer, and elk without a major species
barrier (1), and other members of the cervid family, including reindeer,
caribou, and other species of deer worldwide, may be vulnerable to CWD
infection. Black-tailed deer (a subspecies of mule deer) and European red deer
(Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34).
Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation
(35). Continued study of CWD susceptibility in other cervids is of considerable
interest.
Reasons for Caution There are several reasons for caution with respect to
zoonotic and interspecies CWD transmission. First, there is strong evidence that
distinct CWD strains exist (36). Prion strains are distinguished by varied
incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc
depositions (3,32). Strains have been identified in other natural prion
diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies
transmission of prions from CWD-positive deer and elk isolates resulted in
identification of >2 strains of CWD in rodent models (36), indicating that
CWD strains likely exist in cervids. However, nothing is currently known about
natural distribution and prevalence of CWD strains. Currently, host range and
pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of
CWD may also vary with CWD strain. In addition, diversity in host (cervid) and
target (e.g., human) genotypes further complicates definitive findings of
zoonotic and interspecies transmission potentials of CWD. Intraspecies and
interspecies passage of the CWD agent may also increase the risk for zoonotic
CWD transmission. The CWD prion agent is undergoing serial passage naturally as
the disease continues to emerge. In vitro and in vivo intraspecies transmission
of the CWD agent yields PrPSc with an increased capacity to convert human PrPc
to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and
yield multiple novel prion strains (3,28). The potential for interspecies CWD
transmission (by cohabitating mammals) will only increase as the disease spreads
and CWD prions continue to be shed into the environment. This environmental
passage itself may alter CWD prions or exert selective pressures on CWD strain
mixtures by interactions with soil, which are known to vary with prion strain
(25), or exposure to environmental or gut degradation. Given that prion disease
in humans can be difficult to diagnose and the asymptomatic incubation period
can last decades, continued research, epidemiologic surveillance, and caution in
handling risky material remain prudent as CWD continues to spread and the
opportunity for interspecies transmission increases. Otherwise, similar to what
occurred in the United Kingdom after detection of variant CJD and its subsequent
link to BSE, years of prevention could be lost if zoonotic transmission of CWD
is subsequently identified,
Thursday, February 09, 2012
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
SOME HISTORY ON THIS ;
Subject: Re: CWD TO CATTLE by inoculation (ok, is it three or four???)
Date: Wed, 11 Dec 2002 23:20:41 +0000
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy
Organization: Netscape Online member
To: BSE-L
References:
Dear Dr Miller,
I have to admit it was difficult to me to believe either....but in the end
I just had to realise that it was true.
When I investigated the age at which cattle actually were becoming infected
it was shocking to find that the majority were infected under 1 month of age
(and many of them seemed to be within the first week, although the data on this
was more shakey, and the rest seemed to be infected in a decreasing slope up to
the 7th month.
The question was: just how could the cattle be infected simply so young?
What also was turning out was that I could not find any obvious sign of
multipoint inoculation and it was as if either there was a major dose arriving
at one point or not at all. Again the maths on that was difficult but would
probably stand up to the logic. These figures could only be certain in the
period on either of the feed ban in the UK in 1988: but then again there was no
change in the age distrubution after some other factors are removed since that
point.
For a long time we had been wondering why, during the epidemic, the age
distribution of cases did not change greatly, when the actual amount of
infectivity in the total diet of the battle population may have gone up
10,000fold. Surely, if infection was taking place at many points in an animal's
life then they would have been becoming younger when dying of disease as the
epidemic progressed?..but this was not seen.
So...when you argue that a lamb is unlikely to have been infected
naturally at a single point....I think that this is almost certainly incorrect
and that they are indeed infected when exceedingly young and probably at a
single point. Also I now believe that the amount of infectivity needed to infect
these animals is likely to be very low compared with adults when given orally.
(this was all published in the British Food Journal in 2001)
Steve Dealler
"Janice M. Miller" wrote:
> ######## Bovine Spongiform Encephalopathy
#########
>
> I did not mean to imply that it wouldn't be possible for an animal to
> consume that amount of material, especially over a lifetime. I was
> merely pointing out that it is unlikely a lamb would be naturally
> exposed to that amount of material at a single time point early in its
> life and therefore such a short incubation period would not be expected
> to occur under non-experimental conditions.
>
> >>> flounder@WT.NET 12/09/02 12:35PM >>>
>
>
> hello Dr. Miller,
>
> i was curious about this statement;
>
> > It was not a true natural exposure, however, because they fed
>
> > the lambs 2-5 grams of infectious brain, which is very likely a
>
> > much larger dose than would occur under natural conditions.
>
> how do you come to the conclusion that 2-5 grams is a
> 'much larger dose than would occur under natural conditions',
> considering 1/2 to 1 gram is lethal for a cow ?
>
> "FDA has determined that each animal could have consumed, at most and
> in
> total, five-and-one-half grams - approximately a quarter ounce -- of
> prohibited material. These animals weigh approximately 600 pounds."
>
> http://www.fda.gov/bbs/topics/news/2001/new00752.html
>
> if we look at these studies, we will find that
> the 5.5 grams would be more than sufficient to
> infect a cow, if the feed was tainted with TSEs...TSS
>
> please read page 4, 5 and 6 of some 53;
>
> Scientific Steering Committee
> ORAL EXPOSURE OF HUMANS TO THE BSE AGENT:
> INFECTIVE DOSE AND SPECIES BARRIER
>
> http://europa.eu.int/comm/food/fs/sc/ssc/out79_en.pdf
>
> 9 DR. BROWN: If I am not mistaken, and I can be
> 10 corrected, I think a half a gram is enough in a cow, orally;
> 11 in other words, one good dietary-supplement pill.
>
> [FULL TEXT ABOUT 600 PAGES]
> 3681t2.rtf
> http://www.fda.gov/ohrms/dockets/ac/cber01.htm
>
> thank you,
>
> kind regards,
> terry
>
> Janice M. Miller wrote:
> >
> > With scrapie it's believed that most infections occur at or
> shortly
> > after birth, either from exposure to placenta from the lamb's own
> > infected dam or from another placent of another infected ewe that is
> > lambing at the same time. There are several experiments reported,
> > however, in which older sheep from scrapie-free flocks have been put
> in
> > contact with lambing ewes from scrapie flocks and transmission has
> > occurred. In these cases the incubation period appears to be
> longer.
> > Recently we heard in England that they have been able to reproduce
> > scrapie within 6 months (an incredibly short incubation period for
> that
> > disease) by oral exposure of 2-week old lambs. It was not a true
> > natural exposure, however, because they fed the lambs 2-5 grams of
> > infectious brain, which is very likely a much larger dose than would
> > occur under natural conditions. The effect of age on incubation
> period
> > may reflect the amount of lymphoid tissue available in the
> intestinal
> > tract of lambs because they experience a significant amount of
> atrophy
> > in that tissue diromg the first year of life. I don't remember
> anyone
> > suggesting that age plays a role in either the success of
> transmissions
> > or incubation periods when sheep are inoculated initracerebrally.
> That
> > seems to depend mostly on infectious titer of the inoculum and the
> > genetics of the recipient sheep.
> > In CWD no one has found any evidence that placenta is
> infectious
> > so the source of infectivity for transmission is unknown. In the
> highly
> > contaminated wildlife research facility at Colorado they lose over
> 90%
> > of their deer by about 2 years of age so it is likely that those
> animals
> > are infected at a very young age. In the wild, however, they are
> > reporting some positive animals that are much older so while there
> might
> > be some development of resistance with age, it certainly isn't
> complete.
> > I don't know that anyone has reported doing experiments where
> CWD-free
> > deer of different ages were put into a contaminated environment to
> see
> > if the transmission rates or incubation periods would be influenced
> by
> > age.
> >
> >
> >>>>taotm@EARTHLINK.NET 11/26/02 08:24AM >>>
> >>>
> >
> > Dr. Miller,
> >
> > About a year ago there was a report of from a Colorado DoW staffer
> who
> > recalled seeing scrapie sheep in
> > pens near the sickly-looking deer at the Ft. Collins research
> facility.
> > Although there's some debate about
> > whether those sheep actually had scrapie, given the results of the
> > intercerebral tests-- "... The other
> > sheep, necropsied 35 months after inoculation, showed clinical signs
> > and histopathologic lesions that were
> > indistinguishable from scrapie..."-- has there been any attempt to
> > recreate the alleged conditions at Ft.
> > Collins? In other words, an environmental test where scrapie sheep
> > would be put in close proximity to
> > healthy deer? Clearly there's a huge questions about the mechanics
> of
> > jumping the species barrier. But is
> > it possible that this was the way the CWD prion fire was initially
> lit?
> > Farmed sheep to wild cervids?
> >
> > Also, have there been any tests looking at the age at which an
> animal
> > becomes infected? Are younger,
> > smaller animals more at risk? Does the same dose of infectious
> material
> > as given an adult affect them
> > faster or more intensely?
> >
> > thank you,
> >
> > Janet Ginsburg
> >
> > "Terry S. Singeltary Sr." wrote:
> >
> >>hello Janice,
> >>
> >>many thanks for this update.
> >>
> >> > we do not know if the CWD agent in white-tailed deer
> >> > would be equivalent to that obtained from mule deer.
> >>
> >>i was just reading some data where it states;
> >>
> >>Although few white tailed deer were available for biopsy,
> >>findings were consistent with those in mule deer and
> >>support similarity in lymphoid accumulation of PrPCWD
> >>between the species that has been observed post-mortem.
> >>However, because PrPCWD does not appear to accumulate
> >>in lymphoid tissue to the same degree in elk as deer
> >>(T.R. Spraker, unpublished data)
> >>
> >>i am confused?
> >>
> >>thank you,
> >>kind regards,
> >>
> >>terry
> >>
> >>Janice M. Miller wrote:
> >>
> >
> >>> The statement that 4 cattle have developed evidence of CWD
> >>
> > transmission
> >
> >>>following intracerebral inoculation is correct because an
> >>
> > additional
> >
> >>>animal has been found prion positive subsequent to the 2001 paper
> >>
> > that
> >
> >>>presented preliminary findings after only 2 and a half years of
> >>>observation. Following this message is a summary of the current
> >>
> > status
> >
> >>>of our CWD cross-species transmission experiments in cattle and
> >>
> > sheep.
> >
> >>>This information was prepared in anticipation of questions about
> >>
> > these
> >
> >>>studies that we expected would be raised at the recent annual
> >>
> > meeting of
> >
> >>>the U.S. Animal Health Association.
> >>> I would like to correct one statement in the newspaper
> >>
> > article
> >
> >>>that was attributed to me that is in error. I did not imply that
> >>
> > our
> >
> >>>work thus far could be extrapolated to the situation with
> >>
> > white-tailed
> >
> >>>deer and dairy cattle. While there is no indication that there
> >>
> > should
> >
> >>>be any difference in susceptibility of beef versus dairy cattle, we
> >>
> > do
> >
> >>>not know if the CWD agent in white-tailed deer would be equivalent
> >>
> > to
> >
> >>>that obtained from mule deer. For that reason Dr. Hamir is now
> >>>repeating the original experiment in cattle with brain suspension
> >>
> > from
> >
> >>>affected white-tails as inoculum.
> >>>
> >>>Experimental Transmission of Chronic Wasting Disease (CWD) to
> >>
> > Cattle
> >
> >>>and Sheep
> >>>Progress report - October 15, 2002
> >>>
> >>>Transmission of CWD (mule deer) to cattle:
> >>>
> >>>Background:
> >>>In 1997, 13 calves were inoculated intracerebrally with brain
> >>>suspension from mule deer naturally affected with CWD. During the
> >>
> > first
> >
> >>>3 years, 3 animals were euthanized 23, 24, and 28 months after
> >>>inoculation because of weight loss (2) or sudden death (1).
> >>
> > Although
> >
> >>>microscopic examination of the brains did not show classical
> >>
> > lesions of
> >
> >>>transmissible spongiform encephalopathy (TSE), a specific TSE
> >>
> > marker
> >
> >>>protein, PrPres, was detected by immunohistochemistry (IHC) and
> >>
> > western
> >
> >>>blot . Detailed information on these animals has been published
> >>>previously (A Hamir et al., J Vet Diagn Invest 13: 91-96, 2001).
> >>>
> >>>Update:
> >>>During the 3rd and 4th years of observation, 5 additional animals
> >>
> > have
> >
> >>>been euthanized because of health concerns (primarily chronic joint
> >>
> > and
> >
> >>>foot problems). Although all tests for PrPres are not complete,
> >>
> > IHC
> >
> >>>results indicate that 1 of these animals, necropsied 59 months
> >>
> > after
> >
> >>>inoculation, was positive for PrPres. This animal (# 1746) had not
> >>
> > been
> >
> >>>eating well for approximately 1 week prior to being found
> >>
> > recumbent. At
> >
> >>>necropsy, significant gross lesions consisted of an oblique
> >>
> > fracture of
> >
> >>>L1 vertebral arch with extension into the body, and moderate
> >>
> > multifocal
> >
> >>>hemorrhagic ulceration in the abomasum. Microscopic examination
> >>
> > of
> >
> >>>brain revealed a few isolated neurons with single or multiple
> >>
> > vacuoles,
> >
> >>>but neither neuronal degeneration nor gliosis was observed. IHC
> >>>revealed the presence of PrPres in sections from several areas of
> >>
> > the
> >
> >>>brain.
> >>>
> >>>Summary of findings on this case and data from previous animals:
> >>>
> >>> Necropsy Survival Disease Clinical
> >>>Histo- IHC SAF WB
> >>> No. Route date period course signs
> >>
> > pathology
> >
> >>>________________________________________________________________
> >>>
> >>>1745 i/c 8/18/99 23m 2m +
> >>>+/- + - +
> >>>
> >>>1768 i/c 9/22/99 24m 3m +
> >>>+/- + + +
> >>>
> >>>1744 i/c 1/29/00 28m 3d ±
> >>>- + + +
> >>>
> >>>1749 i/c 5/20/01 44m NA -
> >>> - - NT NT
> >>>
> >>>1748 i/c 6/27/01 45m NA -
> >>>- - NT NT
> >>>
> >>>1743 i/c 8/21/02 59m NA -
> >>>- - Pending Pending
> >>>
> >>>1741 i/c 8/22/02 59m NA -
> >>>- - Pending Pending
> >>>
> >>>1746 i/c 8/27/02 59m 7d ±
> >>>+/- + Pending Pending
> >>>
> >>>NT = not tested; IHC = immunohistochemistry for PrPres; SAF =
> >>
> > scrapie
> >
> >>>associated fibrils; NA = not applicable; WB = Western blot
> >>>(Prionics-Check); + = lesions or antigen present; - = lesions or
> >>>antigen absent; ± = signs/lesions equivocal; i/c = intracerebral;
> >>
> > m =
> >
> >>>months; d = days.
> >>>
> >>>Summary:
> >>>After 5 years of observation we have 4 CWD transmissions to cattle
> >>
> > from
> >
> >>>a group of 13 inoculates. These animals, which were necropsied 23,
> >>
> > 24,
> >
> >>>28, and 59 months after inoculation, did not show the clinical
> >>
> > signs or
> >
> >>>histopathologic lesions typical of a TSE, but PrPres was detected
> >>
> > in
> >
> >>>brain samples. Four other animals that were necropsied during the
> >>
> > 4th
> >
> >>>and 5th years of observation have not shown evidence of prion
> >>
> > disease
> >
> >>>(although not all tests are complete) and the 5 remaining cattle
> >>
> > are
> >
> >>>apparently healthy. Note that this study involved direct
> >>
> > intracerebral
> >
> >>>inoculation of cattle with the CWD agent, which is an unnatural
> >>
> > route of
> >
> >>>exposure. It is likely that transmission by a more natural route,
> >>
> > such
> >
> >>>as oral exposure, would be much more difficult to accomplish.
> >>
> > Cattle
> >
> >>>have been inoculated orally at the University of Wyoming with the
> >>
> > same
> >
> >>>inoculum used for this experiment, and 5 years into the study
> >>
> > these
> >
> >>>animals remain healthy.
> >>>
> >>>
> >>>Experimental Transmission of CWD (mule deer) to sheep
> >>>
> >>>Eight Suffolk sheep from the NADC scrapie-free flock were
> >>
> > inoculated
> >
> >>>intracerebrally with the CWD brain suspension used to inoculate
> >>
> > cattle.
> >
> >>>PRNP genotyping showed that 4 of the sheep were QQ at codon 171 and
> >>
> > the
> >
> >>>other four were QR. Two of the QQ sheep were euthanized during the
> >>
> > 3rd
> >
> >>>year of observation. At necropsy one of these animals had a
> >>
> > urethral
> >
> >>>obstruction and PrPres was not detected in brain or lymphoid
> >>
> > tissues.
> >
> >>>The other sheep, necropsied 35 months after inoculation, showed
> >>
> > clinical
> >
> >>>signs and histopathologic lesions that were indistinguishable from
> >>>scrapie. IHC tests showed typical PrPres accumulations in brain,
> >>>tonsil, and some lymph nodes. The 2 remaining QQ sheep and all 4
> >>
> > QR
> >
> >>>sheep are apparently healthy 39 months after inoculation.
> >>>
> >>>Summary:
> >>>After 3 years of observation we have 1 transmission of CWD to a 171
> >>
> >
> >>>sheep. This animal, which was necropsied 35 months after
> >>
> > inoculation,
> >
> >>>showed clinical signs and histopathologic lesions that were
> >>>indistinguishable from scrapie. Another QQ sheep that was
> >>
> > necropsied
> >
> >>>during the 3rd year showed no evidence of prion disease and all
> >>>remaining sheep (2 QQ and 4 QR) are apparently healthy.
> >>>
> >>>
> >>>>>>flounder@WT.NET 11/23/02 06:54PM >>>
> >>>>>>
> >>>
> >>>1: J Vet Diagn Invest 2001 Jan;13(1):91-6
> >>>
> >>>Preliminary findings on the experimental transmission of chronic
> >>>wasting
> >>>disease agent of mule deer to cattle.
> >>>
> >>>Hamir AN, Cutlip RC, Miller JM, Williams ES, Stack MJ, Miller MW,
> >>>O'Rourke KI, Chaplin MJ.
> >>>
> >>>National Animal Disease Center, ARS, USDA, Ames, IA 50010, USA.
> >>>
> >>>To determine the transmissibility of chronic wasting disease (CWD)
> >>
> > to
> >
> >>>cattle and to provide information about clinical course, lesions,
> >>
> > and
> >
> >>>suitability of currently used diagnostic procedures for detection
> >>
> > of
> >
> >>>CWD
> >>>in cattle, 13 calves were inoculated intracerebrally with brain
> >>>suspension from mule deer naturally affected with CWD. Between 24
> >>
> > and
> >
> >>>27
> >>>months postinoculation, 3 animals became recumbent and were
> >>>euthanized.
> >>>Gross necropsies revealed emaciation in 2 animals and a large
> >>>pulmonary
> >>>abscess in the third. Brains were examined for protease-resistant
> >>>prion
> >>>protein (PrP(res)) by immunohistochemistry and Western blotting
> >>
> > and
> >
> >>>for
> >>>scrapie-associated fibrils (SAFs) by negative-stain electron
> >>>microscopy.
> >>>Microscopic lesions in the brain were subtle in 2 animals and
> >>
> > absent
> >
> >>>in
> >>>the third case. However, all 3 animals were positive for PrP(res)
> >>
> > by
> >
> >>>immunohistochemistry and Western blot, and SAFs were detected in 2
> >>
> > of
> >
> >>>the animals. An uninoculated control animal euthanized during the
> >>
> > same
> >
> >>>period did not have PrP(res) in its brain. These are preliminary
> >>>observations from a currently in-progress experiment. Three years
> >>>after
> >>>the CWD challenge, the 10 remaining inoculated cattle are alive
> >>
> > and
> >
> >>>apparently healthy. These preliminary findings demonstrate that
> >>>diagnostic techniques currently used for bovine spongiform
> >>>encephalopathy (BSE) surveillance would also detect CWD in cattle
> >>>should
> >>>it occur naturally.
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11243374&dopt=Abstract
>
> >>>Sat, Nov 23, 2002
> >>>
> >>>Scientists unsure if CWD can jump species
> >>>
> >>>By Jessica Bock
> >>>Wausau Daily Herald
> >>>jbock@wdhprint.com
> >>>
> >>>snip...
> >>>
> >>>Janice Miller, a veterinarian in charge of the experiment, said
> >>
> > she
> >
> >>>believes previous research shows it is hard for the disease to be
> >>>transmitted naturally from whitetail deer to dairy cattle.
> >>>"Our study says nothing of how it could be transmitted in natural
> >>>surroundings," she said.
> >>>
> >>>Miller has been studying the transmission of CWD from mule deer to
> >>>cattle since 1997. Since then, chronic wasting disease was
> >>
> > transmitted
> >
> >>>to four out of 13 cattle injected with brain tissue from naturally
> >>>infected mule deer, she said.
> >>>
> >>>In Wyoming, Williams has been studying cattle that were given a
> >>>concoction of diseased brain tissue orally, and five years into
> >>
> > the
> >
> >>>study the animals remain healthy, Miller said.
> >>>No one knows if chronic wasting disease could ever spread to
> >>
> > another
> >
> >>>species through natural surroundings.
> >>>
> >>>"Our experience is that it's pretty hard to predict," Miller said.
> >>>
> >>>http://www.wausaudailyherald.com/wdhlocal/277564794712612.shtml
> >>>
> >>>greetings list,
> >>>
> >>> > Since then, chronic wasting disease was
> >>>
> >>> > transmitted to four out of 13 cattle
> >>>
> >>>is this a typo by the media or has another cow gone down
> >>>with CWD since the preliminary findings were found?
> >>>
> >>>TSS
=======================================================
-------- Original Message --------
Subject: Re: CWD TO CATTLE by inoculation (ok,is it three or four OR NOW
FIVE???)
Date: Mon, 23 Jun 2003 12:36:59 –0500
From: "Janice M. Miller"
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
I am happy to provide an update on the experimental inoculation of cattle
and sheep with CWD. These are ongoing experiments and updates are normally
provided via presentations at meetings. Dr. Hamir has prepared a poster of the
following information that will be displayed at 4 upcoming meetings this summer
and fall.
Experimental Transmission of Chronic Wasting Disease (CWD) to Cattle and
Sheep Progress report - June 23, 2003
Experimental Transmission to Cattle
Background: In 1997, 13 calves were inoculated intracerebrally with brain
suspension from mule deer naturally affected with CWD. During the first 3 years,
3 animals were euthanized 23, 24, and 28 months after inoculation because of
weight loss (2) or sudden death (1). Although microscopic examination of the
brains did not show classical lesions of transmissible spongiform encephalopathy
(TSE), a specific TSE marker protein, PrPres, was detected by
immunohistochemistry (IHC) and western blot. Detailed information on these
animals has been published previously (A Hamir et al., J Vet Diagn Invest 13:
91-96, 2001).
Update: During the 3rd, 4th and 6th years of observation, 7 additional
animals have been euthanized due to a variety of health concerns (primarily
chronic joint and foot problems). IHC and western blot results indicate that 2
of these animals, necropsied 59 and 63 months after inoculation, were positive
for PrPres. One animal (# 1746) had not been eating well for approximately 1
week prior to being found recumbent. At necropsy, significant gross lesions
consisted of an oblique fracture of L1 vertebral arch with extension into the
body, and moderate multifocal hemorrhagic ulceration in the abomasum.
Microscopic examination of brain revealed a few isolated neurons with single or
multiple vacuoles, but neither neuronal degeneration nor gliosis was observed.
IHC revealed the presence of PrPres in sections from several areas of the brain.
The other PrPres positive animal (#1742) was euthanized after being found in
lateral recumbency with a body temperature of 104.6 F. It had not shown prior
clinical signs except for some decreased appetite for 2 days. Necropsy revealed
only moderate hepatitis and a small renal infarct due to intravascular
thrombosis.
Summary of findings on all necropsied animals to date:
Ear tag Date of Survival Disease Clinical Histo- IHC WB no. necropsy period
course signs pathology
_____________________________________________________________________ 1745
8/18/99 23m 2m + +/- + + 1768 9/22/99 24m 3m + +/- + + 1744 1/29/00 28m 3d +/- -
+ + 1749 5/20/01 44m NA - - - - 1748 6/27/01 45m NA - - - - 1743 8/21/02 59m NA
- - - - 1741 8/22/02 59m NA - - - - 1746 8/27/02 59m 7d +/- +/- + + 1765
11/27/02 62m 1d +/- +/- - - 1742 12/28/02 63m 2d +/- - + + NT = not tested; IHC
= immunohistochemistry for PrPres; SAF = scrapie associated fibrils; NA = not
applicable; WB = Western blot (Prionics-Check); + = lesions or antigen present;
- = lesions or antigen absent; +/- = signs/lesions equivocal; i/c =
intracerebral; m = months; d = days.
Summary: After 5.75 years of observation we have 5 CWD transmissions to
cattle from a group of 13 inoculates. These animals, which were necropsied 23,
24, 28, 59, and 63 months after inoculation, did not show the clinical signs or
histopathologic lesions typical of a TSE, but PrPres was detected in brain
samples by both immunohistochemistry and western blot. Five other animals
necropsied during the 4th, 5th and 6th years of observation have not shown
evidence of PrPres and the remaining 3 cattle are apparently healthy. Note that
this study involved direct intracerebral inoculation of cattle with the CWD
agent, which is an unnatural route of exposure. Likely, it would be more
difficult to infect cattle by the oral route. Cattle have been inoculated orally
at the University of Wyoming with the same inoculum used in this experiment, and
5.75 years into the study the animals remain healthy (personal communication,
Dr. Beth Williams).
Experimental Transmission of CWD to sheep
Eight Suffolk sheep from the NADC scrapie-free flock were inoculated
intracerebrally with the CWD brain suspension used to inoculate cattle. PRNP
genotyping showed that 4 of the sheep were QQ at codon 171 and the other four
were QR. Two of the QQ sheep were euthanized during the 3rd year of observation.
At necropsy one of these animals had a urethral obstruction and PrPres was not
detected in brain or lymphoid tissues. The other sheep, necropsied 35 months
after inoculation, showed clinical signs and histopathologic lesions that were
indistinguishable from scrapie. IHC tests showed typical PrPres accumulations in
brain, tonsil, and some lymph nodes. The 2 remaining QQ sheep and all 4 QR sheep
are apparently healthy 47 months after inoculation.
Summary: After 4 years of observation we have 1 transmission of CWD to a
171 QQ sheep. This animal, which was necropsied 35 months after inoculation,
showed clinical signs and histopathologic lesions that were indistinguishable
from scrapie. Another QQ sheep that was necropsied during the 3rd year showed no
evidence of prion disease and all remaining sheep (2 QQ and 4 QR) are apparently
healthy.
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-------- Original Message --------
Subject: Re: CWD TO CATTLE by inoculation (ok, is it three or four OR NOW
FIVE???)
Date: Mon, 23 Jun 2003 09:25:27 –0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
Greetings List Members,
i hear now that a 5th cow has gone done with CWD from the studies of Amir
Hamir et al. will Dr. Miller please confirm or deny this please, and possibly
explain why this has not made the news, if in fact this is the case?
seems these cows infected with CWD/TSE did not display the usual BSE
symptoms. i wonder how many more are out there in the field? course, we will
never know unless someone starts rapid TSE/BSE testing in sufficient numbers to
find...
thank you, kind regards, terry
Date: Sat, 23 Nov 2002 18:54:49 -0600 Reply-To: BSE Sender: BSE From:
"Terry S. Singeltary Sr." Subject: CWD TO CATTLE by inoculation (ok, is it three
or four???)
1: J Vet Diagn Invest 2001 Jan;13(1):91-6
Preliminary findings on the experimental transmission of chronic wasting
disease agent of mule deer to cattle.
Hamir AN, Cutlip RC, Miller JM, Williams ES, Stack MJ, Miller MW, O'Rourke
KI, Chaplin MJ.
National Animal Disease Center, ARS, USDA, Ames, IA 50010, USA.
To determine the transmissibility of chronic wasting disease (CWD) to
cattle and to provide information about clinical course, lesions, and
suitability of currently used diagnostic procedures for detection of CWD in
cattle, 13 calves were inoculated intracerebrally with brain suspension from
mule deer naturally affected with CWD. Between 24 and 27 months postinoculation,
3 animals became recumbent and were euthanized. Gross necropsies revealed
emaciation in 2 animals and a large pulmonary abscess in the third. Brains were
examined for protease-resistant prion protein (PrP(res)) by immunohistochemistry
and Western blotting and for scrapie-associated fibrils (SAFs) by negative-stain
electron microscopy. Microscopic lesions in the brain were subtle in 2 animals
and absent in the third case. However, all 3 animals were positive for PrP(res)
by immunohistochemistry and Western blot, and SAFs were detected in 2 of the
animals. An uninoculated control animal euthanized during the same period did
not have PrP(res) in its brain. These are preliminary observations from a
currently in-progress experiment. Three years after the CWD challenge, the 10
remaining inoculated cattle are alive and apparently healthy. These preliminary
findings demonstrate that diagnostic techniques currently used for bovine
spongiform encephalopathy (BSE) surveillance would also detect CWD in cattle
should it occur naturally.
Sat, Nov 23, 2002
Scientists unsure if CWD can jump species
By Jessica Bock Wausau Daily Herald jbock@wdhprint.com
snip...
Janice Miller, a veterinarian in charge of the experiment, said she
believes previous research shows it is hard for the disease to be transmitted
naturally from whitetail deer to dairy cattle. "Our study says nothing of how it
could be transmitted in natural surroundings," she said.
Miller has been studying the transmission of CWD from mule deer to cattle
since 1997. Since then, chronic wasting disease was transmitted to four out of
13 cattle injected with brain tissue from naturally infected mule deer, she
said.
In Wyoming, Williams has been studying cattle that were given a concoction
of diseased brain tissue orally, and five years into the study the animals
remain healthy, Miller said. No one knows if chronic wasting disease could ever
spread to another species through natural surroundings.
"Our experience is that it's pretty hard to predict," Miller said.
greetings list,
> Since then, chronic wasting disease was
> transmitted to four out of 13 cattle
is this a typo by the media or has another cow gone down with CWD since the
preliminary findings were found?
TSS
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Saturday, June 09, 2012
USDA Establishes a Herd Certification Program for Chronic Wasting Disease
in the United States
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
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. The purpose
of these experiments was to determine susceptibility of white-tailed deer (WTD)
to scrapie and to compare the resultant clinical signs, lesions, and molecular
profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD
intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral
and intranasal (IN); n = 5) with a US scrapie isolate.
All deer were inoculated with a 10% (wt/vol) brain homogenate from sheep
with scrapie (1ml IC, 1 ml IN, 30 ml oral). All deer inoculated by the
intracranial route had evidence of PrPSc accumulation. PrPSc was detected in
lymphoid tissues as early as 7 months-post-inoculation (PI) and a single deer
that was necropsied at 15.6 months had widespread distribution of PrPSc
highlighting that PrPSc is widely distributed in the CNS and lymphoid tissues
prior to the onset of clinical signs. IC inoculated deer necropsied after 20
months PI (3/5) had clinical signs, spongiform encephalopathy, and widespread
distribution of PrPSc in neural and lymphoid tissues.
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.
PO-041: Susceptibility of domestic cats to CWD infection
Amy Nalls, Jeanette Hayes-Klug, Kelly Anderson, Davis Seelig, Kevin Carnes,
Susan Kraft, Edward Hoover, Candace Mathiason
Colorado State University; Fort Collins, CO USA
Domestic and non-domestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE); very likely due to consumption of bovine
spongiform encephalopathy (BSE) contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were
inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer
brain homogenate.
Between 40 and 43 months two IC-inoculated cats developed slowly
progressive symptoms including weight loss, anorexia, polydipsia, patterned
motor behaviors, and ataxia”’ultimately mandating euthanasia. PrPCWD was
detected in the brains of these animals by western blot, immunohistochemistry
(IHC), and quaking-induced conversion (RT-QuIC) assays. No clinical signs of TSE
were detected in the remaining primary passage cats at 86 months pi.
Feline-adapted CWD (FelCWD) was sub-passaged into groups (n = 4 or 5) of cats by
IC, PO, and IP/SQ routes.
All 5 IC inoculated cats developed symptoms of disease 20–24 months pi
(approximately half the incubation period of primary passage). Additional
symptoms in these animals included increasing aggressiveness and hyper
responsiveness. FelCWD was demonstrated in the brains of all the affected cats
by western blot and IHC. Currently, 3 of 4 IP/SQ, and 1 of 4 PO inoculated cats
have developed abnormal behavior patterns consistent with the early stage of
feline CWD. Magnetic resonance imaging (MRI) has been performed on 11 cats (6
clinically ill, 2 asymptomatic, and 3 age-matched negative controls).
Abnormalities were detected in 4 of 6 clinically ill cats and included
multifocal signal changes consistent with inflammation, ventricular size
increases, more prominent sulci, and white matter tract cavitation.
These results demonstrate that CWD can be transmitted and adapted to the
domestic cat, and raise the potential for cervid-to-feline transmission in
nature.
SEE ;
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more