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From: TSS ()
Subject: CWD AND ENVIRONMENTAL FACTORS i.e. saliva, fecal shedding and fecal-oral transmission is likely
Date: October 1, 2006 at 6:31 pm PST

CWD Annual Report – 2005

To date, we have developed a reliable, non-lethal method for detecting chronic wasting disease in

mule deer that represented a significant breakthrough in improving the ability to monitor

prevalence of the disease over time and space. We also have demonstrated that chronic wasting

disease can be transmitted indirectly, and that fecal shedding and fecal-oral transmission is likely.

We also have developed epidemic models for chronic wasting disease in captive mule deer that

align well with the independent empirical findings on transmission processes, underscoring the

likely importance of indirect transmission in the ecology of chronic wasting disease in natural

populations.

full text ;

http://www.nrel.colostate.edu/projects/cwd/papers/CWD_ann_rpt_2005_w_figs.pdf

Vet Pathol 42:530–549 (2005)

REVIEW ARTICLE

Chronic Wasting Disease

E. S. WILLIAMS1

Department of Veterinary Sciences, University of Wyoming, Laramie, WY

Abstract. Chronic wasting disease (CWD) is a unique transmissible spongiform encephalopathy (TSE) of

mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus), and Rocky Mountain elk (Cervus elaphus

nelsoni). The natural history of CWD is incompletely understood, but it differs from scrapie and bovine spongiform

encephalopathy (BSE) by virtue of its occurrence in nondomestic and free-ranging species. CWD has

many features in common with scrapie, including early widespread distribution of disease-associated prion

protein (PrPd) in lymphoid tissues, with later involvement of central nervous system (CNS) and peripheral

tissues. This distribution likely contributes to apparent efficiency of horizontal transmission and, in this, is

similar to scrapie and differs from BSE. Clinical features and lesions of CWD are qualitatively similar to the

other animal TSEs. Microscopically, marked spongiform lesions occur in the central nervous system (CNS)

after a prolonged incubation period and variable course of clinical disease. During incubation, PrPd can be

identified in tissues by antibody-based detection systems. Although CWD can be transmitted by intracerebral

inoculation to cattle, sheep, and goats, ongoing studies have not demonstrated that domestic livestock are

susceptible via oral exposure, the presumed natural route of exposure to TSEs. Surveillance efforts for CWD

in captive and free-ranging cervids will continue in concert with similar activities for scrapie and BSE. Eradication

of CWD in farmed cervids is the goal of state, federal, and industry programs, but eradication of CWD

from free-ranging populations of cervids is unlikely with currently available management techniques.

snip...

Transmission

Although the exact method of transmission of CWD

is not known, horizontal and indirect transmission appear

to be the most important routes of spread.99 Epidemiologic

observations suggest that in addition to

transmission within species, CWD can be transmitted

from elk to mule deer and white-tailed deer, from mule

deer to elk, and from mule deer to white-tailed deer.156

Maternal transmission, if it occurs, does not appear to

play a significant role in the epidemiology of the disease.

99 To date, PrPd and infectivity have not been

identified in placentas of deer and elk. This is in contrast

to scrapie, in which high levels of infectivity reside

in the placenta,5,122,143,144 and epidemiologic investigations

have found that transmission at the time of

lambing appears to be important in maintaining scrapie

in flocks.

Results of a series of studies investigating CWD

transmission have recently been published.102 Direct

transmission of CWD between animals occurred, although

the exact mechanism was not determined. The

role of environmental contamination in maintaining infectivity

is not entirely understood; however, controlled

studies showed infectivity remained on pastures

in which CWD-affected deer resided approximately 2

years previously. These studies were conducted in pastures

presumed to be highly contaminated. Thus, extrapolation

to field situations should be done with care,

but these data suggest caution in managing pastures or

paddocks that have housed CWD-affected cervids. In

addition, mule deer were infected by contact with skeletal

remains of CWD-affected deer and surrounding

ground and vegetation. This information bolsters the

need for caution when moving portions of harvested

cervids that contain the highest amount of infectivity,

such as the head and the spine, to areas where CWD

does not exist.

snip...end

full text ;

http://www.vetpathology.org/cgi/reprint/42/5/530.pdf

DRAFT

WYOMING GAME AND FISH DEPARTMENT

CHRONIC WASTING DISEASE MANAGEMENT PLAN

February 17, 2006


snip...

6. Epidemiology of CWD: detection, shedding, and environmental contamination.
Thirty elk were orally inoculated with elk CWD prion in May 2005. Every six weeks, elk are individually housed in metabolic cages for three days. Feces, urine, saliva, and blood are collected. These samples are used to develop and validate an assay capable of detecting minute concentrations of the CWD prion in a variety of substrates. Additional samples for testing are collected from insects, rabbits, rodents, and soil where the CWD-infected elk are housed. This study could determine: 1) how the CWD prion is shed from infected animals; 2) the temporal pattern of such shedding; and 3) the degree and extent of environmental contamination with the CWD prion.

http://gf.state.wy.us/downloads/pdf/CWD2005reviseddraft.pdf

Experimental CWD Infection and Bioassay in the Ferret
Edward A. Hoover', Christina J. Sigurdson', Candace K. Mathiason', Michael W. Miller2, Matthew R. Perroti', Gwyneth A. Eliason', Terry R. Spraker3, and Jason C. Bartz4
'Prion Research Laboratory, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523; 2Colorado Division of Wildlife, Fort Collins, CO 80526; 3Colorado State Veterinary Diagnostic Laboratory, Fort Collins, CO 80523;4Department of Medical Microbiology and Immunology, Creighton University, Omaha, NB 68178

Based on the work of Bartz et al., we have developed the ferret model of CWD infection and employed this system to: (1) compare brain lesions and PrPcwd distribution in brain and lymphoid tissues in ferrets with those in deer, and (2) assay secretions/excretions from deer for CWD prion infectivity. Groups of ferrets were inoculated via the oral or intracerebral (i.c.) route with CWD + vs. CWD- deer brain homogenates, white blood cells, or saliva. Inoculated ferrets were monitored clinically and either sacrificed at pre-determined intervals from 3 to 24 months post inoculation (pi) or when terminal symptoms developed. Ferrets inoculated ic with CWD+ brain developed clinical neurologic disease and were euthanized between 14 and 19 months. Tissues were examined by histopathology, and by immunohistochemical staining, ELISA, and western blotting for Histopathologic lesions indicative of TSE included spongiform vacuolation and neuronal necrosis. PrPcwd was demonstrated in ferret brain by ELISA and western blot assays. In addition, dual immunofluorescent staining revealed PrPcwd localized at astrocyte surface membranes and within neurons. Results to date from ferret bioassay of saliva and blood cells from CWD+ deer will be reported. These studies confirm the susceptibility of the ferret to CWD infection and pose the potential that CWD infectivity can be assayed in this small animal model.

=============================================


Based on epidemiological studies there

is evidence that the disease is transmitted horizontally from infected to susceptible cervids

(Miller and Williams, 2003). Maternal transmission may also occur but seems to play a

subordinate role. Accumulation of PrPres in gut-associated lymphoid tissues during the disease

course suggests agent shedding in faeces and/or saliva as plausible transmission routes

(Sigurdson et al., 1999). Residual infectivity in contaminated environments, either from

excreta or from decomposed carcasses of infected animals, may also be important in

sustaining epidemics.

http://www.efsa.europa.eu/etc/medialib/efsa/science/biohaz/biohaz_opinions/opinion_annexes/500.Par.0001.File.dat/opinion_biohaz12_ch_wast_dis_ef70_report_en1.pdf

CWD

3.4.2 Evidence for lateral transmission


The CWD agent has been demonstrated in lymphoid tissues of the alimentary tract that suggests that the agent may be shed through the alimentary tract (faeces and saliva).

see Annexe 1 on distribution of tissue infectivity (old data)...tss


http://ec.europa.eu/food/fs/sc/ssc/out324_en.pdf

http://72.14.209.104/search?q=cache:s7mfafLPBrYJ:ec.europa.eu/food/fs/sc/ssc/out324_en.pdf+REPORT+ON+CHRONIC+WASTING+DISEASE+AND+TISSUE&hl=en&gl=us&ct=clnk&cd=11


and secondly the possibility of a sylvatic reservoir...

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

Observations of deer and elk in captivity indicate that CWD is contagious though the

exact mechanism(s) of transmission are not yet known. Based on pathogenesis of the disease

it is plausible that the CWD agent exits the body in saliva and feces. The contribution of

82

environmental contamination to the epidemiology of CWD is not specifically known but

observations of cohorts of elk and deer in captivity strongly suggest it is important in areas of

high CWD prevalence and high densities of susceptible species. This is an area of

considerable ongoing research.

http://www.blackwellpublishing.com/products/journals/suppmat/nan/nan477/NAN477sm.pdf


CHRONIC WASTING DISEASE

Review of research published since November 2004

SNIP...

7) EPIDEMIOLOGY AND TRANSMISSION

From enclosures previously used by infected animals

28. Research reviewed in the WIN report showed that healthy cervids could be

infected with CWD by grazing on pastures contaminated with excreta from

infected cervids or with the carcases of diseased cervids. This provided

evidence for environmental transmission of CWD.

29. A more recent experimental study examined the potential for soil to serve as

a reservoir for TSEs by examining the interaction of PrPSc (from an adapted

transmissible mink encephalopathy agent) with common soil minerals

(Johnson et al, 2006). It was demonstrated that substantial PrPSc could be

adsorbed by the clay minerals, kaolinite and montmorillonite as well as

quartz. In addition, significant adsorption to whole soil samples was found.

Furthermore, there was a strong interaction between PrPSc and

montmorillonite. To determine whether prions remained infectious in soil,

clay samples experimentally contaminated with an inoculum were ic

inoculated into hamsters. Symptoms developed in these animals at

approximately the same time as those injected with directly with the inoculum.

The study suggests that TSE infectivity released into soil may be preserved in

a bioavailable form which may contribute to disease transmission. The

authors suggest this study adds to the evidence for environmental

transmission of CWD.

http://www.seac.gov.uk/papers/CWD-review.pdf


Prions Adhere to Soil Minerals and Remain Infectious
Christopher J. Johnson1,2, Kristen E. Phillips3, Peter T. Schramm3, Debbie McKenzie2, Judd M. Aiken1,2, Joel A. Pedersen3,4*

1 Program in Cellular and Molecular Biology, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 2 Department of Animal Health and Biomedical Sciences, School of Veterinary Medicine, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 3 Molecular and Environmental Toxicology Center, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 4 Department of Soil Science, University of Wisconsin Madison, Madison, Wisconsin, United States of America

An unidentified environmental reservoir of infectivity contributes to the natural transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) in sheep, deer, and elk. Prion infectivity may enter soil environments via shedding from diseased animals and decomposition of infected carcasses. Burial of TSE-infected cattle, sheep, and deer as a means of disposal has resulted in unintentional introduction of prions into subsurface environments. We examined the potential for soil to serve as a TSE reservoir by studying the interaction of the disease-associated prion protein (PrPSc) with common soil minerals. In this study, we demonstrated substantial PrPSc adsorption to two clay minerals, quartz, and four whole soil samples. We quantified the PrPSc-binding capacities of each mineral. Furthermore, we observed that PrPSc desorbed from montmorillonite clay was cleaved at an N-terminal site and the interaction between PrPSc and Mte was strong, making desorption of the protein difficult. Despite cleavage and avid binding, PrPSc bound to Mte remained infectious. Results from our study suggest that PrPSc released into soil environments may be preserved in a bioavailable form, perpetuating prion disease epizootics and exposing other species to the infectious agent.

Funding. This work was supported by USEPA grant 4C-R070-NAEX (JAP) and DOD grant DAMD17–03–1–0369 (JMA).

Competing interests. The authors have declared that no competing interests exist.

Editor: David Westaway, University of Toronto, Canada

Received: December 20, 2005; Accepted: March 8, 2006; Published: April 14, 2006

DOI: 10.1371/journal.ppat.0020032

Copyright: © 2006 Johnson et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abbreviations: BH, brain homogenate; BSE, bovine spongiform encephalopathy; CWD, chronic wasting disease; dpi, days postinoculation; Kte, kaolinite; Mte, montmorillonite; PK, proteinase K; PrPC, normal cellular isoform of the prion protein; PrPSc, disease-associated prion protein; TSE, transmissible spongiform encephalopathy

* To whom correspondence should be addressed. E-mail: joelpedersen@wisc.edu

Citation: Johnson CJ, Phillips KE, Schramm PT, McKenzie D, Aiken JM, et al. (2006) Prions Adhere to Soil Minerals and Remain Infectious. PLoS Pathog 2(4): e32

snip...

Discussion
Environmental transmission of prion diseases has been noted for decades [7,8,14]. In this study, we provide evidence indicating that soil and soil minerals serve as a reservoir of TSE infectivity. While extrapolation of in vitro studies to the environment must be made with caution, our findings suggest that PrPSc released from diseased animals may be sequestered near the soil surface, maintaining the TSE agent in an environmental medium with which livestock and wildlife come in contact. Our experiments demonstrate that Mte-bound PrPSc remains infectious and suggest that soil may harbor more TSE agent than previously assumed on the basis of water extraction of prions from garden soil [13].

snip...

In conclusion, soil and soil minerals have the potential to bind PrPSc and maintain infectivity. These findings will serve as the basis for further study on the interaction of PrPSc with other soil components (humic substances, quartz, and other minerals), the stability of soil-bound PrPSc under typical environmental conditions (UV light, freeze-thaw cycles) and the effect of soil microorganisms and extracellular enzymes on protein integrity. Our current results suggest that sorption of PrPSc to clay minerals may limit its migration through the soil column. Maintenance of prion infectivity at the soil surface may contribute to the propagation of CWD and scrapie epizootics and enhance the likelihood of interspecies transmission of these diseases.

snip...full text ;

http://pathogens.plosjournals.org/archive/1553-7374/2/4/pdf/10.1371_journal.ppat.0020032-S.pdf

Environ. Sci. Technol., ASAP Article 10.1021/es060943h S0013-936X(06)00943-6
Web Release Date: September 9, 2006

Copyright © 2006 American Chemical Society
Prion Degradation in Soil: Possible Role of Microbial Enzymes Stimulated by the Decomposition of Buried Carcasses

Delphine Rapp, Patrick Potier, Lucile Jocteur-Monrozier, and Agnès Richaume*

Ecologie Microbienne, Université Claude Bernard Lyon 1 - UMR CNRS 5557 - USC INRA 1193, bat. G. Mendel, 43 Bd du 11 Novembre 1918, 69 622 Villeurbanne Cedex, France

Received for review April 19, 2006

Revised manuscript received July 21, 2006

Accepted July 27, 2006

Abstract:

This study is part of a European project focused on understanding the biotic and abiotic mechanisms involved in the retention and dissemination of transmissible spongiform encephalopathies (TSE) infectivity in soil in order to propose practical recommendations to limit environmental contamination. A 1-year field experiment was conducted with lamb carcasses buried in a pasture soil at three depths (25, 45, and 105 cm). Microbial community response to carcasses was monitored through the potential proteolytic activity and substrate induced respiration (SIR). Soil above carcasses and control soil exhibited low proteolytic capacity, whatever the depth of burial. Contrastingly, in soil beneath the carcasses, proteolysis was stimulated. Decomposing carcasses also stimulated SIR, i.e., microbial biomass, suggesting that proteolytic populations specifically developed on lixiviates from animal tissues. Decomposition of soft tissues occurred within 2 months at subsurface while it lasted at least 1 year at deeper depth where proteolytic activities were season-dependent. The ability of soil proteases to degrade the form of prion protein was shown in vitro and conditions of burial relevant to minimize the risk of prion protein dissemination are discussed.

http://pubs.acs.org/cgi-bin/abstract.cgi/esthag/asap/abs/es060943h.html

70. A member considered that, since the TSE agent is a protein, it was

likely to decay quickly due to the pH of, and bacteria present in,

soil. However, a member pointed out good evidence suggesting

that the Chronic Wasting Disease agent persisted in the

environment. Dr Matthews informed members that a VLA project

on infectivity in sheep exposed to the farm environment indicated

that material on pasture is infectious for at least 2 months.

Members agreed that in view of the resistance of PrPsc to

degradation, evidence from CWD and the VLA studies, it was safer

to assume survival of the agent in soil for a significant amount of

time.

71. In response to members’ questions about the field spreading of

fertiliser, Alan Brewer (Defra) informed the committee that some

dust can arise from the activity, both from the fertiliser distribution

process (that depends on the type of spreading mechanism) and

from tractor wheels kicking up soil in arable situations. But it was

not possible to indicate whether there was any likelihood of dust

particles containing fertiliser drifting onto adjoining fields. He

added that it was recognised as good practice for farmers not to

spread fertiliser into hedges and watercourses.

http://www.seac.gov.uk/minutes/final87.pdf

Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: PRION INFECTION OF MUCOSAL TISSUE


Authors

Bessen, Richard - MONTANA STATE UNIVERSITY
Dejoia, Crista - MONTANA STATE UNIVERSITY
Dlakic, Wendy - MONTANA STATE UNIVERSITY
Sorg, Rebecca - MONTANA STATE UNIVERSITY
O'Connell, Kimberly - MONTANA STATE UNIVERSITY
Tucker, Tammy - MONTANA STATE UNIVERSITY
Hamir, Amirali
Richt, Juergen
Rocke, Tonie - NAT WILDLIFE HEALTH CTR


Submitted to: Chronic Wasting Disease Symposium Proceedings
Publication Type: Abstract
Publication Acceptance Date: June 15, 2005
Publication Date: July 12, 2005
Citation: Bessen, R.A., Dejoia, C., Dlakic, W., Sorg, R., O'Connell, K., Tucker, T., Hamir, A.N., Richt, J.A., Rocke, T. 2005. Prion infection of mucosal tissue [abstract]. 2nd International Chronic Wasting Disease Symposium. p. 38.

Technical Abstract: To investigate the site(s) of prion agent shedding in chronic wasting disease (CWD), we examined the distribution of the prion agent in mucosal tissue from ruminants and rodents with experimental prion disease. We chose the tongue as a peripheral target of prion infection since is a densely innervated tissue at the oral mucosa that we postulate can be a site of CWD agent shedding. The prion agent, PrP**Sc, was present in tongues from elk infected with the CWD agent and sheep infected with the scrapie agent. In hamsters infected with the prion agent, PrP**Sc was found in nerve fibers and skeletal muscle cells as well as in taste cells. In fungiform papillae on the tongue, the distribution of PrP**Sc was consistent with deposition in the taste bud and the surrounding stratified squamous epithelium. These findings suggest that the prion agent can spread from the brain to the tongue along sensory and motor fibers. The presence of the prion agent in the tongue of ruminants and rodents indicates that 1) ingestion of tongue or tongue derived food products can pose a risk to human and animal health, and 2) the localization of the prion agent at the mucosal surface of the tongue could provide a site for prion agent shedding and subsequent transmission to naive hosts.


Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: ABNORMAL PRION PROTEIN IN ECTOPIC LYMPHOID TISSUE IN A KIDNEY OF AN ASYMPTOMATIC WHITE-TAILED DEER EXPERIMENTALLY INOCULATED WITH THE AGENT OF CHRONIC WASTING DISEASE


Authors

Hamir, Amirali
Kunkle, Robert
Miller, Janice - ARS RETIRED
Hall, S - USDA-VS-APHIS-NVSL, AMES


Submitted to: Veterinary Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 14, 2005
Publication Date: May 1, 2006
Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Hall, S.M. 2006. Abnormal prion protein in ectopic lymphoid tissue in a kidney of an asymptomatic white-tailed deer experimentally inoculated with the agent of chronic wasting disease. Veterinary Pathology. 43(3):367-369.

Interpretive Summary: Chronic wasting disease (CWD) is a fatal disease of brain and spinal cord of deer and elk. It belongs to a group of transmissible spongiform encephalopathy (TSE) diseases which includes bovine spongiform encephalopathy or "mad cow disease". Infection by the CWD agent induces accumulations of an abnormal form of protein (called prion or PrP**res) in tissues of nervous and lymphoid systems. This report documents presence of PrP**res within kidney of a white tailed deer that was experimentally inoculated by intracerebral route with CWD. The deer was euthanized and examined at 10 months post inoculation. At that age it did not show any clinical signs of the disease but lesions of TSE were detected in the tissues. These findings confirm early involvement of tissues in white tailed deer. Also, it corroborates the recently published finding of presence of PrP**res in organs other than brain and lymphoid systems in laboratory animals with TSE (scrapie) by demonstration of the same phenomenon in a natural host species.
Technical Abstract: Chronic wasting disease (CWD), a transmissible spongiform encephalopathy (TSE) of deer and elk is one of a group of fatal, neurologic disease that affects several mammalian species, including human beings. Infection by the causative agent induces accumulations of an abnormal form of prion protein (PrP**res) in nervous and lymphoid tissues. This report documents the presence of PrP**res within lymphoid follicles in kidney of a white-tailed deer that had been experimentally inoculated by intracerebral route with CWD 10 months previously. The deer was non-clinical, but spongiform lesions characteristic of TSE were detected in tissues of the central nervous system (CNS) and PrP**res was seen in CNS and in lymphoid tissues by immunohistochemistry. These findings confirm previous reports of early involvement in the obex region of CNS and in lymphoid tissues of white-tailed deer with CWD. Also, the demonstration of PrP**res in kidney corroborates a recently published finding of PrP**res in lymphoid follicles of organs other than CNS and lymphoid tissues in laboratory animals with TSE (scrapie). This report, however, is the first description of a similar phenomenon in a natural host species.


Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: TRANSMISSION OF CHRONIC WASTING DISEASE AGENT OF MULE DEER (CWD**MD) TO SUFFOLK SHEEP BY INTRACEREBRAL ROUTE


Authors

Hamir, Amirali
Kunkle, Robert
Cutlip, Randall - ARS RETIRED
Miller, Janice - ARS RETIRED
Williams, Elizabeth - UNIVERSITY OF WYOMING
Richt, Juergen


Submitted to: European Society of Veterinary Pathology
Publication Type: Abstract
Publication Acceptance Date: June 5, 2006
Publication Date: August 31, 2006
Citation: Hamir, A., Kunkle, R., Cutlip, R., Miller, J., Williams, E., Richt, J. 2006. Transmission of chronic wasting disease agent of mule deer (CWD**md) to Suffolk sheep by intracerebral route [abstract]. European Society of Veterinary Pathology 24th Annual Meeting. Paper No. P63. p. 171-172.

Technical Abstract: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) that has been identified in captive and free-ranging cervids in the U.S. since 1967. To determine the transmissibility of CWD to sheep, 8 Suffolk lambs [4 QQ and 4 QR at codon 171 of prion protein (PRNP) gene] were inoculated intracerebrally with a pooled brain suspension from 28 mule deer naturally affected with CWD (CWD**md). Two other lambs (1 QQ and 1 QR at codon 171 of the PRNP gene) were kept as non-inoculated controls. Within 36 months post inoculation (MPI), 2 animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in the sheep with the clinical signs of TSE and its tissues were positive for the abnormal prion protein (PrP**res) by immunohistochemistry and Western blot. Between 36 and 60 MPI, 3 other sheep were euthanized because of conditions unrelated to TSE. The remaining 3 sheep remained non-clinical at the termination of the study (72 MPI) and were euthanized at that time. One of the 3 animals revealed SE and its tissues were positive for PrP**res. Both sheep positive for PrP**res were homozygous QQ at codon 171. Retrospective examination of the PRNP genotype of the 2 TSE-positive animals revealed that the sheep with clinical prion disease (euthanized at 35 MPI) was heterozygous (AV) and the sheep with the sub-clinical disease (euthanized at 72 MPI) was homozygous (AA) at codon 136 of the PRNP. These findings demonstrate that transmission of the CWD**md agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a significant part in successful transmission and incubation period of CWD**md.


Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

Title: EXPERIMENTAL SECOND PASSAGE OF CHRONIC WASTING DISEASE (CWD(MULE DEER)) AGENT TO CATTLE


Authors

Hamir, Amirali
Kunkle, Robert
Miller, Janice - ARS RETIRED
Greenlee, Justin
Richt, Juergen


Submitted to: Journal of Comparative Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 25, 2005
Publication Date: January 1, 2006
Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Greenlee, J.J., Richt, J.A. 2006. Experimental second passage of chronic wasting disease (CWD(mule deer)) agent to cattle. Journal of Comparative Pathology. 134(1):63-69.

Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.
Technical Abstract: To compare clinicopathological findings of first and second passage of chronic wasting disease (CWD) in cattle, a group of calves (n=6) were intracerebrally inoculated with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and lost weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify CWD PrPres but also develop clinical CNS signs without manifestation of morphologic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, scrapie. The current study confirms previous work that indicates the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of neuropathologic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.

====================================================


CWD USA

http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html

Transmission

Baier, M., S. Norley, J. Schultz, M. Burwinkel, A. Schwarz and C. Riemer. 2003. Prion diseases: infectious and lethal doses following oral challenge. J. of General Virology 84:1927-1929.

Hamir, A.N., J.M. Miller, R.C. Cutlip, M.J. Stack, M.J. Chaplin, and A.L. Jenny. 2003. Preliminary Observations on the Experimental Transmission of Scrapie to Elk (Cervus elaphus nelsoni) by Intracerebral Inoculation. Vet Pathol. 40:81-85.

Hamir, A.N., J.M. Miller, R.C. Cutlip, M.J. Stack, M.J. Chaplin, A.L. Jenny and E.S. Williams. 2003. Experimental inoculation of scrapie and chronic wasting disease agents in raccoons (Procyon lotor). The Veterinary Record 153:121-123.

Lupi, O., 2003. Could ectoparasites act as vectors for prion disease?. International J. of Dermatology. 42:425-429.

Miller, M.W. and E.S. Williams. 2003. Prion disease: Horizontal prion transmission in mule deer. Nature 425:35-36.

Race, R.; Raines, A.; Baron, T.; Miller, M.; Jenny, A.; Williams, E. 2002. Comparison of Abnormal Prion Protein Glycoform Patterns from Transmissible Spongiform Encephalopathy Agent-Infected Deer, Elk, Sheep, and Cattle. Journal of Virology 76(23):12365-12368.

Gould, D.; Voss, J.; Miller, M.; Bachand, A.; Cummings, B.; Frank, A. 2003. Brief Communcations; Survey of cattle in northeast Colorado for evidence of chronic wasting disease: geographical and high-risk targeted sample. Journal Vet. Diagn. Invest. 15: 274-277.

Hunter, N.; Foster, J.; Chong, A.; McCutcheon, S.; Parnham, D.; Eaton, S.; MacKenzie, C.; Houston, F. 2002. Transmission of prion diseases by blood transfusion. Journal of General Virology 83:2897-2905.

Belay, E.D., P. Gambetti, L.B. Schonberger, P. Parchi, D.R. Lyon, S. Capellari, J.H. McQuiston, K. Bradley, G. Dowdle, M. Crutcher and C.R. Nichols. 2001. Creutzfeldt-Jakob disease in unusually young patients who consumed venison. Arch. Neurol. 58(10): 1673-1678.

Hamir, A.N., R.C. Cutlip, J.M. Miller, E.S. Williams, M.J. Stack, M.W. Miller, K.I. O'Rourke and M.J. Chaplin. 2001. Preliminary findings on the experimental transmission of chronic wasting disease agent of mule deer to cattle. J. Vet. Diagn. Invest. 13(1): 91-96.

Hill, A.F., S. Joiner, J. Lineham, M. Desbruslais, P.L Lantos and J. Collinge. 2000. Species-barrier-independent prion replication in apparently resistant species. Proc. Natl. Acad. Sci. 97(18): 10248-10253.

Raymond, G.J., A. Bossers, L.D. Raymond, K.I. O'Rourke, L.E. McHolland, P.K. Bryant III, M.W. Miller, E.S. Williams, M. Smits and B. Caughey. 2000. Evidence of a molecular barrier limiting susceptibility of humans, cattle and sheep to chronic wasting disease. The EMBO Journal 19(17): 4425-4430.

Sigurdson, C.J., E.S. Williams, M.W. Miller, T.R. Spraker, K.I. O'Rourke and E.A. Hoover. 1999. Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus). J. of General Virology 80(10): 2757-2764.

http://www.aphis.usda.gov/vs/nahps/cwd/cwd-research.html#Transmission

2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 7
Terry S. Singeltary Sr.
Vol #:
1

-------- 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."
To: fdadockets@oc.fda.gov


Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed; Availability

Several 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 feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant
materials being fed back to cattle is terribly flawed. without the
_total_ and _mandatory_ ban of all ruminant materials being fed
back 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 recent
findings of deer fawns being infected with CWD, how many could
possibly be sub-clinically infected. until we have a rapid TSE test to
assure us that all deer/elk are free of disease (clinical and sub-clinical),
we must ban not only documented CWD infected deer/elk, but healthy
ones 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 infectivity
in the rump or ass muscle. wether it be low or high, accumulation
will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in the
USA. TME in mink, Scrapie in Sheep and Goats, and unidentified
TSE in USA cattle. all this has been proven, but the TSE in USA
cattle has been totally ignored for decades. i will document this
data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back
to ALL ruminants, until we rapid TSE test (not only deer/elk) but
cattle in sufficient numbers to find (1 million rapid TSE test in
USA cattle annually for 5 years), any partial measures such as the
ones proposed while ignoring sub-clinical TSEs and not rapid TSE
testing cattle, not closing down feed mills that continue to violate the
FDA's BSE feed regulation (21 CFR 589.2000) and not making
freely available those violations, will only continue to spread these
TSE mad cow agents in the USA. I am curious what we will
call a phenotype in a species that is mixed with who knows
how many strains of scrapie, who knows what strain or how many
strains of TSE in USA cattle, and the CWD in deer and elk (no
telling how many strains there), but all of this has been rendered
for animal feeds in the USA for decades. it will get interesting once
someone starts looking in all species, including humans here in the
USA, 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 must
be issued to every family of a victim of TSE. only checking death
certificates 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 make
the same mistakes...

REFERENCES


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
ehoover@lamar.colostate.edu

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.

snip...

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.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757


Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700
From: "Terry S. Singeltary Sr."
Reply-To: BSE-L
To: BSE-L

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

snip...

_animal protein_

http://www.surefed.com/deer.htm

BODE'S GAME FEED SUPPLEMENT #400
A RATION FOR DEER
NET WEIGHT 50 POUNDS
22.6 KG.

snip...

_animal protein_

http://www.bodefeed.com/prod7.htm

Ingredients

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.

http://www.bodefeed.com/prod6.htm
===================================

MORE ANIMAL PROTEIN PRODUCTS FOR DEER

Bode's #1 Game Pellets
A RATION FOR DEER
F3153

GUARANTEED ANALYSIS
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%


Ingredients

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.

FEEDING DIRECTIONS
Feed as Creep Feed with Normal Diet

http://www.bodefeed.com/prod8.htm

INGREDIENTS

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

DIRECTIONS FOR USE

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.

http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
===================================================

DEPARTMENT OF HEALTH & HUMAN SERVICES
PUBLIC HEALTH SERVICE
FOOD AND DRUG ADMINISTRATION

April 9, 2001 WARNING LETTER

01-PHI-12
CERTIFIED MAIL
RETURN RECEIPT REQUESTED

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

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
distinguished
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...tss

http://www.fda.gov/foi/warning_letters/g1115d.pdf


SNIP...FULL TEXT ;

http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm

TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;

*********************************

e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;

*********************************

f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,
net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and
visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###


http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html

##################### Bovine Spongiform Encephalopathy #####################

Subject: SEAC Position statement - Chronic wasting disease in UK deer January 2005 (updated July 2006)
Date: July 17, 2006 at 8:34 am PST

SEAC Statement
January 2005 (updated July 2006)

--------------------------------------------------------------------------------

Position statement - Chronic wasting disease in UK deer
Introduction
1. In 2004, the Food Standards Agency asked SEAC to consider the possible public and animal health implications of chronic wasting disease (CWD), in particular the level of risk posed to consumers of meat from infected animals. The committee also considered the possibility that BSE may be present in UK deer. The committee reconsidered these issues in 2006 in light of new information.

Background
2. CWD has emerged as an endemic transmissible spongiform encephalopathy (TSE) in certain captive and free-ranging species of cervid (deer) in some areas of North America. The disease is characterised by weight loss and behavioural changes in infected animals, usually over a period of weeks or months leading to death. CWD has not been found in the UK or elsewhere in Europe. No definitive or suspected cases of transmission of CWD to humans have been reported.

3. SEAC considered a review of the published, and some unpublished, research on CWD, together with surveillance data on TSEs in European cervids and information on UK cervid populations 1. A further review of the published literature was considered together with additional surveillance data on TSEs in European cervids 2.

Origins
4. The origins of CWD are unknown. On the basis of epidemiological data, it is highly improbable that CWD originated from the recycling of mammalian protein in processed feed. It has been suggested that CWD may have arisen from transmission and adaptation of scrapie from sheep to cervids, as a result of a spontaneous change of endogenous prion protein (PrP) to an abnormal disease-associated form, or from an unknown source.

5. Data supporting any of these possible origins of CWD are either absent or equivocal. Although CWD could have originated from scrapie, the differing properties of the two prion diseases in strain typing bioassays, whilst limited, do not support this hypothesis. Evidence for multiple strains of CWD is equivocal. It seems most likely that CWD arose from a spontaneous change of endogenous PrP resulting in a disease-associated and laterally-transmissible form of PrP, although direct data to support this hypothesis are lacking.

Host range
6. The known natural hosts for CWD are mule deer (Odocoileus hemionus hemionus), black-tailed deer (Odocoileus hemionus columbianus), white-tailed deer (Odocoileus virginianus), Rocky Mountain elk (Cervus elaphus nelsoni) and moose (Alces alces). The prevalence and geographical distribution of CWD in these species appears to be increasing in North America in a manner which is unlikely to be due simply to increased surveillance.

7. There are no direct data relating to the transmissibility of CWD to UK cervid species. However, comparison of a limited number of PrP codons indicates some homology in the endogenous PrP gene of European and North American cervid species. Thus, the possibility that UK cervids may be susceptible to CWD cannot be excluded, in particular red deer (Cervus elaphus elaphus) which are closely related to Rocky Mountain elk.

8. There is no evidence to suggest that CWD is present in UK cervids. However, because surveillance in the UK is very limited, a low level prevalence of CWD cannot be ruled out. The committee endorsed the opinion of the European Food Safety Authority on CWD surveillance in the European Union (2004) 3.

9. Transmission studies using parenteral routes of administration to cattle, sheep and a single goat, together with data from in vitro PrP conversion experiments, suggest that a significant barrier to CWD transmission to these species may exist. No transmission has been evident so far in an on-going oral transmission study in cattle after seven years. However, evidence from transmission experiments in cattle using the intracerebral route suggests that should cattle ever become infected with CWD, the barrier to transmission between cattle would be appreciably lower. In addition, these experiments show that the neuropathology of CWD is very different from BSE allowing CWD to be distinguished from BSE should natural transmission of CWD ever occur. Furthermore, no signs of infection have been observed from monitoring of cattle co-habiting areas with infected cervids, or in cattle, sheep or goats in close contact with infected cervids in research facilities. Thus, although the data are limited, there is currently no evidence to suggest that CWD can be transmitted naturally to cows, sheep or goats, and it is likely that there is a strong species barrier to such transmission.

Routes of transmission
10. Epidemiological data indicate that lateral transmission between infected and susceptible cervids occurring naturally is sufficiently effective to maintain epidemics in both captive and free-living populations. There is good evidence from studies of cervids inhabiting paddocks previously inhabited by infected animals or contaminated with infected carcases, that CWD can be transmitted laterally between animals via the environment. The precise mechanism of transmission is unclear. It is possible that the infectious agent is shed in the saliva, faeces or urine or as a result of decomposition of infected carcases and transferred to other cervids grazing the contaminated areas. It is also possible that some maternal transmission occurs.

11. There have also been suggestions that the lateral transmission of CWD may be influenced by environmental factors.

Pathogenesis
12. Information on the pathogenesis of CWD is limited. The data show that, following oral challenge, PrPCWD is first detected in the oral and gut-associated lymphoid tissues before spreading more widely within the lymphoid system and then to the brain. However, involvement of the retropharyngeal lymph nodes or tonsils in the pathogenesis may not occur in some elk. At the microscopic level, the nature and distribution of the tissue lesions are similar to those found for scrapie. The available data suggest the pathogenesis of CWD is similar to scrapie. CWD infectivity has been detected in the muscle of mule deer.

BSE in UK deer
13. Both captive and free-ranging cervids in the UK may have been exposed to contaminated feed prior to the reinforced mammalian meat and bone meal ban instituted in 1996. A study to look at the potential susceptibility of red deer to BSE has shown no signs of transmission of the disease by the oral route, but this study is still ongoing. Although a theoretical possibility exists, there is no evidence from the very limited surveillance data to suggest that BSE is present in the UK cervid population.

Human health implications
14. Epidemiological data on possible CWD infection of humans are very limited. The possibility that clinical symptoms of CWD in humans differ from those of Creutzfeldt-Jakob Disease (CJD) cannot be excluded. There is no significant difference between the prevalence of CJD in CWD endemic areas and other areas of the world. However, because CJD surveillance in the USA is relatively recent, not all CJD cases may have been identified. Additionally, detection of a small increase in prevalence of such a rare disease is very difficult. Investigation of six cases of prion disease in young people (< 30 years of age) in the USA found no definite causal link with consumption of venison from known CWD endemic areas. The disease characteristics in these cases were indistinguishable from sporadic CJD or Gerstmann-Sträussler-Scheinker syndrome. Likewise, in a study of three hunters (> 54 years of age) diagnosed with sporadic CJD, no link with consumption of venison from CWD endemic areas was found. No causal link was found in an investigation of three men with neurological illnesses who were known to partake in “wild game feasts”. Only one of these subjects was found to have a prion disease and this was also indistinguishable from sporadic CJD.

15. No study has examined the transmission of CWD to non-human primates by the oral route. However, CWD has been transmitted by intracranial inoculation to non-human primates. Transmission experiments using two strains of transgenic mice expressing human PrP, show that these animals do not develop CWD, suggesting a significant species barrier to the transmission of CWD to humans exists. However, these findings must be interpreted with caution as they may not accurately predict the human situation. Data from in vitro experiments on conversion of human PrP by disease-associated forms of PrP, including PrPCWD, are equivocal.

16. The committee concluded there is no evidence of transmission of CWD to humans from consumption of venison, and that there may be significant barriers to transmission. Nevertheless, as the data are extremely limited a risk cannot be ruled out should CWD enter UK herds.

Conclusions
17. There is no evidence that CWD (or BSE) is present in the UK cervid population. However, because only limited surveillance is conducted in the cervid population, a low level prevalence of CWD cannot be ruled out. It is recommended that further surveillance of TSEs in UK cervids is conducted.

18. There is no evidence of transmission of CWD to humans from consumption of meat from infected cervids. Although epidemiological and experimental data on potential transmission of CWD are extremely limited, they suggest that there may be a significant species barrier. It would be helpful if further studies were available assessing the potential species barrier for transmission to humans.

19. Although limited, there is no evidence CWD can be transmitted to cattle, sheep or goats by natural means.

20. In summary, it appears that CWD currently poses relatively little risk to human health, or to the health of cattle, sheep or goats in the UK. Nevertheless, as a risk cannot be excluded a watching brief should be maintained.


SEAC
January 2005 and updated July 2006

1. The information considered by the committee in 2004 is available here.

2. The information considered by the committee in 2006 is available here.

3. http://www.efsa.eu.int/science/biohaz/biohaz_opinions/501_en.html

http://www.seac.gov.uk/statements/state0706.htm


Greetings,


SEAC hypothisized that ;


Origins
4. The origins of CWD are unknown. On the basis of epidemiological data, it is highly improbable that CWD originated from the recycling of mammalian protein in processed feed. It has been suggested that CWD may have arisen from transmission and adaptation of scrapie from sheep to cervids, as a result of a spontaneous change of endogenous prion protein (PrP) to an abnormal disease-associated form, or from an unknown source.

5. Data supporting any of these possible origins of CWD are either absent or equivocal. Although CWD could have originated from scrapie, the differing properties of the two prion diseases in strain typing bioassays, whilst limited, do not support this hypothesis. Evidence for multiple strains of CWD is equivocal. It seems most likely that CWD arose from a spontaneous change of endogenous PrP resulting in a disease-associated and laterally-transmissible form of PrP, although direct data to support this hypothesis are lacking. ................end


IT may not be the origin, but you cannot ignore the fact that feeding of tainted ruminant materials to deer and elk was a fact, and could have amplified and spread the agent along with the potential of horizontal and vertical transmission route. Feeding of TSE tainted materials could have very well played a key roll in the transmission and spreading of the CWD agent to deer and elk. NOT to say it is the only route of transmission, but one cannot ignore the Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ), the FDA warning letters of feeding deer ruminant materials, and the fact it is a known fact that these deer and elk farms have been feeding potentially tainted ruminant materials for years and years to get those trophy racks, and the fact some hunters did the same with ruminant feed, so do dismiss this potential route in my opinion is not scientific. ...TSS


----- Original Message -----
From: mark.dagleish@
To: flounder9@verizon.net
Sent: Friday, June 30, 2006 9:01 AM
Subject: Susceptibility of Red Deer to BSE


Dear Terry,

this study is on going at the moment and, as yet, we have no results. All results will probably appear on the UK Food Standards Agency web pages but I’m afraid we really do not know just how long this study will take to complete as no one has undertaken this work before.


Kind regards.


Yours,


Mark


Dr. Mark Dagleish BVM&S PhD MRCVS

Moredun Research Institute

Pentlands Science Park

Bush Loan, Penicuik,

Near Edinburgh, EH26 0PZ

Scotland, UK

==============

TSS

#################### https://lists.aegee.org/bse-l.html ####################




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