Thursday, May 31, 2012
MDC open house on CWD next steps June 2 in Macon County 
 News from the Central and Northeast regions
Published on: May. 25, 2012
Posted by Joe Jerek 
 JEFFERSON CITY Mo. – The Missouri Department of Conservation (MDC) will 
hold an informational open house on Chronic Wasting Disease (CWD) in Macon 
County on June 2 at New Cambria High School, 501 S. Main St. The public is 
invited to stop by 1-4 p.m. 
MDC staff will provide information on five recently found cases of CWD in 
free-ranging deer in northwest Macon County, explain disease management actions 
the Department is taking, answer questions and provide information on managing 
private land for deer. 
MDC’s disease-management steps to help contain the spread of CWD include 
two regulation changes to the Wildlife Code of Missouri, recommendations on 
transportation and disposal of deer carcasses and continuing CWD sampling of 
deer harvested in the area where CWD has been found. 
 Restriction on Feeding 
The Conservation Commission approved a regulation change at its May 25 
meeting that places a restriction on activities that are likely to unnaturally 
concentrate white-tailed deer and promote the spread of CWD. The ban on the 
placement of grain, salt products, minerals and other consumable natural or 
manufactured products is limited to the area where CWD has been found in Macon 
County and is comprised of Adair, Chariton, Linn, Macon, Randolph and Sullivan 
counties. 
The regulation includes exceptions for backyard feeding of birds and other 
wildlife within 100 feet of any residence or occupied building, or if feed is 
placed in such a manner to reasonably exclude access by deer. The regulation 
also includes exceptions for normal agricultural, forest management, crop and 
wildlife food production practices. 
According to MDC Deer Biologist Jason Sumners, the reason for the 
regulation change is that activities such as feeding and placement of 
minerals/salts that artificially concentrate deer greatly increase the 
likelihood of disease transmission from animal to animal or from soil to animal. 
 Removal of Antler-Point Restriction 
The Conservation Commission also approved a regulation change at its May 25 
meeting for a special harvest provision that rescinds the antler-point 
restriction (four-point rule) in Adair, Chariton, Linn, Macon, Randolph and 
Sullivan counties. 
According to Sumners, the reason for the regulation change is that 
management strategies such as antler-point restrictions, which protect yearling 
males and promote older bucks, have been found to increase prevalence rates and 
further spread the disease. 
Sumners explained that yearling and adult male deer have been found to 
exhibit CWD at much higher rates than yearling and adult females so a reduction 
in the number of male deer can help reduce the spread of CWD. He added that the 
movement of young male deer from their birth range in search of territory and 
mates is also a way of expanding the distribution of CWD. 
 Don’t Remove Carcasses from Area 
MDC also encourages hunters who harvest deer in Adair, Chariton, Linn, 
Macon, Randolph, and Sullivan counties not to take whole deer carcasses or 
carcass parts out of the area where CWD has been found. Exceptions to this 
include meat that is cut and wrapped, meat that has been boned out, quarters or 
other portions of meat with no part of the spinal column or head attached, hides 
or capes from which all excess tissue has been removed, antlers, antlers 
attached to skull plates or skulls cleaned of all muscle and brain tissue, upper 
canine teeth and finished taxidermy products. 
According to Sumners, the reason for this recommendation is that CWD can be 
transmitted from the environment to deer through soil and water that contain 
infected waste and/or infected carcasses. Deer can be infected with CWD but have 
no visible signs or symptoms. Moving harvested deer that still have parts known 
to concentrate CWD (brain, spinal cord, eyes, spleen, and lymph nodes) from the 
area known to have CWD can introduce the disease to other parts of the state 
through the improper disposal of carcasses. 
He explained that hunters should make every attempt to avoid moving the 
head and spinal cord from the area and properly dispose of potentially infected 
deer carcasses, including bones and trimmings, to minimize the risk of exposure 
to uninfected deer. MDC advises hunters to double-bag carcass parts and take 
them directly to a landfill, or place them in trash cans for pick-up. Burying 
carcass waste deep enough to prevent scavengers from digging it up is another 
acceptable option. As a last resort, and only on their own land, hunters can put 
carcass waste back on the landscape. Carcasses should be put as close as 
possible to where the deer was harvested so as to not spread CWD-causing prions 
to new locations. If possible, put the carcass in a location where it will be 
inaccessible to scavengers and other deer. 
 Fall Harvest CWD Sampling 
Sumners added that MDC will also continue to work with hunters who harvest 
deer this fall in Adair, Chariton, Linn, Macon, Randolph and Sullivan counties 
to collect samples for CWD testing. Details on these efforts are being developed 
and will be shared before the 2012 fall deer hunting season. 
For more information on the open house, contact MDC Public Involvement 
Coordinator Michele Baumer at 573-522-4115, ext. 3350, or 
Michele.Baumer@mdc.mo.gov. 
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 
Thursday, February 09, 2012 
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Saturday, February 04, 2012 
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol 
Needs To Be Revised 
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. 
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for 
$465,000 for the Statewide Wildlife Habitat Program in Portage County and 
approve the restrictions on public use of the site. 
snip...see full text and much more here ;
PRODUCT 
Product is custom made deer feed packaged in 100 lb. poly bags. The product 
has no labeling. Recall # V-003-5. 
CODE 
The product has no lot code. All custom made feed purchased between June 
24, 2004 and September 8, 2004. 
RECALLING FIRM/MANUFACTURER 
Farmers Elevator Co, Houston, OH, by telephone and letter dated September 
27, 2004. Firm initiated recall is ongoing. 
REASON 
Feed may contain protein derived from mammalian tissues which is prohibited 
in ruminant feed. 
VOLUME OF PRODUCT IN COMMERCE 
Approximately 6 tons. 
DISTRIBUTION 
OH. 
END OF ENFORCEMENT REPORT FOR October 20, 2004 
################# BSE-L-subscribe-request@uni-karlsruhe.de 
################# 
 Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material 
From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 
–0500
From: "Terry S. Singeltary Sr."
Monday, March 26, 2012 
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE 
http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html
CANADA PLANS TO IMPRISON ANYONE SPEAKING 
ABOUT MAD COW or ANY OTHER DISEASE OUTBREAK, CENSORSHIP IS A TERRIBLE 
THING
TSS
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more
PO-031: Aerosol transmission of chronic wasting disease to white-tailed 
deer 
 Nathaniel Denkers,1 Jeanette Hayes-Klug,1 Kelly Anderson,1 Sally Dahmes,2 
David Osborn,3 Karl Miller,3 Robert Warren,3 Candace Mathiason,1 Edward Hoover1 
 1Colorado State University; Fort Collins, CO USA; 2WASCO Inc.; Monroe, GA 
USA; 3Warnell School of Forestry and Natural Resources, University of Georgia; 
Athens, GA USA 
 Purpose. A signature feature of chronic wasting disease (CWD) is its 
efficient lateral transmission in nature, almost surely by mucosal exposure. Our 
previous studies employing Tg(cerPrP) mice determined that CWD can be 
transmitted to a susceptible host by aerosol exposure, a route with relatively 
little investigation. The present study was designed to determine whether CWD is 
transmissible by aerosol to a native cervid host, white-tailed deer. 
 Materials and Methods. Nine white-tailed deer were exposed to two (2) 
aerosol doses of a 5% w/v CWD+ (n = 6) or CWD- (n = 3) brain homogenate, 
delivered via the nasal passages using a customized aerosol apparatus. At 
3-month intervals post inoculation (mpi), tonsil and recto-anal 
mucosa-associated lymphoid tissue (RAMALT) biopsies were collected and assayed 
for CWD infection by protein misfolding cyclic amplification (PMCA), western 
blotting (WB), and immunohistochemistry (IHC). 
 Results. At 3 mpi and 6 mpi, tonsil and RAMALT biopsies were collected 
from 5 of the 6 CWD + aerosol-exposed deer. Three of the 5 (60%) tested positive 
for CWD by PMCA but not IHC or western blot analysis at 3 mpi. By 6 mpi, 5 of 5 
(100%) were tonsil and/or RAMALT biopsy positive by at least two of the three 
assays. Biopsies were collected from all CWD+ aerosol-exposed deer at 9 mpi, 
with 6 of 6 (100%) tonsil and/ or RAMALT positive by western blot or IHC. At 10 
mpi 3 of the 6 prion-exposed deer have developed early clinical signs of CWD 
infection (hyperphagia, polydypsia, wide leg stance and head/neck 
dorsi-flexion). All sham-inoculated deer are showing no clinical signs and have 
remained CWD negative as assessed by all three assays. Interestingly, the prion 
dose delivered to the deer by aerosol-exposure is estimated to be 20-fold lower 
than the historical oral dose that has resulted in detectable CWD infection at 6 
or 12 mpi. 
 Conclusions. This study documents the first aerosol transmission of CWD in 
deer. These results further infer that aerosolized prions facilitate CWD 
transmission with greater efficiency than does oral exposure to a larger prion 
dose. Thus exposure via the respiratory mucosa may be significant in the facile 
spread of CWD in deer and perhaps in prion transmission overall. 
 PO-073: Multiple routes of prion transepithelial transport in the nasal 
cavity following inhalation 
Anthony Kincaid, Shawn Feilmann, Melissa Clouse, Albert Lorenzo, Jason 
Bartz Creighton University; Omaha, NE USA 
Introduction. Inhalation of either prion-infected brain homogenate or 
aerosolized prions has been shown to cause disease, and in the case of 
inhalation of infected brain homogenate, the nasal route of infection has been 
shown to be 10–100 times more efficient than the oral route. The cell types 
involved in the in vivo transport of prions across the nasal cavity epithelium 
have not been determined. M cells in the follicular associated epithelium have 
been shown to mediate transcellular transport of prions in vitro and in the gut 
of experimentally infected mice. We tested the hypothesis that M-cell mediated 
transport was responsible for prion entry across nasal cavity epithelium 
following inhalation. 
Materials and Methods. Hamsters were inoculated extranasally with 50 or 
100ul of infected (n = 31) or mock-infected (n = 13) brain homogenate. Control 
animals were inoculated with buffer (n = 4) or were untreated (n = 5). Following 
survival periods ranging from 15 to 180 min, animals were perfused, skulls were 
decalcified and nasal cavities were embedded in paraffin. Tissue sections were 
cut and processed immunohistochemically for glial fibrillary acidic protein to 
identify brain homogenate, or for the disease-associated form of the prion 
protein. Tissue sections not further than 112 um apart through the entire extent 
of the nasal cavity were analyzed using light microscopy; photomicrographs were 
obtained wherever inoculum was observed on the surface of, within, or deep to 
the nasal mucosa for each animal. 
Results. Infected or uninfected brain homogenate was identified within the 
nasal cavities of animals at all time points and was seen crossing the nasal 
cavity epithelium within minutes of inoculation; the transepithelial transport 
of brain homogenate continued for up to 3 h after inoculation. Infected or 
uninfected brain homogenate was seen adhering to, or located within, M cells at 
all time points. However, larger volumes of infected or uninfected brain 
homogenate were identified crossing between cells of the olfactory and 
respiratory epithelia in multiple locations. In addition, infected or uninfected 
brain homogenate was identified within the lumen of lymphatic vessels in the 
lamina propria beneath the nasal mucosa at all time points. 
Conclusion. Transepithelial transport of prions across nasal cavity mucosa 
begins within minutes of inhalation and can continue for up to 3 h. While M 
cells appear to transport prions across the follicular associated epithelium, 
larger amounts of prions are transported between the cells of the respiratory 
and olfactory epithelia, where they immediately enter the lymphatic vessels in 
the lamina propria. Thus, inhaled prions can be spread via lymph draining the 
nasal cavity and have access to somatic and autonomic nerves in the lamina 
propria of the nasal cavity. The increased efficiency of the nasal cavity route 
of infection compared with the oral route may be due to the rapid and prolonged 
transport of prions between cells of the respiratory and olfactory 
epithelia.
PO-033: Replication efficiency of soil-bound prions varies with soil type 
Shannon Bartelt-Hunt,1 Samuel Saunders,1 Ronald Shikiya,2 Katie 
Langenfeld,2 Jason Bartz2 1University of Nebraska-Lincoln; Omaha, NE USA; 
2Creighton University; Omaha, NE USA 
Prion sorption to soil is thought to play an important role in the 
transmission of scrapie and chronic wasting disease (CWD) via the environment. 
Sorption of PrP to soil and soil minerals is influenced by the strain and 
species of PrPSc and by soil characteristics. However, the ability of soil-bound 
prions to convert PrPc to PrPSc under these wide-ranging conditions remains 
poorly understood. We developed a semiquantitative protein misfolding cyclic 
amplification (PMCA) protocol to evaluate replication efficiency of soil-bound 
prions. Binding of the hyper (HY) strain of transmissible mink encephalopathy 
(TME) (hamster) prions to a silty clay loam soil yielded a greater-than-1-log 
decrease in PMCA replication efficiency with a corresponding 1.3-log reduction 
in titer. The increased binding of PrPSc to soil over time corresponded with a 
decrease in PMCA replication efficiency. The PMCA efficiency of bound prions 
varied with soil type, where prions bound to clay and organic surfaces exhibited 
significantly lower replication efficiencies while prions bound to sand 
exhibited no apparent difference in replication efficiency compared to unbound 
controls. PMCA results from hamster and CWD agent-infected elk prions yielded 
similar findings. Given that PrPSc adsorption affinity varies with soil type, 
the overall balance between prion adsorption affinity and replication efficiency 
for the dominant soil types of an area may be a significant determinant in the 
environmental transmission of prion diseases. 
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. 
PO-055: Transgenetic modeling of the CWD species barrier to humans 
 Eri Saijo,1 Sehun Kim,2 Claudio Soto,3 Glenn Telling2 1University of 
Kentucky College of Medicine; Fort Collins, CO USA; 2Department of Microbiology, 
Immunology and Pathology; Colorado State University; Fort Collins, CO USA ; 
3Department of Neurology; University of Texas Houston Medical School; Houston, 
TX USA 
 Our recent studies raise significant concerns about the zoonotic potential 
of CWD. First, we showed that tissues consumed by humans derived from deer or 
elk with CWD, including skeletal muscle and antler velvet, harbor infectious 
prions. In other studies, cervid PrPSc converted human PrPC after CWD prions 
were stabilized by successive passages in vitro or in vivo. 
We also identified at least two distinct strains of CWD, referred to as 
CWD1 and CWD2, the host-range properties of which are currently undefined. Other 
studies showed that codon 129, and the corresponding 132 residue in elk, 
significantly influenced the transmission of BSE and CWD prions respectively in 
transgenic (Tg) mouse models. 
We inoculated Tg mice expressing human PrP encoding either methionine (M) 
or valine (V) at codon 129 with deer or elk CWD prions that previously produced 
disease in Tg mice expressing deer PrP with characteristics typical of CWD1 and 
CWD2 strains, as well as CWD prions that had been passaged multiple times in Tg 
mice expressing deer PrP. 
While most Tg mice remained free of signs of prion disease for >260 
days, small numbers of inoculated mice developed multiple, progressive 
neurological signs, that were consistent with prion disease. However, 
examination of brain materials from diseased mice failed to confirm the presence 
of protease-resistant human PrP. These preliminary results are consistent with a 
significant species barrier in humans to these CWD strains, and indicate that 
the 129 polymorphism does not modulate susceptibility. 
 PO-056: PrPCWD profiling of white-tailed deer (Odocoileus virginianus) 
with different Prnp genotypes following experimental oral infection 
 Camilo Duque Velasquez,1 Allen Herbst,1 Chad Johnson,2 Judd Aiken,1 Debbie 
McKenzie1 1Centre for Prions and Protein Folding Diseases; University of 
Alberta; Edmonton, AB Canada; 2Department of Soil Science; University of 
Wisconsin; Madison, WI USA 
 Chronic wasting disease (CWD) affects captive and free-ranging cervid 
populations in North America and farmed cervids of South Korea. CWD and scrapie 
are the only prion diseases in which the transmission occurs horizontally. The 
cervid Prnp gene is polymorphic at various positions. The effect of these 
changes on infection is influenced by the sequence and structure compatibility 
between the host and the infectious source. Prion strains have been described 
virtually in every prion disease and strongly impact disease characteristics 
(clinical symptoms, neuropathological profiles, incubation periods, species 
tropism as well as biochemical and biophysical properties of the abnormally 
folded prion protein). Prion protein sequence differences can result, upon 
subsequent infection, in the generation of novel strains as documented in sheep 
scrapie. We have previously shown that Prnp polymorphisms influence 
susceptibility to CWD in free-ranging white-tailed deer. In CWD-positive deer 
populations, alleles Q95G96 (wt) were over-represented compared to the H95G96 
and Q95S96 alleles. Experimental oral infection of white-tailed deer with known 
Prnp genotypes (with inoculum from CWDpositive wt/wt deer) confirmed the link 
between prion protein primary sequence and the progression of disease. 
Heterozygous interference occurred in varying degrees as evidenced by the 
difference in the extension of the incubation period as an effect of alleles 
Q95S96 and H95G96. Interestingly, the biochemical profiles of the wt/Q95S96 and 
wt/H95G96 isolates resemble the wt/wt, differing only in the amount of protease 
resistant PrPCWD present suggesting that the wt allele is preferentially 
converted. PrPCWD profiling revealed differences between deer with at least one 
wt allele and the H95G96/Q95S96 deer suggesting that this PrPCWD is unique 
compared to the PrPCWD from wt/wt animals. 
PO-057: Host factors influence prion strain adaptation 
 Crystal Meyerett Reid, Mark Zabel Colorado State University; Fort Collins, 
CO USA 
 Background. Chronic Wasting disease (CWD) is one of many prion-mediated 
diseases known as transmissible spongiform encephalopathies (TSEs). There is 
ever-increasing biological and biochemical evidence that prion pathogenesis is 
caused by the conversion of the normal host protein (PrPC) into an abnormal 
disease causing conformation (PrPRES). How prions encipher heritable strain 
properties without nucleic acid remains unclear. Previously we have shown that 
host factors have contributed to the adaptation of an original deer CWD prion 
strain to transgenic mice. 
 Materials and Methods. We assessed strain differences using biological and 
biochemical assays and found that amplified cervid prions and serial-passaged 
cervid prions were significantly different than that of the original cervid 
strain. It is possible that prion mutation and adaptation can broaden the host 
range. Previous reports, however, indicate that there is a strict species 
barrier preventing CWD infection in wildtype mice. 
 Results. Here we show the generation of a mouse-adapted strain of CWD upon 
serial passage into transgenic cervidized mice and then subsequent passage into 
wildtype mice. All wildtype mice remained non-clinical upon first passage but 
became completely susceptible after second passage with similar incubation times 
to those of mice terminally ill from a mouse adapted scrapie strain. Inoculation 
of our mouse adapted CWD strain back into cervidized mice delayed progression to 
terminal disease. 
 Conclusion. We conclude that prion strain adaptation and mutation is 
highly dependent upon host factors and host encoded PrPC primary sequence. Upon 
serial passage the adapted prion strain shares more characteristics with prion 
strains from the new host rather than the original species. 
OR-12: Chronic wasting disease transmission and pathogenesis in cervid and 
non-cervid Species 
Edward A. Hoover, Candace K. Mathiason, Nicholas J. Haley, Timothy D. Kurt, 
Davis M. Seelig, Nathaniel D. Denkers, Amy V. Nalls, Mark D. Zabel, and Glenn C. 
Telling 
 Prion Research Program, Department of Microbiology, Immunology, and 
Pathology; Colorado State University; Fort Collins, CO USA 
 Since its recognition as a TSE in the late 1970s, chronic wasting disease 
(CWD) of cervids has been distinguished by its facile spread and is now 
recognized in 18 states, 2 Canadian provinces, and South Korea. The efficient 
horizontal spread of CWD reflects a prion/host relationship that facilitates 
efficient mucosal uptake, peripheral lymphoid amplification, and dissemination 
by exploiting excretory tissues and their products, helping to establish 
indirect/environmental and well as direct (e.g., salivary) transmission. Recent 
studies from our group also support the likelihood of early life mother to 
offspring and aerosol CWD prion transmission. Studies of cervid CWD exposure by 
natural routes indicate that incubation period for detection of overt infection, 
while still uncertain, may be much longer than originally thought. 
 Several non-cervid species can be infected by CWD experimentally (e.g., 
ferrets, voles, cats) with consequent species-specific disease phenotypes. The 
species-adapted prions so generated can be transmitted by mucosal, i.e., more 
natural, routes. Whether non-cervid species sympatric with deer/elk can be 
infected in nature, however, remains unknown. In vitro CWD prion amplification 
studies, in particular sPMCA, can foreshadow in vivo susceptibility and suggest 
the importance of the PrPC rigid loop region in species barrier permissiveness. 
Trans-species CWD amplification appears to broaden the host range/strain 
characteristics of the resultant prions. The origins of CWD remain unknown, 
however, the existence of multiple CWD prion strains/ quasi-species, the 
mechanisms of prion shedding/dissemination, and the relationship between sheep 
scrapie and CWD merit further investigation. 
PO-060: Transmission of chronic wasting disease from mother to offspring 
Candace Mathiason, Amy Nalls, Stephenie Fullaway, Kelly Anderson, Jeanette 
Hayes-Klug, Nicholas Haley, Edward Hoover 
Colorado State University; Fort Collins, CO USA 
 To investigate the role mother to offspring transmission plays in chronic 
wasting disease (CWD) we have developed a cervid model employing the Reeve’s 
muntjac deer (Muntiacus reevesi). Eight muntjac doe were orally inoculated with 
CWD and tested PrPCWD lymphoid positive by 4 mo post infection. Twelve fawns 
were born to these eight CWD-infected doe, 3 were born viable, 6 were born 
non-viable, and 3 were harvested as fetuses (1 each from first, second or third 
trimester of pregnancy) from CWDinfected doe euthanized at end-stage disease. 
The viable fawns have been monitored for CWD infection by immunohistochemistry 
(IHC) performed on serial tonsil and rectal lymphoid tissue biopsies. One fawn 
that was IHC PrPCWD positive at 40 d of age is now, at 28 mo of age, showing 
early clinical signs associated with CWD infection. Moreover, CWD prions have 
been detected by sPMCA in placenta, brain, spleen and mesenteric lymphoid tissue 
harvested from 5 full-term non-viable fawns, and in fetal placenta and brain 
tissue harvested in utero from the second and third trimester fetuses. 
Additional tissues and pregnancy related fluids from doe and offspring are being 
analyzed for CWD prions. In summary, using the muntjac deer model we have 
demonstrated CWD clinical disease in an offspring born to a CWD-infected doe, 
and in utero transmission of CWD from mother to offspring. These studies provide 
basis to further investigate the mechanisms of maternal transfer of prions. 
 PO-081: Chronic wasting disease in the cat— Similarities to feline 
spongiform encephalopathy (FSE) 
 Davis Seelig, Amy Nalls, Maryanne Flasik, Victoria Frank, Candace 
Mathiason, Edward Hoover Colorado State University; Fort Collins, CO USA 
 Background and Introduction. Chronic wasting disease (CWD) is an 
efficiently transmitted prion disease of cervids with an as yet to be fully 
defined host range. Moreover, the risk that CWD poses to feline predators and 
scavangers, through crossspecies consumption and subsequent transmission, is 
unknown. Previous and ongoing studies in our laboratory evaluating the 
susceptibility of domestic cats (Felis catus) to CWD (Mathiason et. al., 
NeuroPrion 2011, Nalls et. al., NeuroPrion 2012) have documented the 
susceptibility of domestic cats to CWD following intracerebral (IC) inoculation. 
However, many of the pathologic features of feline-adapted CWD, including the 
neural and systemic patterns of PrPCWD accumulation and neuropathology, remain 
unknown. 
 The chief objectives of this work were: 
(1) to design a sensitive, enhanced immunohistochemical (E-IHC) protocol 
for the detection of CWD prions (PrPCWD) in feline tissues; 
(2) to document the systemic distribution of PrPCWD in CWD-infected cats 
through E-IHC; 
(3) to utilize single and multiple-label immunostaining and laser scanning 
confocal microscopy (LSCM) to provide insights into the subcellular patterns of 
PrPCWD accumulation and neuropathologic features of CWD-infected cats; and 
 (4) to compare feline CWD to the other known feline TSE Materials and 
Methods. Periodate-lysine-paraformaldehyde (PLP)-fixed, paraffin-embedded 
(PLP-PE) from terminal, IC-inoculated (n = 9) and sham-inoculated (n = 2), 1st 
and 2nd passage, CWD-infected cats were examined by E-IHC for the presence of 
PrPCWD and its association with markers of cell phenotype and organelles. 
 Results. The most sensitive E-IHC technique for the detection of PrPCWD in 
feline tissues incorporated a combination of slide pretreatment with 
proteinase-K (PK) in concert with tyramide signal amplification (TSA). With this 
protocol, we identified PrPCWD deposits throughout the CNS, which, in the 1st 
passage cats was primarily restricted to the obex, but increased in distribution 
and severity upon 2nd passage to include a number of midbrain nuclei, cortical 
gray matter, the thalamus and hypothalamus, and the hippocampus. Peripheral 
PrPCWD deposits were detected only in the 2nd passage cats, and included the 
enteric nervous system, the Peyer’s patches, and the retropharyngeal and 
mesenteric lymph nodes. PrPCWD was not detected in the sham-inoculated cats. 
Moreover, using multi-label analysis, intracellular PrPCWD aggregates were 
seen in association with neurofilament heavy chain (NFH)-positive neurons and 
GFAP-positive astrocytes. In addition, large aggregates of intracellular PrPCWD 
were identified within LAMP1-positive lysosomes. 
Conclusions. Feline PrPCWD is present in CNS neurons, astrocytes and 
LAMP-1-positive lysosomes. The morphologic overlap between the PrPCWD deposits 
in feline CWD and BSE-origin feline spongiform encephalopathy (FSE), implicates 
the importance of the host as a key determinant in the development of prion 
neuropathology and suggest a signature for detection of potential spontaneous 
feline prion disease. 
PO-099: Estimating the risk of CWD transmission to humans—An interim report 
of a comprehensive study in non-human primates 
 Ann-Christin Schmaedicke DPZ; Goettingen, Germany 
 Chronic Wasting Disease (CWD) is a transmissible prion disease that occurs 
primarily among North American cervid species. CWD has emerged as a prion 
disease in captive as well as freeranging cervids with rising incidence. 
Continuous consumption of cervid-derived products in conjunction with increasing 
CWD prevalence suggests a risk for human exposure to CWD prions. 
 Although surveillance data collected in the North American population did 
not provide epidemiological evidence for CWD transmissions to humans it remains 
unclear whether a biological risk for such transmissions exists or can be 
excluded. In order to gauge the potential transmissibility of CWD to humans, a 
comprehensive CWD risk assessment in cynomolgus macaques has been initiated. To 
test for the CWD interspecies transmission to humans, we used a primate species 
previously shown to mimic the BSE susceptibility of humans. In addition, this 
species is phylogenetically close to humans with a homologous amino acid 
sequence of the prion protein. When we assessed the genotype of macaque PrP, the 
homozygosity for methionine at codon 129 was confirmed in all animals. 
 The zoonotic potential of CWD is evaluated by challenging groups of 
animals via different inoculation routes. General transmissibility of CWD to 
macaques is tested by intracerebral (i.c.) inoculation of brain homogenate from 
CWD-infected white-tailed deer (WTD) and elk. This was either done by direct 
injection of 10 mg CWDWTD to two animals (> 880 dpi) or by surgical 
implantation of CWD-WTD or CWD-elk contaminated steel wires in two animals (> 
750 dpi) or three animals (> 400 dpi), respectively. 
 To address the risk of hunters while field dressing carcasses, we 
inoculated two animals with CWD-WTD by dermal scarification (> 920 dpi). To 
simulate human consumption of CWDinfected food products, we orally challenged 
three animals with 10 g CWD-WTD brain (> 820 dpi) and three animals with 3 kg 
CWD muscle tissue from different cervid species (> 950 dpi) by repeated 
feeding. Mock-inoculated macaques are co-housed in the same cage allowing 
exposure to saliva and faeces of CWDinoculated macaques. 
To date, all inoculated animals remain asymptomatic. Cerebrospinal fluid 
and blood from all animals were and are going to be collected bimonthly, 
processed and stored in a repository. Analysis of these samples using 
ultrasensitive prion detection methods has been initiated. Oral challenge of 50 
mg BSE to cynomolgus macaques can lead to fatal disease only after more than 5 y 
of incubation time (1952 dpi). 
Thus, to estimate whether CWD could be transmitted to macaques or not, we 
assume that observation of challenged animals would be necessary for at least 
8–10 y. 
 PO-248: TSE infectivity survives burial for five years with little 
reduction in titer 
Allister Smith, Robert Somerville, Karen Fernie The Roslin Institute and 
R(D)SVS; University of Edinburgh; Edinburgh, UK 
BSE infected animals, BSE-contaminated materials and other sources of TSE 
(prion) infection, such as carcasses from scrapie infected sheep, CWD infected 
deer and cadavers of individuals infected with CJD may all end up in the 
environment through burial or other methods of disposal. They may continue to 
act as a reservoir of TSE infectivity if cattle or other susceptible animals 
were to be exposed to these sources in the future. In order to address these 
concerns, we performed two large scale demonstration experiments under field 
conditions which were designed to mimic some of the ways by which TSE infected 
materials may have been disposed of. The project examined the fate of TSE 
infectivity over a period of five years in two scenarios; when the infectivity 
was contained within bovine heads and when the infectivity was buried without 
any containment. Two soil types were compared: a sandy loam and a clay loam. We 
used the 301V TSE strain which was derived by serial passage of BSE in VM 
mice.
TSE infectivity was recovered from all the heads exhumed annually for five 
years from both types of soil, with little reduction in the amount of 
infectivity throughout the period of the experiment. Small amounts of 
infectivity were found in the soil immediately surrounding the heads, but not in 
samples remote from them. Similarly there was no evidence of significant lateral 
movement of infectivity from the buried bolus. However large amounts of TSE 
infectivity were recovered at the site of burial of both boluses. There was 
limited vertical upward movement of infectivity from the bolus buried in clay 
soil and downward movement from the bolus buried in sandy soil.
Now that these experiments are completed we conclude that TSE infectivity 
is likely to survive burial for long periods of time with minimal loss of 
infectivity and restricted movement from the site of burial. These experiments 
emphasize that the environment is a viable reservoir for retaining large 
quantities of TSE infectivity, and reinforce the importance of risk assessment 
when disposing of this type of infectious material. 
see more here ; 
Epidemiology Update March 23, 2006 
As of today, 13 locations and 32 movements of cattle have been examined 
with 27 of those being substantially completed. Additional investigations of 
locations and herds will continue. In addition, state and federal officials have 
confirmed that a black bull calf was born in 2005 to the index animal (the red 
cow). The calf was taken by the owner to a local stockyard in July 2005 where 
the calf died. The calf was appropriately disposed of in a local landfill and 
did not enter the human or animal food chain. http://www.aphis.usda.gov/newsroom/hot_issues/bse/bse_al_epi-update.shtml 
> The calf was appropriately disposed of in a local 
> landfill and did not enter the human or animal food chain. 
 Wednesday, May 30, 2012
PO-248: TSE infectivity survives burial for five years with little 
reduction in titer 
TSS
    Friday, May 25, 2012
Chronic Wasting Disease CWD found in a farmed red deer from Ramsey County Minnesota
News Release
For immediate release: Friday, May 25, 2012
Contact: Malissa Fritz, BAH Communications Director, 651-201-6830
Chronic Wasting Disease found in a farmed red deer from Ramsey County
Mandatory surveillance program leads to detection of the disease
St. Paul, Minn – The Minnesota Board of Animal Health today announced that 
a farmed red deer from a Ramsey County herd tested positive for Chronic Wasting 
Disease (CWD). 
The brain stem from a two-year-old female red deer was submitted for 
testing at the University of Minnesota Veterinary Diagnostic Laboratory, where 
preliminary results were positive for CWD. The National Veterinary Services 
Laboratory today confirmed the positive test. The Board of Animal Health has 
placed the herd under quarantine and is working with the owners to determine the 
herd’s future. 
The red deer died on the farm on May 10. The animal was tested for the 
disease as part of Minnesota’s mandatory CWD surveillance program, which has 
been in place since 2003. Farmed cervidae producers in Minnesota must CWD test 
all deer and elk over 16 months of age that die or are slaughtered. 
This herd has been registered with the Board of Animal Health since 2000. 
“This herd is an example of farmers who take great care in the management of 
their animals,” said Dr. Paul Anderson, assistant director of the Board of 
Animal Health. “In their 12 years of herd registration with the Board, this 
producer has met all of the requirements.” 
The Board of Animal Health is coordinating with the Minnesota Department of 
Natural Resources (DNR). The DNR is currently evaluating the situation and will 
likely test wild white-tailed deer in the area this fall.
CWD is a fatal brain and nervous system disease found in cervidae in 
certain parts of North America. The disease is caused by an abnormally shaped 
protein called a prion, which can damage brain and nerve tissue. Infected 
animals may show signs of the disease including progressive loss of body weight, 
behavioral changes, staggering, increased water consumption and drooling. In 
later stages of the disease, animals become emaciated (thus “wasting” disease). 
According to state health officials and the federal Centers for Disease 
Control and Prevention, there is no evidence that CWD can be transmitted to 
humans. 
For more information on CWD and the Board of Animal Health, visit 
www.bah.state.mn.us.
--30--
Chronic wasting disease found in a red deer from North Oaks farm herd
By Dennis Lien
Posted:   05/25/2012 12:01:00 AM CDT
May 26, 2012 1:45 AM GMTUpdated:   05/25/2012 08:45:21 PM CDT
A farmed red deer from a large northern Ramsey County herd has tested 
positive for chronic wasting disease. 
The Minnesota Board of Animal Health said the 2-year-old female deer died 
on the farm May 10, and a required examination of its brain stem tested positive 
for the fatal brain and nervous system disease affecting elk and deer. 
The 500-head North Oaks herd remains under quarantine, and officials are 
trying to figure out how the disease got there and what to do with the rest of 
the red deer, a large species native to Europe and Asia. 
It marks the fifth case of farmed cervids testing positive in Minnesota for 
chronic wasting disease, according to Dr. Paul Anderson, a board veterinarian. 
Three were elk; the fourth, a white-tailed deer. 
In those instances, including the most recent one in Olmsted County in 
2009, all other herd members were slaughtered and tested for the disease. 
"It's way too early to tell (in this case),'' said Anderson, noting the 
investigation will take weeks. 
"The one thing I will say, this particular operation has had absolutely 
perfect surveillance for CWD,'' he added. "They have never missed an animal they 
needed to test, and all the animals have tested negative. This farm is one of 
the best-run in the state, and it's going to take some work to see if we can 
figure out where this came from.'' 
A man answering a telephone number listed at northoaksfarms.com declined to 
comment. 
"I would refer you to the Board of Animal Health. We're working closely 
with them. Goodbye,'' he said and hung up. 
That herd of red deer has been registered with the Board of Animal Health 
since 2000. 
Chronic wasting disease, which is found in elk and deer in parts of North 
America, is caused by an abnormally shaped protein called a prion, which can 
damage brain and nerve tissue. Infected animals show progressive loss of body 
weight with accompanying behavioral changes, including staggering, drinking 
large amounts of water, excessive urinating and drooling. 
There is no evidence the disease can be transmitted to humans or other 
animals such as cattle or sheep, according to federal and state health experts. 
Authorities believe it most likely is transmitted by animal-to-animal contact or 
exposure to contaminated habitat. 
The disease can have a long incubation period, making it difficult to 
figure out how animals became infected. 
In the North Oaks case, the brain stem from the red deer was submitted to 
the University of Minnesota Veterinary Diagnostic Laboratory, where preliminary 
results were positive. The U.S. Department of Agriculture's National Veterinary 
Services Laboratory in Ames, Iowa, confirmed the positive test Friday, May 25. 
The deer was tested as part of the state's mandatory CWD surveillance 
program. 
Since 2003, Minnesota has required registration and chronic wasting disease 
surveillance programs for farmed cervid herds. When animals 16 months or older 
die or are slaughtered, herd owners must submit brain samples for testing. 
The Minnesota Department of Natural Resources plans to meet with the board 
soon and likely will test wild white-tailed deer in the area. 
"We haven't had any reports of sick deer in the area,'' said Lou 
Cornicelli, DNR wildlife research manager. 
Although the other farmed herds have been destroyed, Anderson said 
decisions are made on a case-by-case basis. 
"Whenever something like this happens, we do what is best for the herd and 
figure out a way to make sure this disease is eradicated,'' Anderson said. 
Dennis Lien can be reached at 651-228-5588.
CHRONIC WASTING DISEASE UPDATE September 6, 2002
Minnesota has announced the finding of CWD in a captive elk in Aitkin 
County. The animal was a five-year-old male. It had been purchased from a 
captive facility in Stearns County in August of 2000. The herd where the elk was 
found has been placed under quarantine as has two additional facilities where 
the infected elk had resided prior to it coming to the farm in Aitkin County. 
Minnesota DNR officials will test wild deer in the area to determine if there is 
any sign of CWD in the free-ranging population. This is the first case of CWD in 
either captive or freeranging cervids in Minnesota. Several more states have 
passed bans on the importation of deer and elk carcasses from states where CWD 
has been found in wild animals. Previously the states of Colorado, Illinois and 
Iowa and the province of Manitoba had passed such bans. The states of Vermont, 
Oregon and Missouri have enacted similar bans. Numerous states have issue 
voluntary advisories to their out-of-state hunters encouraging them not to bring 
the carcass or carcass parts of deer and elk into their state. The bans do 
permit the importation of boned out meat, hides or cape with no meat attached, 
clean skull cap with antler attached, finished taxidermy heads or the ivories of 
elk. The state of Georgia has recently banned the importation of live cervids 
into that state also. Some citizens of Colorado have formed a new political 
action group called Colorado Wildlife Defense (just happens that the acronym is 
CWD). The stated goal of this group are; Elimination of big game diseases, 
especially CWD; promotion of healthy wildlife habitat; promotion of 
scientifically sound wildlife research; promotion of a discussion of the ethics 
of hunting and wildlife management; education of the hunting and non hunting 
public. Their action plan calls for; requiring double fencing of all game farms 
at owners expense; all game farmers provide annual proof of bonding; prohibit 
new licenses for deer and elk farms; prohibit expansion in acreage of existing 
game farms; prohibit the transfer of game farm licenses; prohibit charging for 
hunting behind high wire; prohibit blocking of traditional migratory paths by 
high fences; requiring game farms to maintain environmental controls and 
prohibit the escape of contaminated water or soil; requiring immediate reporting 
of missing deer or elk from game farms; and requiring all game farm deer and elk 
to be tested for brucellosis and TB. Wisconsin has announced that 7 more 
free-ranging deer have tested positive for CWD. They have expanded their 
eradication zone by an additional 15 square miles to cover these findings. The 
total number of free-ranging CWD positive in Wisconsin is now 31 white-tail 
deer.
In 2000, a elk farmer in Wisconsin received elk from a CWD exposed herd in 
Colorado. At that time, the farmer advised the Wisconsin Department of 
Agriculture that both animals from the exposed herd in Colorado were dead. He 
has now advised Wisconsin Ag. that he was mistaken and that one of the animals 
is still alive in his herd. The second draft of the implementation documents for 
the National CWD Plan was distributed to committee members and others on Friday, 
August 30. The final documents are due to APHIS and USFWS on Friday, September 
13. The herd of captive elk in Oklahoma that had been exposed to CWD will be 
destroyed this week. This herd had an elk test positive for CWD in 1997 but the 
depopulation of the herd was not agreed to by the owners and federal 
representatives until this week. Since the discovery of CWD in the herd, the 
remaining animals have been under quarantine, however, in the meantime the herd 
has dropped from 150 animals to 74. Due to a lack of communication, not all of 
the 76 animals that died in the interim were tested for CWD. All remaining 
animals will be tested but the true degree of infection rate of the herd will 
never be known.
The owners of the facility will not be permitted to restock the area with 
cervids for a period of five years. A New York based organization, BioTech 
Research Fund I LLC has committed a $1 million line of credit to fund 
commercialization of tests for brain-wasting disorders and production of various 
vaccines to Gene-Thera of Wheat Ridge, Colorado. Gene-Thera has spent three 
years developing new ways not only to diagnose CWD, but create vaccines for mad 
cow disease, E. coli contaminants and foot-and-mouth disease. Its tests for CWD 
have been successful in more than 100 samples from Colorado and Wisconsin 
according to company officials. Gene-Thera plans to license and market some o 
fits disease test kits by the end of the year, then begin volume distribution by 
mid-2003. The abstracts of the presentations from the CWD Conference in Denver 
August 6 and 7 have been posted on the Colorado Division of Wildlife web site. 
You will need adobe acrobat reader to read them. 
The Division web site is: http://wildlife.state.co.us/CWD/Symposium_booklet.pdf 
If you don’t have adobe acrobat, you can download it free at http://www.adobe.com/products/acrobat/readstep.html
Minnesota: Second case in a game farmed elk discovered in Stearns Co. 
This is a trace forward from the previously affected game farm in Aitkins 
Co. An additional game farm in Benton Co is under quarantine.
snip...
Supporting Documents: Colorado: CWD-Exposed Elk Used in 1990 Study- 
Wildlife officials call W. Slope move a mistake Date: January 17, 2003 Source: 
Denver Post Contacts: Theo Stein Environment Writer
The Colorado Division of Wildlife knowingly used a herd of captive elk 
exposed to chronic wasting disease in a grazing study on the Western Slope in 
January 1990, possibly introducing the disease to the elk-rich area. "It was a 
bad call," said Jeff Ver Steeg, the division's top game manager. "I can't deny 
it." About 150 wild elk were allowed to graze in the same pens near Maybell 
after the research herd was removed and may have picked up the abnormal protein 
that causes the disease from the feces and urine left by the captive elk. While 
the Division of Wildlife has expressed concern before that its animals might 
have helped spread CWD, this is the first time the agency has acknowledged it 
knowingly moved elk exposed to CWD deep into an area where the disease was not 
known to already exist. Studies that could help determine the source of CWD on 
the Western Slope are incomplete, and officials say what data that do exist are 
so new and so spotty they may not provide all the answers. So far, it appears 
that less than 1 percent of deer and elk in the area are infected, compared with 
as much as 15 to 20 percent in hotspots in northeastern Colorado. But as 
wildlife officials grapple with CWD's appearance in northwestern Colorado, 
officials now admit the decision to continue the grazing study over the 
objections of some biologists was an error. At the time, biologists wanted to 
see whether elk grazing on winter range depleted forage that ranchers wanted for 
fattening cattle in spring. "I think in hindsight a lot of good people probably 
did some dumb things, myself included," said Bruce Gill, a retired wildlife 
manager who oversaw research efforts and remembers the debate over the project. 
"Had we known CWD would explode into such a potentially volatile ecologic and 
economic issue, we wouldn't have done it." Elk ranchers, who have been blamed 
for exporting the disease from its stronghold on the Colorado and Wyoming plains 
to seven states and two Canadian provinces, say the agency's belated disclosure 
smacks of a coverup. "It's pure negligence," said Jerry Perkins, a Delta banker 
and rancher who is now demanding a legislative inquiry. "If I'd have moved 
animals I knew to be infected around like that, I'd be in jail." Grand Junction 
veterinarian and sportsman Dick Steele said he faults the agency for not 
disclosing information about CWD-exposed research animals before October, when 
information was posted on the Division of Wildlife website. "This went way 
beyond poor judgment," he said. "My main concern is that this has been hidden 
for the last 12 years. It would have been real important to our decision-making 
process on how to deal with CWD." While the Maybell information is new, Perkins 
and other ranchers have long suspected Division of Wildlife research facilities 
near Meeker and Kremmling, which temporarily housed mule deer kept in heavily 
infected pens at the Fort Collins facility, have leaked CWD to the wild. Fear of 
an outbreak led the agency to sample 450 deer around the Meeker and Kremmling 
facilities. None tested positive, but the sample size was only large enough to 
detect cases if the infection rate was greater than 1 percent. This fall, tests 
on 23,000 deer and elk submitted by hunters statewide have revealed 48 CWD cases 
north of Interstate 70 and west of the Continental Divide. Biologists believe 
the infection rate in that area, which includes the Maybell, Meeker and 
Kremmling sites, is still well below 1 percent. But CWD has never been contained 
in a wild population, so experts fear the problem will grow worse.
The Division of Wildlife says it will be months before a statistical 
analysis of the fall's sampling results can be completed, an exercise that may 
shed light on the disease's origin on the Western Slope. "We're just not going 
to speculate at this point," said Ver Steeg of the possible Maybell connection. 
"This is one possibility, but certainly not the only possibility." Some 
biologists think a defunct elk ranch near Pagoda, which had dozens of 
unexplained deaths in the mid-'90s, is another, a suggestion Perkins rejects. 
"It may be inconclusive to them," said Perkins. "It isn't inconclusive to 
us."
To date, 19 CWD-positive 
animals have been found on six Wisconsin farms. All have been white-tailed deer 
except for one elk imported from a Minnesota herd later found to be infected. 
More than 8,000 farm-raised deer and elk have been tested in Wisconsin, and 
about 540 herds are enrolled in the CWD monitoring program. 
Subject: CWD disease detected on Lac qui Parle County cervid farm 
southwestern Minnesota (2006-03-15) Date: March 15, 2006 at 12:36 pm PST
Chronic wasting disease detected on Lac qui Parle County cervid farm 
(2006-03-15) The Board of Animal Health announced today that chronic wasting 
disease (CWD) has been detected in one domestic white-tailed deer on a cervid 
farm in Lac qui Parle County, which is located in southwestern Minnesota.
Immediately, DNR officials will conduct a local deer survey to determine 
the number of wild deer in the area. It is expected that not many deer will be 
found because the area is highly agricultural, with little deer habitat 
surrounding the farm. DNR will conduct opportunistic sampling of deer, like road 
kills, in the immediate area now and will conduct intensive hunter-harvested 
surveillance during the 2006 firearm deer season.
Although this positive animal is a captive deer, DNR has conducted 
surveillance for CWD in wild deer in the area. The farm is located near the 
northern boundary of deer permit area 447, where wild deer surveillance for CWD 
last occurred in 2003.
Lou Cornicelli, DNR big game program coordinator, said, "In 2003, we 
conducted wild deer CWD surveillance in adjoining permit areas 433, 446 and 447. 
In total, we collected 392 samples from those permit areas during the regular 
firearm deer season and CWD was not detected."
The sampling of wild deer was designed statistically to have a 95 percent 
confidence of detecting a 1 percent infection rate, according to Mike DonCarlos, 
DNR wildlife programs manager.
"This situation is very similar to the positive elk farm discovered in 
Stearns County in 2003, which followed the first discovery of CWD in an Aitkin 
County elk farm," DonCarlos said. “The DNR response will be similar to the 
Stearns County action and will include an initial assessment of wild deer 
populations in the area and development of a surveillance program for next 
fall."
From 2002 to 2004, DNR staff collected nearly 28,000 CWD samples statewide 
and no disease found in the wild herd.
"The intensive surveillance conducted in 2003 indicated CWD was not present 
in wild deer," Cornicelli said. “In addition, all indications are that this 
positive captive deer has not contacted any wild deer, but we will conduct 
additional surveillance this fall to be sure."
Subject: CWD disease detected on Lac qui Parle County cervid farm 
southwestern Minnesota (2006-03-15) Date: March 15, 2006 at 12:36 pm PST Chronic 
wasting disease detected on Lac qui Parle County cervid farm (2006-03-15) The 
Board of Animal Health announced today that chronic wasting disease (CWD) has 
been detected in one domestic white-tailed deer on a cervid farm in Lac qui 
Parle County, which is located in southwestern Minnesota.
Immediately, DNR officials will conduct a local deer survey to determine 
the number of wild deer in the area. It is expected that not many deer will be 
found because the area is highly agricultural, with little deer habitat 
surrounding the farm. DNR will conduct opportunistic sampling of deer, like road 
kills, in the immediate area now and will conduct intensive hunter-harvested 
surveillance during the 2006 firearm deer season.
Although this positive animal is a captive deer, DNR has conducted 
surveillance for CWD in wild deer in the area. The farm is located near the 
northern boundary of deer permit area 447, where wild deer surveillance for CWD 
last occurred in 2003.
Lou Cornicelli, DNR big game program coordinator, said, "In 2003, we 
conducted wild deer CWD surveillance in adjoining permit areas 433, 446 and 447. 
In total, we collected 392 samples from those permit areas during the regular 
firearm deer season and CWD was not detected."
The sampling of wild deer was designed statistically to have a 95 percent 
confidence of detecting a 1 percent infection rate, according to Mike DonCarlos, 
DNR wildlife programs manager.
"This situation is very similar to the positive elk farm discovered in 
Stearns County in 2003, which followed the first discovery of CWD in an Aitkin 
County elk farm," DonCarlos said. “The DNR response will be similar to the 
Stearns County action and will include an initial assessment of wild deer 
populations in the area and development of a surveillance program for next 
fall."
From 2002 to 2004, DNR staff collected nearly 28,000 CWD samples statewide 
and no disease found in the wild herd.
"The intensive surveillance conducted in 2003 indicated CWD was not present 
in wild deer," Cornicelli said. “In addition, all indications are that this 
positive captive deer has not contacted any wild deer, but we will conduct 
additional surveillance this fall to be sure."
*** 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). 
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). 
SNIP... 
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, SNIP...SEE FULL TEXT ; 
SNIP...SEE FULL TEXT ; 
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 *** 
WHICH CAME FIRST, THE CART OR THE HORSE $$$
PLEASE STUDY THIS MAP, COMPARE FARMED CWD TO WILD CWD...TSS
please see full text ;
Saturday, February 18, 2012 
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease 
CDC Volume 18, Number 3—March 2012 
see much more here ; 
Thursday, February 09, 2012 
50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE
Saturday, February 04, 2012 
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol 
Needs To Be Revised 
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. 
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for 
$465,000 for the Statewide Wildlife Habitat Program in Portage County and 
approve the restrictions on public use of the site. 
snip...see full text and much more here ;
SNIP...SEE FULL TEXT ; 
CJD9/10022 
October 1994 
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge 
Spencers Lane BerksWell Coventry CV7 7BZ 
Dear Mr Elmhirst, 
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT 
Thank you for your recent letter concerning the publication of the third 
annual report from the CJD Surveillance Unit. I am sorry that you are 
dissatisfied with the way in which this report was published. 
The Surveillance Unit is a completely independant outside body and the 
Department of Health is committed to publishing their reports as soon as they 
become available. In the circumstances it is not the practice to circulate the 
report for comment since the findings of the report would not be amended. In 
future we can ensure that the British Deer Farmers Association receives a copy 
of the report in advance of publication. 
The Chief Medical Officer has undertaken to keep the public fully informed 
of the results of any research in respect of CJD. This report was entirely the 
work of the unit and was produced completely independantly of the the 
Department. 
The statistical results reqarding the consumption of venison was put into 
perspective in the body of the report and was not mentioned at all in the press 
release. Media attention regarding this report was low key but gave a realistic 
presentation of the statistical findings of the Unit. This approach to 
publication was successful in that consumption of venison was highlighted only 
once by the media ie. in the News at one television proqramme. 
I believe that a further statement about the report, or indeed statistical 
links between CJD and consumption of venison, would increase, and quite possibly 
give damaging credence, to the whole issue. From the low key media reports of 
which I am aware it seems unlikely that venison consumption will suffer 
adversely, if at all. 
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf 
THIRD CJD REPORT UK 1994 
snip... 
Consumption of venison and veal was much less widespread among both cases 
and controls. For both of these meats, there was evidence of a trend with 
increasing frequency of consumption being associated with increasing risk of 
CJD. These associations were largely unchanged when attention was restricted to 
pairs with data obtained from relatives. ... 
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER 
AND ELK ; 
Thursday, May 26, 2011 
Travel History, Hunting, and Venison Consumption Related to Prion Disease 
Exposure, 2006-2007 FoodNet Population Survey 
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 
858-863, June 2011. 
NOR IS THE FDA recalling this CWD positive elk meat for the well being of 
the dead elk ; 
Wednesday, March 18, 2009 
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat 
derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS 
AND FIELD CORRECTIONS: FOODS CLASS II 
now, let’s see what the authors said about this casual link, personal 
communications years ago. see where it is stated NO STRONG evidence. so, does 
this mean there IS casual evidence ???? 
“Our conclusion stating that we found no strong evidence of CWD 
transmission to humans” 
From: TSS (216-119-163-189.ipset45.wt.net) 
Subject: CWD aka MAD DEER/ELK TO HUMANS ??? 
Date: September 30, 2002 at 7:06 am PST 
From: "Belay, Ermias" 
To: 
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias" 
Sent: Monday, September 30, 2002 9:22 AM 
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS 
Dear Sir/Madam, 
In the Archives of Neurology you quoted (the abstract of which was attached 
to your email), we did not say CWD in humans will present like variant CJD. 
That assumption would be wrong. I encourage you to read the whole article 
and call me if you have questions or need more clarification (phone: 
404-639-3091). Also, we do not claim that "no-one has ever been infected with 
prion disease from eating venison." Our conclusion stating that we found no 
strong evidence of CWD transmission to humans in the article you quoted or in 
any other forum is limited to the patients we investigated. 
Ermias Belay, M.D. Centers for Disease Control and Prevention 
-----Original Message----- 
From: 
Sent: Sunday, September 29, 2002 10:15 AM 
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV 
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS 
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS 
Thursday, April 03, 2008 
A prion disease of cervids: Chronic wasting disease 
2008 1: Vet Res. 2008 Apr 3;39(4):41 
A prion disease of cervids: Chronic wasting disease 
Sigurdson CJ. 
snip... 
*** twenty-seven CJD patients who regularly consumed venison were reported 
to the Surveillance Center***, 
snip... 
full text ; 
Saturday, March 5, 2011 
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE 
RISE IN NORTH AMERICA 
Sunday, February 12, 2012 
National Prion Disease Pathology Surveillance Center Cases Examined1 
(August 19, 2011) including Texas 
TSS


