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From: TSS ()
Subject: Experimental transmission of chronic wasting disease agent from mule deer to cattle by the intracerebral route MAY 2005
Date: June 22, 2005 at 11:33 am PST

1: J Vet Diagn Invest. 2005 May;17(3):276-81.

Experimental transmission of chronic wasting disease agent from mule deer to cattle by the intracerebral route.

Hamir AN, Kunkle RA, Cutlip RC, Miller JM, O'Rourke KI, Williams ES, Miller MW, Stack MJ, Chaplin MJ, Richt JA.

National Animal Disease Center, ARS, USDA, 2300 Dayton Avenue, PO Box 70, Ames, IA 50010, USA.

This communication reports final observations on experimental transmission of chronic wasting disease (CWD) from mule deer to cattle by the intracerebral route. Thirteen calves were inoculated intracerebrally with brain suspension from mule deer naturally affected with CWD. Three other calves were kept as uninoculated controls. The experiment was terminated 6 years after inoculation. During that time, abnormal prion protein (PrP(res)) was demonstrated in the central nervous system (CNS) of 5 cattle by both immunohistochemistry and Western blot. However, microscopic lesions suggestive of spongiform encephalopathy (SE) in the brains of these PrP(res)-positive animals were subtle in 3 cases and absent in 2 cases. Analysis of the gene encoding bovine PRNP revealed homozygosity for alleles encoding 6 octapeptide repeats, serine (S) at codon 46, and S at codon 146 in all samples. Findings of this study show that although PrP(res) amplification occurred after direct inoculation into the brain, none of the affected animals had classic histopathologic lesions of SE. Furthermore, only 38% of the inoculated cattle demonstrated amplification of PrP(res). Although intracerebral inoculation is an unnatural route of exposure, this experiment shows that CWD transmission in cattle could have long incubation periods (up to 5 years). This finding suggests that oral exposure of cattle to CWD agent, a more natural potential route of exposure, would require not only a much larger dose of inoculum but also may not result in amplification of PrP(res) within CNS tissues during the normal lifespan of cattle.

PMID: 15945388 [PubMed - in process]





Scientific Steering Committee

Chronic wasting disease






3.3.1 Transmissibility of CWD

There are certain key questions with respect to transmissibility:

1. Can CWD be transmitted artificially to other species, e.g. sheep, cattle, humans?

2. What is the natural transmissibility to other species ?

3. Can transmissions inform on possible similarities between the agent and BSE,

natural scrapie or another know TSE source, or does the evidence suggest a novel


Several experimental studies to transmit CWD have been conducted, most by intracerebral

(IC) inoculation. Whilst such studies provide information on susceptibility to the

most efficient means of interspecies transmission, they do not inform on interspecies

susceptibility by natural routes of transmission. For the latter oral or other possible

natural exposure route studies are considered the most appropriate. Intracerebral inoculation studies:

 Mule deer-CWD has been successfully transmitted to ferrets (Mustela putorius furo)

by the intracerebral (IC) route (Williams et al., 1982) but failed to transmit to Syrian

golden hamsters (Mesocricetus auratus) even after multiple attempts (Williams and

Young, 1992). Primary transmission into ferrets resulted in an incubation period of

17-21 months. On subsequent passage this shortened with a 5 months incubation

period by the third ferret passage. Unlike mule deer-CWD, ferret-passaged CWD was

transmissible to Syrian golden hamsters and increasing the number of transmission

passes of CWD in ferrets increased the pathogenicity of the agent for hamsters (Bartz

et al, 1998).

 Transmission of mule deer-CWD to mice is possible, but with a very low efficiency at

primary transmission to a panel of mouse strains (RIII, C57BL and VM) and results

in incubation periods in excess of 500 days. Serial passage in each mouse strain

produced clinical disease in all challenged mouse strain at each passage. The

phenotype of disease produced in the mice differed from that of previously strain


typed sources, including scrapie and BSE sources, suggesting that the CWD agent is a

unique strain of TSE pathogen (Bruce et al., 2000).

 IC inoculation of mule deer-CWD into squirrel monkeys (Saimiri sciureus) was

successful in one animal and mink are also susceptible to IC inoculation of mule deer

CWD (Williams and Young, 1992).

 IC inoculation into one four months old goat with CWD agent resulted in an

incubation time of about 6 years. This is longer than what would be expected with

scrapie (Williams and Young, 1992).

 CWD transmission to raccoons (Procyon lotor) remains unsuccessful to date at three

years after inoculation (Hamir et al., 2003) but a difference in incubation time was

observed after IC infection into raccoons when comparing infection with TME (6

months) and scrapie (2 years) in cattle.

 Studies in progress at the National Animal Disease Centre (NADC) have shown

preliminary evidence of the transmission of mule deer-CWD to sheep. To date, 1 out

of 8 sheep inoculated IC with CWD brain suspension has shown clinical signs at 35

months post inoculation. Histopathological changes indistinguishable from those of

scrapie were found and IHC examinations of the brain, tonsil and some lymph nodes

proved positive. (Janice Miller, Personal Comm.).

 On-going research on the species barrier is indicating that there is a substantial

biological barrier to transmission of CWD from deer to cattle. Preliminary data from

experiments in progress in Colorado, Wyoming, and Iowa indicate that only a few

calves develop disease after challenge with CWD pathogen from affected mule deer.

In 3 calves euthanised between 24 and 27 months post-inoculation (IC), microscopic

lesions in the brain were subtle or absent. However, all 3 animals were positive for

PrPres by immunohistochemistry (IHC) and Western blot. Three years after

challenge, the 10 remaining inoculated cattle were alive and apparently healthy

(Hamir et al, 2001; Hamir, 2002). Oral and other natural exposure route studies

 Homologous CWD has been transmitted by oral inoculation in mule deer, whitetailed

deer, and elk in pathogenesis studies that are nearly complete. In addition,

homologous CWD has been transmitted in elk at a low dose (0.1 g pooled CWD-elk

brain) by oral exposure (Williams, pers. Comm.).

 Cattle have been inoculated orally with a brain pool from CWD affected mule deer at

the University of Wyoming and have not developed any evidence of transmission

more than 5 years following exposure. These studies are scheduled to run for 10

years. In addition, bovine calves have been orally inoculated with CWD brain pools

from mule deer and from elk; these calves are being sequentially necropsied and

results are not yet available (Williams, pers comm).

 Cattle living in close contact with infected deer and elk have not developed the

disease during the first five years of a 10-year study. Twenty-four cattle were housed

with resident deer and elk with endemic CWD, in two wildlife research facilities in

Wyoming and Colorado. These studies started in 1997 and to date there is no

evidence of transmission of CWD to cattle through contact. Control deer have all

succumbed to CWD (Williams, 2002).

 Brains from cattle over 5 years of age and from different ranches within an enzootic

area of CWD were examined with H&E and IHC stains and all were found negative

(Gould et al, 2003).

3.3.2 Susceptibility of deer and elk to other TSEs

Scrapie has been successfully transmitted to 3/5 elk after IC inoculation (Hamir et

al., 2003). There is apparently no ongoing work at present to attempt transmission of

scrapie to mule deer.




Although CWD is not similar to BSE in terms of epidemiology in that there is no

evidence of natural spread of the disease to phylogenetic families other than the cervidae

it may theoretically pose a risk for animal and human food safety.



There is no evidence that CWD can be transmitted to humans consuming meat or

handling infected cervids or their products, however this possibility cannot be ruled out.

The World Health Organisation recommends that people not consume animal products

from any animal infected with a TSE disease and public health policies in Canada and the

US are consistent with this direction.

 In Canada, all adult cervids slaughtered under commercial arrangements in the

provinces of Saskatchewan, Manitoba and Alberta are tested for CWD and carcasses

are only released upon receipt of a negative result. Offals may be disposed off by

incineration or deep burial before test results are known. Once a farmed cervid is

diagnosed with CWD, the infected animal and all cervids exposed to positive animals

are destroyed and the carcasses disposed of by incineration or deep burial. Antler

velvet from test negative animals in the herd is released from official control.

 In NA some health officials advise hunters not to consume meat from animals known

to be infected with CWD. In addition, they suggest hunters take simple precautions

when field dressing deer or elk taken in areas where the disease is found. Although, in

the USA the consumption of meat from CWD affected animals is discouraged,

however, there is no ban. So, affected meat probably has been consumed for decades

in Colorado and Wyoming (Dr. Williams, Personal communication).

 When an animal is slaughtered in the United States, some animals are tested for CWD

depending on individual State regulations. The carcass is stored until result of the test

is returned (test takes one week) and when negative then the carcass is released. In

case the carcass is positive, further steps will vary from state to state.

 Special slaughterhouses for farmed animals do not always exist: sometimes livestock

slaughter plants are used for game animals but they have to handle the different

species at different times and clean in between but the rules vary from state to state.

 Fate of road killed deer is not a USDA policy but differs from state to state with

considerable variation from location to location.

 Viscera and other carcass remnants of hunted animals remain in situ (offals etc…).



Although CWD is not similar to BSE in terms of epidemiology in that there is no

evidence of natural spread of the disease to phylogenetic families other than the cervidae

it may still pose a risk for animal and human food safety.

 What happens with possible affected carcasses of hunted or slaughtered farmed deer

or elk was very much depending on the state, however, the FDA has recently

provided new guidance to state public health and agriculture officials throughout the

US. FDA does not permit material from CWD positive animals or animals at high

risk for CWD to be used as an ingredient in feed for any animal and specifically

requiring that renderers do not accept any deer or elk from CWD epizootic areas for

any animal feed. This is an extension of the 1997 FDA regulations (feed ban) that put

into place the exclusion of ruminant MBM from ruminant feed. This ruling

specifically excluded deer and elk from MBM.

 In Canada there are no mandatory controls on rendering carcasses and offal from

cervids other than those tested positive for CWD or animals that have been exposed

to test positive animals. However, the Canadian Renderers’ Association has a

voluntary ban on the rendering of cervids. Canada prohibits the feeding of ruminant

derived proteins to ruminants.


Recently, the Center for Disease Control (CDC) has issued a new statement

concerning CWD and possible human infection: "Although it is generally prudent to

avoid consuming food derived from any animal with evidence of a TSE, to date, there is

no evidence that CWD has been transmitted or can be transmitted to humans under

natural conditions". However, the CDC has renewed surveillance efforts in order to rule

out a link between CWD and vCJD. While, to date there has been one case of vCJD

reported in US (contracted in the UK), the CDC is working with ongoing investigations

in Wyoming and Colorado to track cases of CJD or suspected CJD.


CDC reported on the epidemiological investigations carried out on three patients

who died of degenerative neurological illness during the period 1993-1999 and who were

hunter and/or had a history of consuming venison during wild game feasts. All three

patients were aged over 55 and developed neurological symptoms prior to death.

Sporadic CJD was confirmed in one case as the cause of death (CDC, 2003).

Belay et al., (2001) Recent reports on of 3 unusually young CJD patients (aged 28,

28 and 30 years) who regularly consumed deer or elk meat, which created concern about

the zoonotic transmission of CWD. Investigations, however, by CDC found that these

were all cases of sporadic CJD of different types. In the USA the occurrence of CJD in

persons 30 years or younger is rare (during 1979-1996, only 12 such CJD cases were

reported to the CDC and 8 of these resulted from the use of contaminated growth

hormone or dura maters grafts). Against the background of the occurrence and

recognition of vCJD in 1996 it is difficult to make an epidemiological distinction between

an increased incidence of CJD that might represent an indication of a novel exogenous

source of infection and an increased ascertainment of CJD cases in young patients due to

better surveillance. Belay et al., (2001), from the National Centre for Infectious Diseases

have examined the hypothesis that a causal link could be made between the disease in

these 3 patients and CWD. They reviewed medical records and interviewed family

members and state wildlife and agriculture officials. Brain tissue samples were examined

using histopathologic, immunohistochemical, immunoblotting, or prion gene analysis

methods. The investigation assessed the presence or absence of CJD risk factors,

associations with deer and elk hunting in CWD- enzootic areas and comparison of the

evidence from the 3 patients with that of a zoonotic link between vCJD and bovine

spongiform encephalopathy. None of the patients had established CJD risk factors or a

history of travel to Europe. Two of the patients hunted game animals and one was a

daughter of a hunter. Unlike patients with vCJD, the 3 patients did not express a common

phenotype of the disease, which did not suggest a causal link between CWD and CJD

(there was also heterogeneity among the three patients on the codon 129 : Met/Met,

Val/Val and Met/Val respectively). Molecular phenotyping characteristics for the 2

patients studied gave type 1 on Western Blot according to Parchi et al.(1997), which

differs from that of vCJD.


In conclusion, the CDC report on the CJD in the patients aged over 55 years and

the investigation of Belay et al. (2001) related to the young CJD patients found no strong

evidence for a causal link between CWD and CJD. Both, however, concluded as well

that ongoing national surveillance for CJD and other neurological cases will remain

important for continuing to assess the risk, if any, of CWD transmission to humans.

Race et al., (2002) described abnormal PrP glycoforms of CWD in comparison to

PrP from scrapie and BSE. Analysis of these abnormal PrP glycoform patterns from

CWD affected deer and elk, scrapie-affected sheep and cattle and cattle with BSE failed

to identify patterns capable of reliably distinguishing these transmissible spongiform

encephalopathy diseases. However, PrP-res patterns sometimes differed among

individual animals, suggesting the possibility of multiple CWD strains.


In answering question two, there was a need for a risk assessment to be carried out

and to consider the imports of game meat from cervids and or live animal imports from

the USA and Canada, if any.

Data provided by the US and Canada preliminary indicate that there is no export of

live cervids into Europe. If licences for export to EU-countries were granted it could be

traced back that these were related to single hunter-related trophies (skin, antlers) by

private persons. Data provided by Eurostat confirm the data supplied by USA and

Canada that there is no import of live cervids into EU countries originating from Canada

or US.

Data on game meat provided by Eurostat fall under two different entries related to ‘game


 Period 1988-1992 entry is indicated as: ‘Fresh, chilled or frozen meat and edible

offal of game (excluding of rabbits, hares and swine)’

 Period 1993-2001 entry is indicated as: ‘Meat and edible meat offal of game,

fresh, chilled, or frozen (excluding rabbits, hares, pigs and quails)’.

A table in Annexe 2 gives the data as provided by Eurostat for the two above-mentioned

entries as exported from USA and Canada.


In summary over the period 1988-1992 a total of 0,4 ton and 80,1 ton was

exported from Canada and USA respectively to the EU. The exports from Canada were

to France, UK and the Netherlands and exports from USA were mainly to UK (79,1 ton)

and the rest to France. During the period 1993-2001 a total of 0,7 ton and 120,6 ton were

exported from Canada and the USA respectively. The main importer from the USA was

UK with 103,8 ton and the remaining importing countries were France Netherlands

Germany, Spain and Austria.

There are no data available on exports of cervid embryo’s and semen from Canada

and the USA and also no import data in the EU. The current, planned and proposed

surveillance studies in Europe were discussed earlier. Related to the current activities in

Europe further surveillance should be encouraged in order to provide more detailed base

line data as the current studies are assessed as insufficient to detect a CWD infection in

cervids would it be present.



Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy

(TSE) of certain species of native North American deer (mule deer and white–tailed deer,

and Rocky Mountain elk. A number of States/Provinces in the USA and Canada, (North

America, NA) have reported cases in free-ranging and farmed cervids. There are no

reports of CWD in areas outside NA with the exception of a single animal imported into

Korea from Canada.

The natural host range of CWD has so far remained confined to cervids. On-going

experimental transmission studies have still not been able to show transmission of CWD

from deer to cattle. Additionally, genetic studies show a relatively large phylogenetic


difference in PrP sequence between Cervidae, Bovidae and Humans. Those differences

suggest an appreciable species barrier for possible transmission of CWD to cattle and

humans. However, since the basis of the transmission barrier in relation to the TSE is

complex and not solely a function of PrP sequence of donor and recipient it remains

theoretically possible that the CWD-agent could infect humans. Infected animals have a

widespread tissue distribution of disease-specific PrP and presumably also infectivity in

those tissues from an early stage in the incubation period.

Epidemiological data have shown that CWD is readily spread by lateral

transmission in cervid populations. In experimental studies, oral exposure to only very

small doses of infective material resulted in disease in cervid animals.

Surveillance data do not as yet provide information on accurate figures of the

prevalence of the disease in NA and the risk factors are not well understood. Some

control measures for farmed deer are in place. However, movement of free-ranging deer

provides a major difficulty for control strategies. The origin of the disease is unknown

and the lack of any connection with other animal TSEs provides no clues as to the

potential for CWD to be pathogenic for man. Available information indicates that there is

only negligible trade in live cervids originating in NA to EU but there are indications of

imports of small annual tonnage of edible products from game. It is unclear what, if any,

trade exists in antler, embryos or semen from cervids between NA and EU countries.

Research and surveillance programs on CWD in farmed or wild Cervidae in Europe

did not exist until recently and thus the available data do not allow to draw conclusions

about CWD in the Cervidae population in Europe.


With regard to the initial question of the mandate, a theoretical risk for prion

transmission to humans consuming products of CWD affected-cervids of all ages in

countries where CWD exists cannot be excluded. Similarly, transmission risk of prions to

domestic animals cannot be excluded. There is therefore a scientific basis on which to

exclude tissues from animals that carry a CWD risk, from human or animal feed chains.

However, the early and widespread involvement of tissues in CWD infected animals

does not allow to define a SRM list, neither to define any lower age cut off as has been

defined for cattle in relation to BSE. Neither is there sufficient knowledge to define

exclusions or amendment of any SRM rule on the basis of relative genetic resistance to

infection as has been proposed for sheep and goats in the event that evidence indicates

the probable natural occurrence of BSE in these species 5.

Although available information indicates imports of live Cervidae from NA to EU

and trade in meat products from cervid species as being negligible, it is important to

reach certainty that no transfer of risk takes place through trade of live cervids and its

derived products.

At present, there are no scientific data that CWD is occurring in Cervidae elsewhere

than in those countries from which it has been previously reported. However, systematic

TSE surveillance of cervid populations has either been absent or has only just started in

European countries. Until results of such surveillance become available no conclusion

can be drawn with regard to the occurrence of CWD or similar TSE in the cervid

population of Europe.

Phone: (509) 335-6020
Fax: (509) 335-8328
Room 3003
PULLMAN, WA, 99164-6630

Project List

Bse and Other Tses Ruminant Herbivors: Diagnosis, Transmission and Genetics Appropriated (D)
Accession Number: 404978

Ovine Prion & Viral Infections: Scrapie & Ovine Progressive Pneumonia, Diagnosis & Control Appropriated (D)
Accession Number: 405202

Scrapie Control Through Prp Genetics: Production Traits and Economic Implications Specific Cooperative Agreement (S)
Accession Number: 405525

Prp-Cwd Profiles in White Tailed Deer and Elk with Naturally Occuring Chronic Wasting Disease Specific Cooperative Agreement (S)
Accession Number: 405528

Characterization of Ovine Placental Cell Lines Supporting Prp-Sc Propagation Specific Cooperative Agreement (S)
Accession Number: 405529

A Transgenic Mouse Model for Chronic Wasting Disease Specific Cooperative Agreement (S)
Accession Number: 405724

The Role of Environmental Contamination in Transmission of Chronic Wasting Disease Specific Cooperative Agreement (S)
Accession Number: 405855

Eradication of Ovine Scrapie Tse Through Selective Genetics Using a Two-Flock Model Specific Cooperative Agreement (S)
Accession Number: 407203

Evaluation of Western Blotting Methods Using Samples with Or Without Sodium Phosphotungstic Acid Precipitation for Diagnosis of Scrapie and Chromic Wasting Disease - (24-Jan-05)

Experimental Transmission of Chronic Wasting Disease (Cwd Mule Deer) Agent to Cattle by Intracerebral Route - (03-Jan-05)

Experimental Transmission of Chronic Wasting Disease Agent to Cattle by Intracerebral Route: Final Outcome of the Study - (29-Sep-04)

Polymorphisms in the Prion Precursor Functional Gene But Not the Pseudogene Are Associated with Susceptibility to Chronic Wasting Disease in White-Tailed Deer
O'Rourke, K.I., Spraker, T.R., Hamburg, L.K., Besser, T.E., Brayton, K.A., Knowles, D.P. 2004. Polymorphisms in the prion precursor functional gene but not the pseudogene are associated with susceptibilty to chronic wasting disease in white-tailed deer. Journal of General Virology. 85:1339-1346.

Resistance to Scrapie in Prp Arr/arq Heterozygous Sheep Is Not Caused by Preferential Allelic Usage
Caplazi, P., Orourke, K.I., Baszler, T.V. 2004. Resistance to scrapie in prp arr/arq heterozygous sheep is not caused by preferential allelic usage. Journal of Clinical Pathology. 57:647-650.

Chronic Wasting Disease Genetics and Molecular Biology in Three Cervid Species - (15-Nov-03)

A Processed Pseudogene Contributes to Apparent Mule Deer Prion Gene Heterogeneity
Brayton, K.A., O'Rourke, K.I., Lyda, A.K., Miller, M.W., Knowles, D.P. A processed pseudogene contributes to apparent mule deer prion gene heterogeneity. Gene. 2003. v. 326. p. 167-173.

Variable Patterns of Prp-Cwd Distribution in Obex and Cranial Lymphoid Tissues of Rocky Mountain Elk with Nonclinical Chronic Wasting Disease
Spraker, T.R., Balachandran, A., Zhuang, D., Orourke, K.I. 2004. Variable patterns of prp-cwd distribution in obex and cranial lymphoid tissues of rocky mountain elk with nonclinical chronic wasting disease. Veterinary Record. 155(10): 295-302.

Transmission of Sheep Scrapie to Elk (Cervus Elaphus Nelsoni) by Intracerebral Inoculation
Hamir, A.N., Miller, J.M., Cutlip, R.C., Richt, J.A., Kunkle, R.A., O'Rourke, K.I., Jenny, A.L., Stack, M.J., Chaplin, M.J. 2003. Transmission of sheep scrapie to elk (Cervus elaphus nelsoni) by intracerebral inoculation. 46th Annual Meeting of the American Association of Veterinary Laboratory Diagnosticians. p. 210.

Experimental Cross-Species Transmission of Chronic Wasting Disease (Cwd-Mule Deer) to Domestic Livestock at the National Animal Disease Center: An Update
Hamir, A.N., Cutlip, R.C., Miller, J.M., Richt, J.A., Kunkle, R.A., Williams, E., Stack, M.J., Chaplin, M.J., Miller, M., O'Rourke, K.I. 2003. Experimental cross-species transmission of chronic wasting disease (CWD-mule deer) to domestic livestock at the National Animal Disease Center: An update [Abstract]. 46th Annual Meeting of the American Association of Veterinary Laboratory Diagnosticians. p. 209.

Histamine As An Aid to Biopsy of Third Eyelid Lymphoid Tissue in Sheep
Bender, S., Alverson, J., Herrmann, L.M., O'Rourke, K.I. 2004. Histamine as an aid to biopsy of third eyelid lymphoid tissue in sheep. Veterinary Record. 154: 662-663.

Transmission of Sheep Scrapie to Elk (Cervus Elaphus Nelsoni) by Intracerebral Inoculation
Hamir, A.N., Miller, J.M., Cutlip, R.C., Richt, J.A., Kunkle, R.A., O'Rourke, K.I., Jenny, A.L., Stack, M.J., Chaplin, M.J. 2003. Transmission of sheep scrapie to elk (Cervus elaphus nelsoni) by intracerebral inoculation [Abstract]. International Conference on Emerging Zoonoses. p. 92.

Experimental Cross-Species Transmission of Chronic Wasting Disease to Domestic Livestock at the National Animal Disease Center: An Update
Hamir, A.N., Cutlip, R.C., Miller, J.M., Richt, J.A., Kunkle, R.A., Williams, E., Stack, M., Miller, M.W., O'Rourke, K.I., Chaplin, M.J. 2003. Experimental cross-species transmission of chronic wasting disease to domestic livestock at the National Animal Disease Center: An update [Abstract]. International Conference on Emerging Zoonoses. p. 91.

Transmission of Sheep Scrapie to Elk (Cervus Elaphus Nelsoni) by Intracerebral Inoculation
Hamir, A.N., Miller, J.M., Cutlip, R.C., Richt, J.A., Kunkle, R.A., O'Rourke, K.I., Jenny, A.L., Stack, M.J., Chaplin, M.J. 2003. Transmission of sheep scrapie to elk (Cervus elaphus nelsoni) by intracerebral inoculation [Abstract]. 52nd Annual Wildlife Disease Association Annual Meeting. p. 135.

Experimental Cross-Species Transmission of Chronic Wasting Disease (Cwd-Mule Deer) to Domestic Livestock at the National Animal Disease Center: An Update
Hamir, A.N., Cutlip, R.C., Miller, J.M., Richt, J.A., Kunkle, R.A., Williams, E., Stack, M., Chaplin, M., Miller, M., O'Rourke, K.I. 2003. Experimental cross-species transmission of chronic wasting disease (CWD-mule deer) to domestic livestock at the National Animal Disease Center: An update [Abstract]. 52nd Annual Wildlife Disease Association Conference. p. 134.

Transmission of Sheep Scrapie to Elk (Cervus Elaphus Nelsoni) by Intracerebral Inoculation

Experimental Cross-Species Transmission of Chronic Wasting Disease (Cwd-Mule Deer) to Domestic Livestock at the National Animal Disease Center: An Update

Differences in Production Traits Between Scrapie Resistant and Scrapie Susceptible Ewes
Proc. Western Sec. Amer Soc Anim Sci 2003, 54:101

Abundant Prp-Cwd in Tonsil from Mule Deer with Preclinical Chronic Wasting Disease
O'Rourke, K.I., Zhuang, D., Lyda, A.K., Gomez, G., Williams, E.S., Tuo, W., Miller, M.W. Abundant PrP-CWD in tonsil from mule deer with preclinical chronic wasting disease. Journal of Diagnostic Investigation. 2003. v. 15. 320-323.

Transmission of Transmissible Mink Encephalopathy (Tme) to Raccoons (Procyon Lotor) by Intracerebral Inoculation
Hamir, A.N., Miller, J.M., O'Rourke, K.I., Bartz, J.C., Stack, M.J., Chaplin, M.J. 2004. Transmission of transmissible mink encephalopathy (TME) to raccoons (Procyon lotor) by intracerebral inoculation. Journal of Veterinary Diagnostic Investigation. 16(1):57-63.

Preclinical Diagnosis of Chronic Wasting Disease in Captive Mule Deer (Odocoileus Heminonus) and White Tailed Deer (Odocoileus Virginianus) Using Tonsillar Biopsy
Wild, M.A., Spraker, T.R., Sigurdson, C.J., Orourke, K.I., Miller, M.A. 2002. Preclinical diagnosis of chronic wasting disease in captive mule deer (odocoileus heminonus) and white tailed deer (odocoileus virginianus) using tonsillar biopsy. Journal of General Virology. 83: 2629-2634.

Active Surveillance for Scrapie Utilizing Third Eyelid Biopsy and Genetic Susceptibility Testing in Flocks of Sheep in Wyoming - (20-Jun-02)

Distribution of Protease-Resistant Prion Protein and Spongiform Encephalopathy in Free-Ranging Mule Deer (Odocoileus Hemionus) with Chronic Wasting Disease
Spraker, T.R., Zink, R.R., Cummings, B.A., Sigurdson, C.J., Miller, M.W., O'Rourke, K.I. Distribution of protease-resistant prion protein and spongiform encephalopathy in free-ranging mule deer (Odocoileus hemionus) with chronic wasting disease. Veterinary Pathology. 2002. v. 39. p. 546-556.

Immunohistochemical Detection and Distribution of Prion Protein in a Goat with Natural Scrapie - (11-Jun-02)

Immunohistochemical Detection and Localization of Prion Protein in a Goat with Natural Scrapie - (03-Jun-02)

Pregnancy Status and Fetal Prion Genetics Determine Prp-Sc Accumulation in Placentomes of Scrapie Infected Sheep - (25-Mar-02)

Validation of Monoclonal Antibody F99/97.6.1 for Immunohistochemical Staining of Brain and Tonsil in Mule Deer (Odocoileus Hemionus) with Chronic Wasting Disease - (10-Sep-01)

Validation of Monoclonal Antibody F99/97.6.1 for Immunohistochemical Staining of Brain and Tonsil in Mule Deer (Odocoileus Hemionus) with Chronic Wasting Disease - (10-Sep-01)

Comparison of Histological Lesions and Immunohistochemical Staining of Proteinase Resistant Prion Protein in a Naturally Occurring Spongiform Encephalopathy of Free-Ranging Mule Deer - (01-Aug-01)

Immunohistochemical Detection of Prion Protein (Prp-Sc) and Epidemiological Study of Bse in Korea - (01-Apr-01)

Prp-C and Prp-Sc at the Fetal-Maternal Interface - (27-Mar-01)

Cellular Prion Protein Is Expressed on Pbmc But Not Platelets of Normal and Scrapie-Infected Sheep - (28-Dec-00)

Preliminary Findings on the Experimental Transmission of Chronic Wasting Disease (Cwd) Agent of Mule Deer to Cattle - (07-Nov-00)

Ovine Scrapie: New Tools for Control of An Old Disease
Orourke, K.I. 2001. Ovine scrapie: new tools for control of an old disease. Veterinary Clinics of North America. p. 283-300.

Evidence of a Molecular Barrier Limiting Susceptibility of Humans, Cattle and Sheep to Chronic Wasting Disease - (13-Jul-00)

Immunohistochemical Detection of Scrapie Prion Proteins in Clinically Normal Sheep in Pennsylvania - (27-Jun-00)

Reducing the Risk of Scrapie in Goat Herds Housed with Flocks of Sheep - (15-Jun-00)

Identification of An Epitope in the C-Terminus of Normal Prion Protein Whose Expression Is Modulated by Binding Events in the N-Terminus - (13-Jun-00)

Preclinical Diagnosis of Scrapie by Immunohistochemistry of Third Eyelid Lymphoid Tissue - (01-Jun-00)

Preclinical Diagnosis of Ovine Scrapie by Immunohistochemistry of Third Eyelid Lymphoid Tissue Using a Pan-Specific Monoclonal Antibody Cocktail - (31-Mar-00)

The Predominant Isoform of Ovine Placental and Uterine Prp Is Proteinase K Sensitive, N-Terminal Truncated and Glycosylated - (03-Mar-00)

Prp Genotypes of Captive and Free-Ranging Rocky Mountain Elk (Cervus Elaphus Nelsoni) with Chronic Wasting Disease - (01-Jul-99)

Oral Transmission and Early Lymphoid Tropism of Chronic Wasting Disease Prpres in Mule Deer Fawns - (16-Jun-99)

Antemortem, Postmortem, and Genetic Testing in Scrapie Control - (01-Jun-99)

Scrapie Diagnosis in the Live Animal: Third Eyelid Lymphoid Tissue Biopsy Technique - (05-May-99)

Immunoreactivity of the Monoclonal Antibody F89/160.1.5 for the Human Prion Protein - (19-Jan-99)

Related news articles

Research on BSE "Cousin" Is Top Postdoc Project

Page Modified: 06/22/2005

CDC - Chronic Wasting Disease and Potential Transmission to Humans
In addition, domestic cattle, sheep, and goat residing in research ... The lack
of evidence of a link between CWD transmission and unusual cases of CJD, ... - 95k -

CDC - Environmental Sources of Prion Transmission in Mule Deer
Whether transmission of the chronic wasting disease (CWD) prion among cervids
requires ... A review of the epidemiology of scrapie in sheep. Rev Sci Tech. ... - 53k

THESE two reports that follow from the OIE about CWD, i take with a grain of salt some of there assessments. FOR one, deer and elk HAVE been fed feed tainted with the TSE agent for decades. ALSO, the TSE agent transmits freely by oral route to deer and elk;

Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,
Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy
Range Road, University of Wyoming, Laramie, WY 82070, USA 2
Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, CO 80526-2097, USA3
Colorado State University Veterinary Diagnostic Laboratory, 300 West
Drake Road, Fort Collins, CO 80523-1671, USA4
Animal Disease Research Unit, Agricultural Research Service, US
Department of Agriculture, 337 Bustad Hall, Washington State University,
Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a
brain homogenate prepared from mule deer with naturally occurring
chronic wasting disease (CWD), a prion-induced transmissible spongiform
encephalopathy. Fawns were necropsied and examined for PrP res, the
abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days
post-inoculation (p.i.) using an immunohistochemistry assay modified to
enhance sensitivity. PrPres was detected in alimentary-tract-associated
lymphoid tissues (one or more of the following: retropharyngeal lymph
node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42
days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No
PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural
tissue of any fawn. PrPres-specific staining was markedly enhanced by
sequential tissue treatment with formic acid, proteinase K and hydrated
autoclaving prior to immunohistochemical staining with monoclonal
antibody F89/160.1.5. These results indicate that CWD PrP res can be
detected in lymphoid tissues draining the alimentary tract within a few
weeks after oral exposure to infectious prions and may reflect the
initial pathway of CWD infection in deer. The rapid infection of deer
fawns following exposure by the most plausible natural route is
consistent with the efficient horizontal transmission of CWD in nature
and enables accelerated studies of transmission and pathogenesis in the
native species.


These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the
earliest post-exposure period, CWD PrPres was traced to the lymphoid
tissues draining the oral and intestinal mucosa (i.e. the
retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and
ileocaecal lymph nodes), which probably received the highest initial
exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum
and spleen in a 10-month-old naturally infected lamb by mouse bioassay.
Eight of nine sheep had infectivity in the retropharyngeal lymph node.
He concluded that the tissue distribution suggested primary infection
via the gastrointestinal tract. The tissue distribution of PrPres in the
early stages of infection in the fawns is strikingly similar to that
seen in naturally infected sheep with scrapie. These findings support
oral exposure as a natural route of CWD infection in deer and support
oral inoculation as a reasonable exposure route for experimental studies
of CWD.


now, just what is in that deer feed? _ANIMAL PROTEIN_

Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: BSE-L

8420-20.5% Antler Developer
For Deer and Game in the wild
Guaranteed Analysis Ingredients / Products Feeding Directions


_animal protein_

22.6 KG.


_animal protein_


Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products 15%, Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Pyosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol
(source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,
Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline
Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine
Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.


Bode's #1 Game Pellets

Crude Protein (Min) 16%
Crude Fat (Min) 2.0%
Crude Fiber (Max) 19%
Calcium (Ca) (Min) 1.25%
Calcium (Ca) (Max) 1.75%
Phosphorus (P) (Min) 1.0%
Salt (Min) .30%
Salt (Max) .70%


Grain Products, Plant Protein Products, Processed Grain By-Products,
Forage Products, Roughage Products, 15% Molasses Products,
__Animal Protein Products__,
Monocalcium Phosphate, Dicalcium Phosphate, Salt,
Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol
(source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement,
Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, Choline
Chloride, Folic Acid, Menadione Sodium Bisulfite Complex, Pyridoxine
Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, Zinc
Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried
Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum,
Artificial Flavors added.

Feed as Creep Feed with Normal Diet


Grain Products, Roughage Products (not more than 35%), Processed Grain
By-Products, Plant Protein Products, Forage Products,
__Animal Protein Products__,
L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium
Phosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic
Copper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite,
Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide,
Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A
Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium
Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite
Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,
Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate


Deer Builder Pellets is designed to be fed to deer under range
conditions or deer that require higher levels of protein. Feed to deer
during gestation, fawning, lactation, antler growth and pre-rut, all
phases which require a higher level of nutrition. Provide adequate
amounts of good quality roughage and fresh water at all times.


April 9, 2001 WARNING LETTER


Brian J. Raymond, Owner
Sandy Lake Mills
26 Mill Street
P.O. Box 117
Sandy Lake, PA 16145

Tel: 215-597-4390

Dear Mr. Raymond:

Food and Drug Administration Investigator Gregory E. Beichner conducted
an inspection of your animal feed manufacturing operation, located in
Sandy Lake, Pennsylvania, on March 23,
2001, and determined that your firm manufactures animal feeds including
feeds containing prohibited materials. The inspection found significant
deviations from the requirements set forth in
Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins
Prohibited in Ruminant Feed. The regulation is intended to prevent the
establishment and amplification of Bovine Spongiform Encephalopathy
(BSE) . Such deviations cause products being manufactured at this
facility to be misbranded within the meaning of Section 403(f), of the
Federal Food, Drug, and Cosmetic
Act (the Act).

Our investigation found failure to label your
swine feed with the required cautionary statement "Do Not Feed to cattle
or other Ruminants" The FDA suggests that the statement be
by different type-size or color or other means of highlighting the
statement so that it is easily noticed by a purchaser.

In addition, we note that you are using approximately 140 pounds of
cracked corn to flush your mixer used in the manufacture of animal
feeds containing prohibited material. This
flushed material is fed to wild game including deer, a ruminant animal.
Feed material which may potentially contain prohibited material should
not be fed to ruminant animals which may become part of the food chain.

The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal
feed use, you are responsible for assuring that your overall operation
and the products you manufacture and distribute are in compliance with
the law. We have enclosed a copy of FDA's Small Entity Compliance Guide
to assist you with complying with the regulation... blah, blah, blah...


full text TSS submission to FDA;

-------- Original Message -------- 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."

Greetings FDA,i would kindly like to comment on;Docket 03D-0186FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; AvailabilitySeveral factors on this apparent voluntary proposal disturbs me greatly,please allow me to point them out;1. MY first point is the failure of the partial ruminant-to-ruminant feedban of 8/4/97. this partial and voluntary feed ban of some ruminantmaterials being fed back to cattle is terribly flawed. without the_total_ and _mandatory_ ban of all ruminant materials being fedback to ruminants including cattle, sheep, goat, deer, elk and mink,chickens, fish (all farmed animals for human/animal consumption),this half ass measure will fail terribly, as in the past decades... 2. WHAT about sub-clinical TSE in deer and elk? with the recentfindings of deer fawns being infected with CWD, how many couldpossibly be sub-clinically infected. until we have a rapid TSE test toassure us that all deer/elk are free of disease (clinical and sub-clinical),we must ban not only documented CWD infected deer/elk, but healthyones as well. it this is not done, they system will fail...3. WE must ban not only CNS (SRMs specified risk materials),but ALL tissues. recent new and old findings support infectivityin the rump or ass muscle. wether it be low or high, accumulationwill play a crucial role in TSEs.4. THERE are and have been for some time many TSEs in theUSA. TME in mink, Scrapie in Sheep and Goats, and unidentifiedTSE in USA cattle. all this has been proven, but the TSE in USAcattle has been totally ignored for decades. i will document thisdata below in my references.5. UNTIL we ban all ruminant by-products from being fed backto ALL ruminants, until we rapid TSE test (not only deer/elk) butcattle in sufficient numbers to find (1 million rapid TSE test inUSA cattle annually for 5 years), any partial measures such as theones proposed while ignoring sub-clinical TSEs and not rapid TSEtesting cattle, not closing down feed mills that continue to violate theFDA's BSE feed regulation (21 CFR 589.2000) and not makingfreely available those violations, will only continue to spread theseTSE mad cow agents in the USA. I am curious what we willcall a phenotype in a species that is mixed with who knowshow many strains of scrapie, who knows what strain or how manystrains of TSE in USA cattle, and the CWD in deer and elk (notelling how many strains there), but all of this has been renderedfor animal feeds in the USA for decades. it will get interesting oncesomeone starts looking in all species, including humans here in theUSA, but this has yet to happen... 6. IT is paramount that CJD be made reportable in every state(especially ''sporadic'' cjd), and that a CJD Questionnaire mustbe issued to every family of a victim of TSE. only checking deathcertificates will not be sufficient. this has been proven as well(see below HISTORY OF CJD -- CJD QUESTIONNAIRE)7. WE must learn from our past mistakes, not continue to makethe same mistakes... REFERENCES

PDF] Chronic wasting disease in deer and elk in North America
File Format: PDF/Adobe Acrobat
Chronic wasting disease (CWD) is a naturally-occurring prion. disease of native
North American ... Preliminary findings on the experimental transmission of ... 2102/E.S.%20WILLIAM%20and%20Miller.pdf - Similar pages

File Format: PDF/Adobe Acrobat
as diverse as cross-species transmission studies and empirical ... Oral transmission
and. early lymphoid tropism of chronic wasting disease PrP ...


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