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 


