4 replies [Last post]
Offline
Location: S.E. Wisconsin
Joined: 01/14/2006
Posts: 76
CWD in Wisconsin

The DNR does not have a leg to stand on when it comes to the facts about CWD. It is very obvius that this CWD kill is really about them forceing us to lower the population by useing this disease as an excuse. They will not allow us to discuss CWD at the meetings and hearings that we attend claiming its not up for debate becuase its a biological problem... Thats just horse crap! The reason they won't let us discuss it is cuase we would easly win any argument about CWD.

OK, 1st of all. this disease cannot be removed from our herd EVER useing the plan currently provided by the DNR becuase the disease lives dormant in the enviroment indefinatly. There current plan is to get the population down to 5 animails per square mile.
If there are deer in an area that has CWD liveing in the enviroment, as long as there are any deer, they can get infected. Here are some quotes from the Wisconsin DNR's CWD pro. Matt Verdon:

When I asked how he could think he could stop the disease by ERADICATION of the herd.

Quote:
Simply put, with the size of the infected area and the factors involved, deer eradication is unrealistic as a means to control the disease.

-Matt
Q Matthew Verdon
Chronic Wasting Disease Data Coordinator
Bureau of Wildlife Management
Wisconsin Department of Natural Resources

Question: Can this disease be stopped by killing all the deer?

Quote:
Even if we kill all the deer in the infected area there isn't a guarantee the disease will not return

Matt
Q Matthew Verdon
Chronic Wasting Disease Data Coordinator
Bureau of Wildlife Management
Wisconsin Department of Natural Resources

Questoin: Does the disease lie in the ground dormant until the next generation of deer come through?

Quote:
There has been research done that shows the disease can be obtained from the environment

Matt
Q Matthew Verdon
Chronic Wasting Disease Data Coordinator
Bureau of Wildlife Management
Wisconsin Department of Natural Resources

Question: What percentage of the deer herd does it affect, If left unchecked?

Quote:
It is unknown how high the infection rate would get if we let the disease go unchecked. Looking on a section level (1 square mile) the highest we have seen is 10-12% of the adult population infected.

Matt
Q Matthew Verdon
Chronic Wasting Disease Data Coordinator
Bureau of Wildlife Management
Wisconsin Department of Natural Resources

That one is interesting... Notice he says ADULT population. In a sqaure mile the adult population is about 5 adult deer. That would meen .5% of the deer in the highest area have the disease... Good reason to kill them all hey???

By the way, how about the rumors the DNR spread about the disease killing people, remember that crap all over the news??? I sure do. Well after over 30 years of researching this disease out West, they have not been able to get it to react to humans. These deer are dieing in the woods... Right? There getting hit by cars too, and dyeing, right? Anybody seeing dead coyotes and crows? How about fox's? And all the other critters that eat these deer... and every part of them. Shouldn't these animals be turning up dead all over the place if this desease was trasferable? I questioned the DNR about it:

I asked him why the WDNR is trying to falsely lead people into beleiveing this disease can be transferred to humans? Why are they warning me not to eat the meat on the card they mailed me? Matt, is this some sort of scare tactic??? here is his return email:

Quote:
Thank you for your comments. The DNR has never stated that CWD is transferable to humans or other animals.

-Matt

I emailed him about the safety issues, Why is he allowing rifles in zones where they were banned for safety reasons? Why are they encouraging large numbers of hunters to shoot at any deer, or anything that moves? Why have a 3 month gun season? I mentioned the guy in Madison who shot the Llamba. and he said

Quote:
Thank you for your comments. It is the responsibility of every hunter to determine what they are shooting at, whether hunting deer, pheasant, turkey, bear, etc..

Yea.... That makes me feel real safe, Hey? Do you guys want to take your kids hunting out there???

I am asking everybody who is concered about the future of hunting in Wisconsin to consider spending a few hours writeing the Govener, Radio stations, Newspapers, Hunting and politacal magazines. Send this link all over Wisconsin. I garruntee they are not going to stop expanding the zones unless we stop them. Together we can make a differance.

Offline
Joined: 01/01/2006
Posts: 230
CWD in Wisconsin

hey there big Big buck serial killer,

i thought you might be interested in some 'sound science'.

my opinion is meaningless, but the science is not easily available
(well, it's easier now than it was 8 years ago), but for the ones that want
it, and will read it and try and understand it, it's really very interesting, and very deadly. 100% deadly for those that go clinical. but for those interested;

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 - bob
Miller, Janice - ARS RETIRED
Greenlee, Justin
Richt, Juergen

Submitted to: Journal Of Comparative Pathology
Publication Acceptance Date: July 25, 2005
Publication Date: N/A

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.

Last Modified: 12/30/2005

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_11...

Title: Experimental Transmission of Chronic Wasting Disease Agent to Cattle by Intracerebral Route

Authors

Hamir, Amirali
Kunkle, Robert - bob
Cutlip, Randall - ARS RETIRED
Miller, Janice - ARS RETIRED
O'Rourke, Katherine
Williams, Elizabeth - UNIVERSITY OF WYOMING
Miller, Michael - COLORADO DIV WILDLIFE
Stack, Mick - VET SERVICES AGENCY, UK
Chaplin, Melanie - VET SERVICES AGENCY, UK
Richt, Juergen

Submitted to: Journal Of Veterinary Diagnostic Investigation
Publication Acceptance Date: January 3, 2005
Publication Date: May 1, 2005
Citation: Hamir, A.N., Kunkle, R.A., Cutlip, R.C., Miller, J.M., Orourke, K.I., Williams, E.S., Miller, M.W., Stack, M.J., Chaplin, M.J., Richt, J. 2005. Experimental Transmission Of Chronic Wasting Disease Agent To Cattle By Intracerebral Route. Journal Of Veterinary Diagnostic Investigation. 17:276-281.

Interpretive Summary: This communication reports final observations on experimental transmission of chronic wasting disease (CWD) from mule deer to cattle. Thirteen calves were inoculated into the brain with brain suspension from mule deer naturally affected with CWD. Three other calves were kept as uninoculated controls. The experiment was terminated 6 years post inoculation (PI). During that time, abnormal prion protein was demonstrated in the brain and spinal cord of 5 cattle by laboratory tests. However, consistent clinical signs and microscopic changes were not seen in any of these cattle. Age related changes were seen in both inoculated and control cattle. Findings of this study show that only 38% of the inoculated cattle were positive for CWD agent. Although inoculation directly into the brain is an unnatural route of exposure, and is the most severe challenge possible, 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 CWD agent within brain and spinal cord tissues during the normal lifespan of cattle. It is possible that a second bovine passage of material (cattle brain infected with CWD) from this study may result in a larger incidence of affected cattle with a shortened incubation time, and may produce different clinical and pathological findings. Such a study is now in progress. Also, experimental inoculations of cattle with CWD isolates from white-tailed deer and elk are needed to compare findings with the present study and these studies will be initiated in the near future. Impact: Results of this study show that although cattle inoculated directly into the brain with CWD succumb to the disease, the attack rate was rather small (38%) with this unnatural route of transmission. It is speculated that the oral route of infection may not result in replication of the agent during normal lifespan of cattle.
Technical Abstract: 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 post inoculation (PI). During that time, abnormal prion protein (PrPres) was demonstrated in the central nervous system (CNS) of 5 cattle by both immunohistochemistry (IHC) and Western blot (WB). However, microscopic lesions suggestive of spongiform encephalopathy in the brains of these PrPres positive animals were subtle in 3 cases and absent in 2 cases. The 3 uninoculated control cattle and 8 other inoculated animals euthanized during this time did not have PrPres in their CNS. Degenerative changes indicative of neuroaxonal dystrophy (NAD) were seen in dorsal medulla oblongata and appeared to be related to advancing age in both inoculated and control cattle. 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 PrPres amplification occurred following direct inoculation into the brain, none of the affected animals had classic histopathologic lesions of spongiform encephalopathy. Furthermore, only 38% of the inoculated cattle demonstrated amplification of PrPres. Although intracerebral inoculation is an unnatural route of exposure, and is the most severe challenge possible, 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 PrPres within CNS tissues during the normal lifespan of cattle.

Last Modified: 12/30/2005

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_11...

Research Project: Molecular Biology and Pathogenesis of Arboviruses
Location: Laramie, Wyoming

Title: Inhibition of Protease-Resistant Prion Protein Formation in a Transformed Deer Cell Line Infected with Chronic Wasting Disease

Authors

Raymond, Gregory - NIAID, NIH, HAMILTON, MT
Olsen, Emily - NIAID, NIH, HAMILTON, MT
Lee, Kil Sun - NIAID, NIH, HAMILTON, MT
Raymond, Lynne - NIAID, NIH, HAMILTON, MT
Bryant, P. Kruger - kruger
Baron, Gerald - NIAID, NIH, HAMILTON, MT
Caughey, Winslow - NIAID, NIH, HAMILTON, MT
Kocisko, David - NIAID, NIH, HAMILTON, MT
Mcholland, Linda
Favara, Cynthia - NIAID, NIH, HAMILTON, MT
Langeveld, Jan P.M. - LELYSTAD, THE NETHERLANDS
Van Zijderveld, Fred - LELYSTAD, THE NETHERLANDS
Mayer, Richard - dick
Miller, Michael - COLO DIVISION OF WILDLIFE
Williams, Elizabeth - UW DEPT OF VET SCI
Caughey, Byron - NIAIN, NIH, HAMILTON, MT

Submitted to: Journal Of Virology
Publication Acceptance Date: October 17, 2005
Publication Date: January 1, 2006
Citation: Raymond, G.J., Olsen, E.A., Lee, K., Raymond, L.D., Bryant, P.K., Baron, G.S., Caughey, W.S., Kocisko, D.A., Mcholland, L.E., Favara, C., Langeveld, J., Van Zijderveld, F.G., Mayer, R.T., Miller, M.W., Williams, E.S., Caughey, B. 2006. Inhibition Of Protease-Resistant Prion Protein Formation In A Transformed Deer Cell Line Infected With Chronic Wasting Disease. Journal Of Virology. 80(2):1-9.

Interpretive Summary: Chronic wasting disease (CWD) is an emerging transmissible spongiform encephalopathy (prion disease) of North American cervids, i.e., mule deer, white-tailed deer, and elk (wapiti). To facilitate in vitro studies of CWD, we have developed a transformed deer cell line that is persistently infected with CWD. Primary cultures derived from uninfected mule deer brain tissue were transformed by transfection with a plasmid containing the simian virus 40 genome. A transformed cell line (MDB) was exposed to microsomes prepared from the brainstem of a CWD-affected mule deer. CWD-associated, protease-resistant prion protein (PrPCWD) was used as an indicator of CWD infection. Although no PrPCWD was detected in any of these cultures after two passes, dilution cloning of cells yielded one PrPCWD-positive clone out of 51. This clone, designated MDBCWD, has maintained stable PrPCWD production through 32 serial passes thus far. A second round of dilution cloning yielded 20 PrPCWD-positive subclones out of 30, one of which was designated MDBCWD2. The MDBCWD2 cell line was positive for fibronectin and negative for microtubule-associated protein 2 (a neuronal marker) and glial fibrillary acidic protein (an activated astrocyte marker), consistent with derivation from brain fibroblasts (e.g., meningeal fibroblasts). Two inhibitors of rodent scrapie protease-resistant PrP accumulation, pentosan polysulfate and a porphyrin compound, indium (III) meso-tetra(4-sulfonatophenyl)porphine chloride, potently blocked PrPCWD accumulation in MDBCWD cells. This demonstrates the utility of these cells in a rapid in vitro screening assay for PrPCWD inhibitors and suggests that these compounds have potential to be active against CWD in vivo.
Technical Abstract: Chronic wasting disease (CWD) is an emerging transmissible spongiform encephalopathy (prion disease) of North American cervids, i.e., mule deer, white-tailed deer, and elk (wapiti). To facilitate in vitro studies of CWD, we have developed a transformed deer cell line that is persistently infected with CWD. Primary cultures derived from uninfected mule deer brain tissue were transformed by transfection with a plasmid containing the simian virus 40 genome. A transformed cell line (MDB) was exposed to microsomes prepared from the brainstem of a CWD-affected mule deer. CWD-associated, protease-resistant prion protein (PrPCWD) was used as an indicator of CWD infection. Although no PrPCWD was detected in any of these cultures after two passes, dilution cloning of cells yielded one PrPCWD-positive clone out of 51. This clone, designated MDBCWD, has maintained stable PrPCWD production through 32 serial passes thus far. A second round of dilution cloning yielded 20 PrPCWD-positive subclones out of 30, one of which was designated MDBCWD2. The MDBCWD2 cell line was positive for fibronectin and negative for microtubule-associated protein 2 (a neuronal marker) and glial fibrillary acidic protein (an activated astrocyte marker), consistent with derivation from brain fibroblasts (e.g., meningeal fibroblasts). Two inhibitors of rodent scrapie protease-resistant PrP accumulation, pentosan polysulfate and a porphyrin compound, indium (III) meso-tetra(4-sulfonatophenyl)porphine chloride, potently blocked PrPCWD accumulation in MDBCWD cells. This demonstrates the utility of these cells in a rapid in vitro screening assay for PrPCWD inhibitors and suggests that these compounds have potential to be active against CWD in vivo.

Project Team

Mecham, James - Jim
Drolet, Barbara
Wilson, William
Letchworth, Geoffrey
Schmidtmann, Edward
Mayer, Richard - Dick

Publications

Publications

Related National Programs

Animal Health (103)
Veterinary, Medical and Urban Entomology (104)

Related Projects

Vesicular Stomatitis Virus Persistence in Convalescent Animals
Research on Arthropod-Borne Diseases of Livestock and Wildlife
Development of Sers Assays for West Nile Virus

Last Modified: 12/30/2005

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_11...

CHRONIC WASTING DISEASE OF ELK AND DEER AND CREUTZFELDT-JAKOB DISEASE: COMPARATIVE ANALYSIS OF THE SCRAPIE PRION PROTEIN*

Zhiliang Xie‡, Katherine I. O’Rourke§, Zhiqian Dong‡, Allen L. Jenny¶, Julie A. Langenberg║, Ermias D. Belay#, Lawrence B. Schonberger#, Robert B. Petersen‡, Wenquan Zou‡, Qingzhong Kong‡, Pierluigi Gambetti‡, and Shu G. Chen‡&

From the ‡Institute of Pathology and National Prion Disease Pathology Surveillance Center, Case Western Reserve University, Cleveland, OH 44106; §USDA Agricultural Research Services, Animal Disease Research Unit, Pullman, WA 99164; ¶USDA National Veterinary Services Laboratories, Ames, Iowa 50010; ║Wildlife Health Program, Bureau of Wildlife Management, Wisconsin Department of Natural Resources, Madison, WI 53707 and #Centers for Disease Control and Prevention, National Center for Infectious Diseases, Division of Viral and Rickettsial Diseases, Atlanta, GA 30333.

& To whom correspondence should be addressed: Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106. Tel: (216) 368-8925; Fax: (216) 368-2546; E-mail: shu.chen@case.edu.

Running Title: PrPSc in CWD and CJD

Chronic wasting disease (CWD), a transmissible prion disease that affects elk and deer, poses new challenges to animal and human public health. Although the transmission of CWD to humans has not been proven, it remains a possibility. If this were to occur, it is important to know whether the "acquired" human prion disease would show a phenotype including the scrapie prion protein (PrPSc) features that differ from those associated with human sporadic prion disease. In this study, we have compared the pathological profiles and PrPSc characteristics in brains of CWD-affected elk and deer with that in subjects with sporadic Creutzfeldt-Jakob disease (CJD), as well as CJD-affected subjects who might have been exposed to CWD, using histopathology, immunohistochemistry, immunoblotting, conformation stability assay (CSA) and N-terminal protein sequencing. Spongiform changes and intense PrPSc staining were present in several brain regions of CWD-affected animals. Immunoblotting revealed three proteinase K (PK)-resistant bands in CWD, representing different glycoforms of PrPSc. Following deglycosylation, the unglycosylated PK-resistant PrPSc of CWD migrated at 21kDa with an electrophoretic mobility similar to that of type 1 human PrPSc present in sporadic CJD affecting subjects homozygous for methionine at codon 129 (sCJDMM1). N-terminal sequencing showed that the PK cleavage site of PrPSc in CWD occurred at residues 82 and 78, similar to that of PrPSc in sCJDMM1. Furthermore, CSA also showed no significant difference between elk CWD PrPSc and the PrPSc species associated with sCJDMM1. However, there was a major difference in glycoform ratio of PrPSc between CWD and sCJDMM1 affecting both CWD-exposed and non-exposed subjects. Moreover, PrPSc of CWD exhibited a distinct constellation of glycoforms distinguishable from that of sCJDMM1 in two-dimensional immunoblots. These findings underline the importance of detailed PrPSc characterization in trying to detect novel forms of acquired prion disease. ...

=====================================================
please note that scrapie transmits to primates by there non-forced oral consumption of scrapie tainted material.

J Infect Dis 1980 Aug;142(2):205-8

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis...

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

From: TSS ()
Subject: Re: Interspecies Transmission of Chronic Wasting Disease Prions to
Squirrel Monkeys (Saimiri sciureus)
Date: October 19, 2005 at 11:21 am PST

JOURNAL OURNAL OF VIROLOGY IROLOGY, Nov. 2005, p. 13794–13796 Vol. 79, No.
21
0022-538X/05/$08.00 !0 doi:10.1128/JVI.79.21.13794–13796.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
NOTES
Interspecies Transmission of Chronic Wasting Disease Prions to
Squirrel Monkeys (Saimiri sciureus sciureus)
Richard F. Marsh, 1† Anthony nthony E. Kincaid, 2 Richard A. Bessen, 3 and
Jason C. Bartz Bartz4*
Department of Animal Health and Biomedical Sciences, University of
Wisconsin, Madison 53706 537061; Department of
Physical Therapy Therapy2 and Department of Medical Microbiology and
Immunology, 4 Creighton University, Omaha,
Nebraska 68178; and Department of Veterinary Molecular Biology, Montana
State University, Bozeman, Montana 59718 597183
Received 3 May 2005/Accepted 10 August 2005
Chronic wasting disease (CWD) is an emerging prion disease of deer and elk.
The risk of CWD transmission
to humans following exposure to CWD-infected tissues is unknown. To assess
the susceptibility of nonhuman
primates to CWD, two squirrel monkeys were inoculated with brain tissue from
a CWD-infected mule deer. The
CWD-inoculated squirrel monkeys developed a progressive neurodegenerative
disease and were euthanized at
31 and 34 months postinfection. Brain tissue from the CWD-infected squirrel
monkeys contained the abnormal
isoform of the prion protein, PrP-res, and displayed spongiform
degeneration. This is the first reported
transmission of CWD to primates.
Chronic wasting disease (CWD) is a prion disease of elk and
deer in North America that was first identified at cervid re- research
search facilities in Colorado and Wyoming in the late 1960s
(17, 18). CWD has been identified on cervid game farms from
Montana to New York and has been diagnosed in wild deer
and elk in Colorado, Wyoming, Nebraska, South Dakota, Wis- Wisconsin,
consin, New Mexico, Illinois, and Utah and in Saskatchewan,
Canada (1, 14, 15). The geographic distribution of CWD in
deer and elk has been expanding and will likely result in an
increase in human exposure to the CWD agent. Although
there have been no cases of human prion disease linked to
CWD infection, the risk of interspecies transmission of CWD
to humans following consumption of CWD-infected tissues is
uncertain (5, 13).
One approach to assess the susceptibility of humans to an- animal
imal prion diseases is by experimental transmission to nonhu- nonhuman
man primates (9–11). To investigate the susceptibility of non- nonhuman
human primates to CWD, two adult female squirrel monkeys
(Saimiri sciureus sciureus) were intracerebrally (i.c.) inoculated with 200
"l of a 20% (wt/vol) brain homogenate from a female mule
deer in the clinical phase of CWD (inoculum was a gift from
Elizabeth Williams, Department of Veterinary Sciences, Uni- University
versity of Wyoming, Laramie, WY). Both CWD-inoculated
squirrel monkeys developed a progressive neurological disease
and were euthanized at the terminal stages of disease at 31 and
34 months postinfection, respectively (data on clinical symp- symptoms
toms and the time to onset of disease were not available).
To determine whether the abnormal form of the prion pro- protein,
tein, PrP-res, was present in the CWD-infected squirrel mon- monkeys,
keys, brain homogenates were analyzed by Western blotting as
previously described using the anti-PrP monoclonal antibody
6H4 (Prionics AG, Switzerland) (2). For this analysis, a 5%
(wt/vol) brain homogenate in Dulbecco’s phosphate-buf buffered fered
saline (Mediatech, Inc.) from CWD-infected squirrel monkeys,
a CWD-infected elk, or an uninfected mouse was either di- digested
gested with proteinase K (PK) (4 U/ml; United States Bio- Biochemical)
chemical) fo for 1 h a r at 37°C with agitation or was not digested
with PK. In the samples that were not digested with PK, PrP
migrated between 21 and 35 kDa in the CWD-infected squirrel
monkeys (Fig. 1, lanes 1 and 2) and between 30 and 35 kDa in
the CWD-infected elk (Fig. 1, lane 3) and in the uninfected
mouse sample (Fig. 1, lane 4). In the samples that were di- digested
gested with PK, PrP-res were detected in the two CWD-in- infected
fected squirrel monkeys (Fig. 1, lanes 5 and 6) and in the
CWD-infected elk sample (Fig. 1, lane 7). In the PK-digested
uninfected mouse brain, PrP was not detected (Fig. 1, lane 8),
indicating that PK digestion completely removed the PK-sen- sensitive
sitive isoform of PrP. In both CWD-infected squirrel monkeys,
the migration of the three PrP-res polypeptides on sodium
dodecyl sulfate-polyacrylamide gels was similar. The diglyco- diglycosylated
sylated PrP-res polypeptide migrated at 30 kDa similar to what
has been reported for squirrel monkeys infected with sporadic
Creutzfeldt-Jakob disease (CJD), kuru, and scrapie (4). The
relative abundance of PrP-res in the brain from the squirrel
monkey that was sacrificed at 34 months postinfection (Fig. 1,
lane 5) was greater than that in the squirrel monkey sacrificed
at 31 months postinfection (Fig. 1, lane 6) and may represent
dif differences ferences in the state of disease progression when the
animals
were sacrificed.
Histological examination of the brain, brain stem, and spinal
cord from the squirrel monkey that was euthanized at 31
months postinfection revealed widespread spongiform changes
that are consistent with CWD-induced neurodegeneration.
* Corresponding author. Mailing address: Department of Medical
Microbiology and Immunology, Creighton University, 2500 California
Plaza, Omaha, NE 68178. Phone: (402) 280-1811. Fax: (402) 280-1875.
E-mail: jbartz@creighton.edu.
† Deceased.
13794
Spongiform lesions in the neuropil were predominantly located
in subcortical gray matter structures of the forebrain. There
was widespread spongiform change in the putamen, caudate
nucleus, nucleus accumbens, lateral and medial hypothalamus,
hippocampal formation (CA 1), amygdala, and dorsomedial
thalamus (Fig. 2). Dif Diffuse fuse spongiosis was found in the interpe-
interpeduncular
duncular nucleus and substantia nigra in the midbrain and in
the reticular formation of the pons and medulla. Due to the
limited number of histological sections, a detailed comparison
of the neuropathology in CWD-infected squirrel monkeys and
other prion transmission studies in squirrel monkeys was not
possible.
The time to terminal disease following inoculation of squir- squirrel
rel monkeys with the CWD agent, 31 and 34 months, was
longer than for squirrel monkeys that were i.c. inoculated with
transmissible mink encephalopathy agent (9 to 12 months) and
scrapie agent (16 months) but is within the reported range of
the time to terminal disease following i.c. inoculation with
sporadic CJD (11 to 37 months) and kuru (10 to 48 months) (6,
8). This variation in disease progression following experimen- experimental
tal transmission of sporadic CJD, kuru, and CWD to squirrel
monkeys could be due to dif differences ferences in the inoculation dose,
strain of the prion agent, or the ability to establish infection
upon interspecies transmission. Regardless, this study illus- illustrates
trates that a nonhuman primate can develop a prion disease
following i.c. inoculation with a brain homogenate from a
CWD-infected mule deer.
Direct comparison of the ability of the CWD agent to cause
disease in squirrel monkeys following experimental i.c. inocu- inoculation
lation and the susceptibility of humans to CWD infection must
be interpreted with caution. Although squirrel monkeys are
susceptible to experimental infection with kuru and CJD, they
are also susceptible to experimental infection with scrapie (8),
and there is no epidemiological evidence to suggest that
scrapie can be transmitted to humans (16). These data suggest,
following direct cerebral inoculation, squirrel monkeys may
not be a good experimental model for assessing human sus- susceptibility
ceptibility to animal prion diseases. Oral exposure is the likely
natural route of human exposure to CWD, and in experimental
animals, this route is much less ef efficient ficient at causing disease
than
i.c. inoculation (3, 7, 12). Therefore, the ability of scrapie and
CWD to cause disease in primates by oral infection needs to be
established to further resolve the issue of susceptibility of hu- humans
mans to CWD infection.
Richard Marsh, who performed the experimental transmission of
CWD to squirrel monkeys, died in 1997 before these experiments were
completed. Due to the emergence of CWD in deer and elk and the
potential risk for CWD transmission to humans, we present his find- findings
ings with additional tissue analysis.
We thank Al Jenny, USDA-APHIS-VS-NVSL for the gift of the
CWD-infected elk tissue.
We dedicate the manuscript to Elizabeth Williams for her pioneer- pioneering
ing work on CWD.
REFERENCES
1. Animal and Plant Health Inspection Services, Marketing and Regulatory
Programs, U.S. Department of Agriculture. 2005. [Online.] http://www.aphis
.usda.gov/vs/nahps/cwd/cwd-distribution.html.
FIG. 1. Deposition of the abnormal isoform of the prion protein,
PrP-res, in the brain of squirrel monkeys inoculated with chronic
wasting disease. Western blot analysis of 250- "g tissue equivalents of
brain homogenates digested with proteinase K or not digested with
proteinase K was performed. The brain homogenates were from a
CWD-infected squirrel monkey that was sacrificed at 34 months (lanes
1 and 5) or at 31 months postinfection (lanes 2 and 6), a CWD-infected
elk (lanes 3 and 7), and an uninfected mouse (lanes 4 and 8). The
arrow indicates the location of the 29-kDa molecular mass marker.
FIG. 2. Spongiform degeneration in brain tissue from a squirrel
monkey inoculated with chronic wasting disease and euthanized at 31
months postinfection. (A) Low-power view of the lentiform nucleus,
showing the distribution of spongiform changes in the putamen (Pu)
and lack of spongiosis in the globus pallidus (Gp). Ac, anterior com-
commissure.
missure. (B) High-power view of the area outlined in panel A that
exhibits widespread spongiosis. Bars # 100 microns.
VOL OL. 79, 2005 NOTES 13795
2. Bartz, J. C., J. M. Aiken, and R. A. Bessen. 2004. Delay in onset of
prion
disease for the HY strain of transmissible mink encephalopathy as a result
of
prior peripheral inoculation with the replication-deficient DY strain. J.
Gen.
Virol. 85: 265–273.
3. Bartz, J. C., A. E. Kincaid, and R. A. Bessen. 2003. Rapid prion
neuroinva- neuroinvasion
sion following tongue infection. J. Virol. 77: 583–591.
4. Beekes, M., E. Baldauf, S. Cassens, H. Diringer, P. Keyes, A. C. Scott,
G. A.
Wells, P. Brown, C. J. Gibbs, Jr., and D. C. Gajdusek. 1995. Western blot
mapping of disease-specific amyloid in various animal species and humans
with transmissible spongiform encephalopathies using a high-yield purifica-
purification
tion method. J. Gen. Virol. 76: 2567–2576.
5. Belay, E. D., P. Gambetti, L. B. Schonberger, P. Parchi, D. R. Lyon, S.
Capellari, J. H. McQuiston, K. Bradley, G. Dowdle, J. M. Crutcher, and
C. R. Nichols. 2001. Creutzfeldt-Jakob disease in unusually young patients
who consumed venison. Arch. Neurol. 58: 1673–1678.
6. Brown, P., C. J. Gibbs, Jr., P. Rodgers-Johnson, D. M. Asher, M. P.
Sulima,
A. Bacote, L. G. Goldfarb, and D. C. Gajdusek. 1994. Human spongiform
encephalopathy: the National Institutes of Health series of 300 cases of
experimentally transmitted disease. Ann. Neurol. 35: 513–529.
7. Diringer, H., J. Roehmel, and M. Beekes. 1998. Ef Effect fect of repeated
oral
infection of hamsters with scrapie. J. Gen. Virol. 79: 609–612.
8. Gibbs, C. J., Jr., and D. C. Gajdusek. 1973. Experimental subacute
spongi- spongiform
form virus encephalopathies in primates and other laboratory animals. Sci-
Science
ence 182: 67–68.
9. Gibbs, C. J., Jr., and D. C. Gajdusek. 1972. Transmission of scrapie to
the
cynomolgus monkey (Macaca fascicularis). Nature 236: 73–74.
10. Lasmezas, C. I., J. P. Deslys, R. Demaimay, K. T. Adjou, F. Lamoury, D.
Dormont, O. Robain, J. Ironside, and J. J. Hauw. 1996. BSE transmission to
macaques. Nature 381: 743–744.
11. Lasmezas, C. I., J. G. Fournier, V. Nouvel, H. Boe, D. Marce, F.
Lamoury, N.
Kopp, J. J. Hauw, J. Ironside, M. Bruce, D. Dormont, and J. P. Deslys. 2001.
Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt-Jakob disease: implications for human health.
Proc. Natl. Acad. Sci. USA 98: 4142–4147.
12. Prusiner, S. B., S. P. Cochran, and M. P. Alpers. 1985. Transmission of
scrapie in hamsters. J. Infect. Dis. 152: 971–978.
13. Raymond, G. J., A. Bossers, L. D. Raymond, K. I. O’Rourke, L. E. McHol-
McHolland,
land, P. K. Bryant, 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. EMBO J. 19: 4425–4430.
14. Sigurdson, C. J., and M. W. Miller. 2003. Other animal prion diseases.
Br.
Med. Bull. 66: 199–212.
15. Spraker, T. R., M. W. Miller, E. S. Williams, D. M. Getzy, W. J. Adrian,
G. G. Schoonveld, R. A. Spowart, K. I. O’Rourke, J. M. Miller, and P. A.
Merz. 1997. Spongiform encephalopathy in free-ranging mule deer
(Odocoileus hemionus), white-tailed deer (Odocoileus virginianus) and
Rocky Mountain elk (Cervus elaphus nelsoni) in northcentral Colorado.
J. Wildl. Dis. 33: 1–6.
16. van Duijn, C. M., N. Delasnerie-Laupretre, C. Masullo, I. Zerr, R. de
Silva,
D. P. Wientjens, J. P. Brandel, T. Weber, V. Bonavita, M. Zeidler, A. Alp-
Alperovitch,
erovitch, S. Poser, E. Granieri, A. Hofman, R. G. Will, and European Union
(EU) Collaborative Study Group of Creutzfeldt-Jakob disease (CJD). 1998.
Case-control study of risk factors of Creutzfeldt-Jakob disease in Europe
during 1993–95. Lancet 351: 1081–1085.
17. Williams, E. S., and S. Young. 1980. Chronic wasting disease of captive
mule
deer: a spongiform encephalopathy. J Wildl. Dis. 16: 89–98.
18. Williams, E. S., and S. Young. 1982. Spongiform encephalopathy of Rocky
Mountain elk. J. Wildl. Dis. 18: 465–471.
13796 NOTES J. VIROL IROL.TSS

Journal of Wildlife Diseases, 41(3), 2005, pp. 503-511
© Wildlife Disease Association 2005
RELATIVE VULNERABILITY OF CHRONIC WASTING DISEASE INFECTED MULE DEER TO
VEHICLE COLLISIONS
Caroline E. Krumm1,2, Mary M. Conner3 and Michael W. Miller1,4
1 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect
Road, Fort Collins, Colorado 80526-2097, USA
2 Natural Resource Ecology Laboratory, Colorado State University, Fort
Collins, Colorado 80523, USA
3 Department of Forest, Range, and Wildlife Sciences, Utah State University,
Logan, Utah 84322, USA
4 Corresponding author (email: mike.miller@state.co.us)

ABSTRACT: We estimated chronic wasting disease (CWD) prevalence among
vehicle-killed mule deer (Odocoileus hemionus) in select data analysis units
(DAUs) in northern Colorado, USA, and compared these with estimated CWD
prevalence among mule deer of the same sex sampled in the vicinity of
collision sites to assess relative vulnerability of CWD-infected individuals
to vehicle collisions. Twenty-five of 171 vehicle-killed mule deer tested
positive for CWD (overall prevalence=0.146, 95% confidence interval
[CI]=0.097–0.208); 173 of 2,317 deer sampled in the vicinity of these
vehicle-killed deer tested positive (overall prevalence=0.075, 95%
CI=0.064–0.085). In nine of ten DAUxsex comparisons, relative risk of CWD
infection tended to be higher among vehicle-killed deer (range of estimated
relative risks=1.6–15.9). Spongiform encephalopathy was detected in 12 of 20
(60%; 95% CI=39–81%) CWD-positive deer killed by vehicles and in 79 of 180
(44%; 95% CI=37–52%) CWD-positive deer detected via random sampling
(relative risk=1.37; 95% CI=0.92–2.03), suggesting that infected deer killed
by vehicles tended to be in later stages of disease than those killed by
hunters. Our data offer evidence that CWD-infected mule deer may be
relatively vulnerable to vehicle collisions. It follows that sampling of
vehicle-killed mule deer may be exploited to increase efficiency of
surveillance programs designed to detect new foci of CWD infection;
moreover, evidence of increased susceptibility to vehicle collisions may aid
in understanding vulnerability of CWD-infected individuals to other forms of
death, particularly predation.
Key words: Chronic wasting disease (CWD), mule deer, Odocoileus hemionus,
predator-prey, prion, surveillance, transmissible spongiform encephalopathy,
vehicle collision.

http://www.jwildlifedis.org/cgi/content/abstract/41/3/503maxtoshow=&HITS...

The common practice of feeding
herbivore deer back to other deer, especially in the captive deer population
is seen as a
major route for spreading CWD. In 1995 alone, Wisconsin Department of
Natural
Resources (DNR) records show that 26,488 road-killed Wisconsin deer were
rendered into
feed. This feed was used to feed other ruminants, notably cattle and other
deer. Since there
was nothing remarkable about 1995, this figure can be taken as an annual
road-kill average
in Wisconsin. If any of the 26,488 animals was infected with CWD, then CWD
was passed
via the rendering process to both deer and cattle. And, lest there be doubt
that CWD can
transmit to cattle, a recently published experimental study has
unequivocally demonstrated
transmission of the CWD agent to cattle by intra-cerebral inoculation (26).

http://www.nidsci.org/pdf/cattledeaths_tse_epidemic.pdf

-
-0 nra NATlONAL RENDERERS ASSOCIATION, Inc.
. Sutte 207 . 4 3 4 3 ,03 8O&b~h,Fal~ 3~’ Alexandria, Virgmta 22314
TEL. (703) 683-0155 . FAX. (703) 683-2626
OFFICES: WASHINGTON, DC . LONDON . HONG KONG . MEXICOCITY
July 7,2003
Dockets Management Branch (HFA-305)
Food and Drug Administration
5630 Fishers Lane
Room 1061
Rockville, MD 20852
RE: Docket Number 030-0186
“Guidance for Industry: use of Material.from Deer and Elk in Animal Feed”
To Whom it May Concern:
The National Renderers Association appreciates the opportunity to submit our
comments in response to the draft guidance published May 14,2003 by the Food
and
Drug Administration concerning the use of material from deer and elk in
animal feed.
The National Renderers Association is the trade association for the
rendering
industry in the United States and Canada. There are 41 member companies that
operate
183 rendering plants throughout the United States and Canada. Of our 4 1
member
companies, 35 are independent renderers and six are packer renderers.
- We represent well over 95% of the independent rendering industry in the
United
States and Canada.
The leadership of the NRA has met several times with FDA and CVM officials
regarding the Chronic Wasting Disease (CWD) issue. We have offered our input
in the
disposal of deer and elk.
Rendered deer and elk represent a very small portion of the raw material
processed by renderers every year. In fact many renderers do not render this
material at
all. However, rendering deer and elk during hunting seasons is very
important for several
renderers as they are providing a service to their regular processor
suppliers. The volume
of raw material is significant in some areas.
The NRA was invited by the FDA-CVM to participate at a CWD Workshop on
May 16,2003 at Rockville, Maryland. Several NRA members who are directly
involved
with the disposal of deer and elk in states where CWD is known to exist
attended and
participated at this workshop. We ask that their comments and presentations
be
considered as part of our comments to this draft guidance.
The NRA believes the BSE feed regulation (21 CFR 589.2000) was promulgated
for the purpose of prohibiting certain feeds for ruminant animals. We
believed this was
to include deer and elk. However, FDA has determined otherwise as it relates
to CWD.
The FDA has now determined that material from CWD-positive animals may not
be used in any animal feed or feed ingredients. It also recommends that
material from
animals from high-risk areas no longer be entered into the animal feed
system.
We appreciate that FDA in section V of the draft guidance continues to
consider
materials from deer and elk not considered at high risk for CWD to be
acceptable for use
in non-ruminant animal feeds in accordance with current agency regulations
21 CFR
589.2000.
We do question why animals from high-risk areas that test negative to CWD
would not be eligible to be in accordance with the feed regulation as well.
NRA members are making individual decisions on the handling of deer and elk.
Our members who choose to continue rendering deer and elk are aware of the
draft
guidance and will be in accordance.
Additional rules and regulations are not necessary and we do not recommend
any
further rulemaking beyond the guidance.
If we can be of any further assistance, please feel free to call on us.
Sincerely,
President

http://www.fda.gov/ohrms/dockets/dailys/03/jul03/071703/03d-0186-c000005...
vol1.pdf

http://www.fda.gov/cvm/guidance/dguide158.pdf.

http://www.fda.gov/bbs/topics/ANSWERS/2003/ANS01220.html

CONTAINS NON-BINDING RECOMMENDATIONS
158
Guidance for Industry
Use of Material from Deer and Elk in Animal Feed
DRAFT GUIDANCE
This draft guidance is being distributed for comment purposes only.
Comments and suggestions regarding this draft guidance should be sent to
the Dockets
Management Branch (HFA-305), Food and Drug Administration, 5630 Fishers
Lane,
Room 1061, Rockville, MD 20852. Comments may also be submitted
electronically on
the Internet at http://www.fda.gov/dockets/ecomments. Once on this
Internet site, select
"[03D-0186][Use of Material from Deer and Elk in Animal Feed]" and
follow the
directions. All written comments should be identified with Docket No.
03D-0186.
For questions regarding this draft document, contact Burt Pritchett,
Center for Veterinary
Medicine (HFV- 222), Food and Drug Administration, 7500 Standish Place,
Rockville,
MD 20855, 301-827-0177. E-mail: bpritche@cvm.fda.gov
Additional copies of this draft guidance document may be requested from the
Communications Staff (HFV-12), Center for Veterinary Medicine, Food and Drug
Administration, 7500 Standish Place, Rockville, MD 20855, and may be
viewed on the
Internet at http://www.fda.gov/cvm.
U.S. Department of Health and Human Services
Food and Drug Administration
Center for Veterinary Medicine
May 14, 2003
CONTAINS NON-BINDING RECOMMENDATIONS
1
158
Guidance for Industry1
Use of Material from Deer and Elk in Animal Feed
I. Introduction
FDA’s guidance documents, including this guidance, do not establish legally
enforceable responsibilities. Instead, guidances describe the Agency’s
current
thinking on a topic and should be viewed only as recommendations, unless
specific regulatory or statutory requirements are cited. The use of the word
“should” in Agency guidances means that something is suggested or
recommended, but not required.
Under FDA’s BSE feed regulation (21 CFR 589.2000) most material from
deer and elk is
prohibited for use in feed for ruminant animals. This draft guidance
document describes
FDA’s recommendations regarding the use in all animal feed of all
material from deer and
elk that are positive for Chronic Wasting Disease (CWD) or are
considered at high risk for
CWD. The potential risks from CWD to humans or non-cervid animals such
as poultry and
swine are not well understood. However, because of recent recognition
that CWD is
spreading rapidly in white-tailed deer, and because CWD’s route of
transmission is poorly
understood, FDA is making recommendations regarding the use in animal
feed of rendered
materials from deer and elk that are CWD-positive or that are at high
risk for CWD.
II. Background
CWD is a neurological (brain) disease of farmed and wild deer and elk
that belong in the
animal family cervidae (cervids). Only deer and elk are known to be
susceptible to CWD
by natural transmission. The disease has been found in farmed and wild
mule deer,
white-tailed deer, North American elk, and in farmed black-tailed deer.
CWD belongs to
a family of animal and human diseases called transmissible spongiform
encephalopathies
1 This draft guidance has been prepared by the Division of Animal Feeds
in the Center for Veterinary Medicine
(CVM) at the Food and Drug Administration.
This draft guidance, when finalized, will represent the Food and Drug
Administration’s current thinking on the use of material from deer and elk
in animal feed. It does not create or confer any rights for or on any person
and does not operate to bind FDA or the public. You can use an alternative
approach if the approach satisfies the requirements of applicable
statutes or
regulations. If you want to discuss an alternative approach, contact the FDA
staff responsible for implementing this guidance. If you cannot identify the
appropriate FDA staff, call the appropriate number listed on the title
page of
this guidance.
CONTAINS NON-BINDING RECOMMENDATIONS
2
(TSEs). These include bovine spongiform encephalopathy (BSE or “mad cow”
disease)
in cattle; scrapie in sheep and goats; and classical and variant
Creutzfeldt-Jakob diseases
(CJD and vCJD) in humans. There is no known treatment for these
diseases, and there is
no vaccine to prevent them. In addition, although validated postmortem
diagnostic tests
are available, there are no validated diagnostic tests for CWD that can
be used to test for
the disease in live animals.
III. Use in animal feed of material from CWD-positive deer and elk
Material from CWD-positive animals may not be used in any animal feed or
feed
ingredients. Pursuant to Sec. 402(a)(5) of the Federal Food, Drug, and
Cosmetic Act,
animal feed and feed ingredients containing material from a CWD-positive
animal would
be considered adulterated. FDA recommends that any such adulterated feed
or feed
ingredients be recalled or otherwise removed from the marketplace.
IV. Use in animal feed of material from deer and elk considered at high
risk for CWD
Deer and elk considered at high risk for CWD include: (1) animals from
areas declared
by State officials to be endemic for CWD and/or to be CWD eradication
zones; and (2)
deer and elk that at some time during the 60-month period immediately
before the time of
slaughter were in a captive herd that contained a CWD-positive animal.
FDA recommends that materials from deer and elk considered at high risk
for CWD no
longer be entered into the animal feed system. Under present
circumstances, FDA is not
recommending that feed made from deer and elk from a non-endemic area be
recalled if a
State later declares the area endemic for CWD or a CWD eradication zone.
In addition,
at this time, FDA is not recommending that feed made from deer and elk
believed to be
from a captive herd that contained no CWD-positive animals be recalled
if that herd is
subsequently found to contain a CWD-positive animal.
V. Use in animal feed of material from deer and elk NOT considered at
high risk
for CWD
FDA continues to consider materials from deer and elk NOT considered at
high risk for
CWD to be acceptable for use in NON-RUMINANT animal feeds in accordance with
current agency regulations, 21 CFR 589.2000. Deer and elk not considered
at high risk
include: (1) deer and elk from areas not declared by State officials to
be endemic for
CWD and/or to be CWD eradication zones; and (2) deer and elk that were
not at some
time during the 60-month period immediately before the time of slaughter
in a captive
herd that contained a CWD-positive animal.

http://www.fda.gov/cvm/guidance/dguide158.pdf

FDA Issues Draft Guidance on Deer and Elk in Animal Feed, Hosts Industry
Meeting

The Food and Drug Administration (FDA) announced the availability of a draft
guidance for industry entitled, “Use of Material from Deer and Elk in Animal
Feed.” It is similar to the guidance issued last year. When finalized, the
guidance document will describe FDA’s recommendations regarding the use of
all material from deer and elk that are positive, or at high risk, for
chronic wasting disease (CWD), a neurological disease of farmed and wild
deer and elk that belong in the cervidae animal family. The draft guidance
recommends that any material from CWD-positive animals, or deer and elk
considered to be at high risk for CWD, not be used in any animal feed or
feed ingredients. Presently, under FDA’s bovine spongiform encephalopathy
feed regulation (21 CFR 589.2000), most material from deer and elk is
prohibited for use in feed for ruminant animals. FDA anticipates finalizing
the document in late August, prior to the start of the next deer hunting
season.

According to the document, the potential risks from CWD to humans or
non-cervid animals such as poultry or swine are not well understood.
However, because of recent recognition that CWD is spreading rapidly in
white-tailed deer and because the disease’s route of transmission is poorly
understood, the FDA is making the additional feed ban recommendations.

The FDA Center for Veterinary Medicine (CVM) hosted a daylong meeting in May
2003 that included representatives from the National Renderers Association
(NRA), federal and state regulatory officials from the FDA, U.S. Department
of Agriculture, Department of Interior, Environmental Protection Agency,
Colorado, Illinois, Indiana, Minnesota, New Mexico, Wisconsin, and Wyoming,
along with the Canadian Food Inspection Agency. The purpose of the meeting
was to review the missteps that were taken in the fall of 2002 regarding
CWD.

According to CVM Director Stephen Sundlof, the agency wanted to make the
2003 hunting season smoother. Key issues discussed were rendering, state
surveillance programs, and improper disposal. Representing the NRA were
Second Vice Chairman Dave Kaluzny II, Immediate Past Chairman Mike
Langenhorst, Mark Myers and David Kirstein, both of National By-Products,
Inc., Ross Hamilton and Matt Taylor, both of Darling International, Inc.,
and NRA staff members Tom Cook and Dr. Peter Nersessian.

Copies of the draft guidance document are available on the CVM home page at
http://www.fda.gov/cvm, or from the Dockets Management Branch Web site at
http://www.fda.gov/ohrms/dockets/default.htm.

August 2003 Render

http://www.rendermagazine.com/August2003/FDAIssuesDraftGuidance.html

December 2002 Render

http://www.rendermagazine.com/December2002/CWDPostiveAnimals.html

The Food and Drug Administration issued an order this week telling rendering
companies to avoid deer and elk carcasses from endemic areas. The rendering
companies that pick up carcasses from local meat lockers say they won't sort
the deer, so they won't pick up any.

http://news.minnesota.publicradio.org/features/200211/19_hetlandc_sodakcwd/

Oregon

http://www.dfw.state.or.us/OARs/200.pdf

As a Processor, How Can I Dispose of Deer?
Three rendering companies currently plan to pickup inedible venison at
processing plants.
1.) Superior Services, Sheboygan, WI 888-688-4005 ext. 159 Attn: Paul
Herrmann
2.) National By-Products, Berlin, WI 920-361-2092
3.) Darling International, Blue Earth, MN 507-526-3296

http://www.dnr.state.wi.us/org/land/wildlife/Whealth/issues/Cwd/CWDfacts...

Guidelines for Rendering Carcasses

The following is a list of unacceptable species and materials for rendering
carcasses with National By-Products, Inc.

Unacceptable Species
All animal species shall be accepted EXCEPT:

* Adult sheep and goats
* Dogs and cats
* Deer or elk tested positive for Chronic Wasting Disease (CWD).
* Deer or elk originating from endemic areas or eradication zones for
CWD as specified by the Department of Natural Resources, unless they have
been tested negative for CWD.
* Cattle tested positive for Bovine Spongiform Encephalopathy (BSE).

WHAT ABOUT SUB-CLINICAL TSEs ???...TSS

* Animals inoculated with infectious agents.
* Transgenic animals, potentially transgenic animals, "no-takes" in the
production of transgenic animals, and off-spring of transgenic animals.
* Small research animals (e.g., rabbits, rats, mice, birds, etc.)
* Human tissues and organs.

http://www.iacuc.uiuc.edu/rendering.html

RENDERING ALTERNATIVES FOR DEER PROCESSORS
BY STEVE KRUT
November 13, 2002
On November 12, the Center for Veterinary Medicine, a component of the U.S.
Food & Drug Administration,
issued a notice that materials from deer or elk that have or are likely to
have Chronic Wasting Disease (CWD) cannot
be used as an ingredient in feed for any animal species.
An immediate result was that a significant part of the rendering industry
told customers they would not pick up any
materials from cervids. Game processors were left scrambling for disposal
alternatives.
The FDA notice said the prohibition against deer or elk materials in animal
feeds would apply to cervids which tested
positive for CWD, farm-raised herds which tested positive, free-ranging
animals from endemic areas in Colorado and
Wyoming, deer from the eradication zone in Wisconsin and deer from any new
area designated as having shown
CWD infection. Renderers, concerned they could not be certain that any deer
or elk are CWD free without testing, sent
statements to processors they would not pick up any bone or other material
from deer or elk. The FDA, while not
demonstrating any scientific evidence that CWD can be harmful to humans or
to animals, such as cattle or hogs,
termed its directive “prudent.”
The most common alternative for processors to dispose of this material is an
approved landfill. These facilities are
sealed so that they can decompose the material and not have it, or the prion
which supposedly carries CWD, leach
into the ground water system. Most landfills are municipally operated and
their decision on whether to accept such
materials is determined by the state agency responsible for environmental
protection.
AAMP has contacted the U.S. Environmental Protection Agency to secure a
letter asserting that the agency has no
problem with this disposal method. However, game processors should protect
themselves by obtaining permission for
dumping cervid materials in the landfill. Transportation to these facilities
must be accomplished in sealed containers,
which may require a permit in some jurisdiction. This is to assure no
leakage of materials during transport. Dumpsters
could be used, but AAMP strongly suggests notifying the hauling company or
landfill that deer or elk materials will be
deposited and obtaining permission.
Burying materials on private land or on unapproved sites may violate local,
state or federal laws.
Some processors have considered accepting only boneless venison for further
processing to eliminate disposal
problems. Others have suggested returning bone and other waste materials to
the hunter. Both of these concepts
may solve the problem for the plant operator, but may accelerate the CWD
problem by having waste materials
dispersed in open fields, near watercourses or in unacceptable places by
hunters who have not disposal sites.
Special Report
P.O. Box 269, Elizabethtown, PA 17022
Phone: 717/367-1168 Fax: 717/367-9096
Web: http://www.aamp.com Email: aamp@aamp.com
Another approach for disposal may be composting. AAMP can provide a list of
existing composting sites (check the
AAMP website http://www.aamp.com for updates).
Individuals interested in developing their own composting operations may
obtain additional information from a
composting video produced by Cornell University with sponsorship from AAMP.
The video is priced at $25 plus $5
shipping and handling and can be ordered through the AAMP office.
Some states and universities have waste reduction systems that use a
chemical process to digest the materials
quickly and kill and CWD prion. For more information on this process, check
out the Agri-Lyzer heading on the
AAMP website.
These systems are now produced in smaller sizes and can be transported on a
small trailer. Priced in the $60,000
to $80,000 range, they could be utilized by multiple plants and could serve
as an off-season income source for
disposal of road kill, dead pets, restaurant grease, or even bio-hazard
materials.
AAMP is continuing to press for government assistance with CWD research,
control, and disposal concerns.

http://www.aamp.com/foodsafety/documents/RenderingAlternatives.pdf

CWD was first recognized in 1967 in captive deer on a Colorado wildlife
research facility. It occurs endemically in wild deer in contiguous sections
of northcentral Colorado and southeastern Wyoming and episodically on elk
farms along the eastern border states of the Rocky Mountains. No disease in
humans or other animals has been attributed to CWD, but the potential for
disease is very real: infected tissues could be eaten by predators or
enjoyed by aficionados of wild game, and carcasses could be rendered for
feed that (by error) could find its way to cattle. Regional hunters and elk
farmers have been alerted to the risks, but more attention at the national
level is urgently needed.

http://www.cdc.gov/ncidod/eid/vol7no3_supp/brown.htm

Pennsylvania’s
Chronic Wasting Disease
Response Plan
September 2005

Vehicle-killed deer have traditionally been picked up by PGC
employees/volunteers and PENN DOT contractors and taken to rendering plants
or to local
landfills. Although deer disposal pits were widely used in the 1970s and
1980s, their use is
limited today.

http://www.agriculture.state.pa.us/agriculture/lib/agriculture/animalhea...
iles/chronicwastingresponseplanjuly05.pdf

-------- 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

Six white-tailed deer fawns test positive for CWD

MADISON -- Six fawns in the area of south central Wisconsin where
chronic wasting disease has been found in white-tailed deer have tested
positive for the disease, according to Department of Natural Resources
wildlife health officials. These are the youngest wild white-tailed deer
detected with chronic wasting disease (CWD) to date.

Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of
fawns sampled were between the ages of 5 to 9 months, though some were
as young as 1 month. Two of the six fawns with CWD detected were 5 to 6
months old. All six of the positive fawns were taken from the core area
of the CWD eradication zone where the highest numbers of positive deer
have been identified.

snip...

http://www.dnr.state.wi.us/org/caer/ce/news/on/2003/on20030513.htm#art4

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

Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH
FINDINGS RELEVANT TO CJD AND BSE

A team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the
National Academy of Sciences, on new evidence for the existence of a
'sub-clinical' form of BSE in mice which was unknown until now.

The scientists took a closer look at what is known as the 'species
barrier' - the main protective factor which limits the ability of
prions2 to jump from one species to infect another. They found the mice
had a 'sub-clinical' form of disease where they carried high levels of
infectivity but did not develop the clinical disease during their normal
lifespan. The idea that individuals can carry a disease and show no
clinical symptoms is not new. It is commonly seen in conventional
infectious diseases.

Researchers tried to infect laboratory mice with hamster prions3 called
Sc237 and found that the mice showed no apparent signs of disease.
However, on closer inspection they found that the mice had high levels
of mouse prions in their brains. This was surprising because it has
always been assumed that hamster prions could not cause the disease in
mice, even when injected directly into the brain.

In addition the researchers showed that this new sub-clinical infection
could be easily passed on when injected into healthy mice and hamsters.

The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of
prions. While some barriers are quite small (for instance BSE easily
infects mice), other combinations of strain and species show a seemingly
impenetrable barrier. Traditionally, the particular barrier studied here
was assumed to be robust.

Professor John Collinge said: "These results have a number of important
implications. They suggest that we should re-think how we measure
species barriers in the laboratory, and that we should not assume that
just because one species appears resistant to a strain of prions they
have been exposed to, that they do not silently carry the infection.
This research raises the possibility, which has been mentioned before,
that apparently healthy cattle could harbour, but never show signs of, BSE.

"This is a timely and unexpected result, increasing what we know about
prion disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best
to safeguard health and reduce the risk that theoretically, prion
disease could be contracted through medical and surgical procedures."

ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS
SET BY THE JOURNAL.

FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011
(OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR
PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO
TRAVEL COMMITME

Offline
Joined: 01/01/2006
Posts: 230
CWD in Wisconsin

snip...

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

CWD/TSEs & ENVIRONMENT CONTAMINATION

I believe it to be very irresponsible to dispose
of clinical/sub-clinial cases of CWD or any animal
with TSEs in landfills...

TSS

Aguzzi warns of CWD danger

The TSE family of diseases also includes chronic wasting disease (CWD)
in deer, a condition that has spread in the US in recent years (Nature
416, 569; 2002). Speaking at the Days of Molecular Medicine conference
in La Jolla in March, prion expert Adriano Aguzzi issued a strong
warning against underestimating this form of TSE.

"For more than a decade, the US has by-and-large considered mad cows
to be an exquisitely European problem. The perceived need to protect
US citizens from this alien threat has even prompted the deferral of
blood donors from Europe," he said. "Yet the threat-from-within
posed by CWD needs careful consideration, since the evidence that CWD
is less dangerous to humans than BSE is less-than-complete. Aguzzi
went on to point out that CWD is arguably the most mysterious of all
prion diseases.

"Its horizontal spread among the wild population is exceedingly
efficient, and appears to have reached a prevalence unprecedented even
by BSE in the UK at its peak. The pathogenesis of CWD, therefore,
deserves a vigorous research effort. Europeans also need to think
about this problem, and it would be timely and appropriate to increase
CWD surveillance in Europe too." Aguzzi has secured funding from the
National Institutes of Health to investigate CWD, and the effort will
be lead by Christina Sigurdson in his department at the University of
Zurich. KAREN BIRMINGHAM, LONDON

This quote from Dr. Gambetti is especially significant since he is the
rather cautious TSE researcher under contract with the Centers for Disease
Control to examine the brains of individuals who have died of CJD.
-----------------

Pierluigi Gambetti, director of the National Prion Disease Pathology
Surveillance Center at Case Western Reserve University in Cleveland,
said all deer should be tested for chronic wasting disease before any
processing is done.

"There is no way around it," he said. "Nobody should touch that meat
unless it has been tested."

http://www.ledger-enquirer.com/mld/...ion/3954298.htm

TSEs And The Environment

The LANCET
Volume 351, Number 9110 18 April 1998

BSE: the final resting place

How to dispose of dangerous waste is a question that has vexed the human
race for hundreds of years. The answer has usually been to get it out of
sight--burn it or bury it. In Periclean Athens, victims of the plague
were incinerated in funeral pyres; in 14th century Venice, a law
stipulated that Black Death corpses should be buried to a minimum depth
of 5 feet; and now, as the 20th century draws to a close, we are
challenged by everything from industrial mercury to the smouldering
reactors of decommissioned atomic submarines.

The Irish Department of Agriculture will convene an expert panel on
April 27-29 to discuss the disposal of tissues from animals with bovine
spongiform encephalopathy (BSE). Proper disposal of tissues from
infected cattle has implications for both human and animal safety.
Safety for human beings is an issue because there is now unassailable if
still indirect evidence that BSE causes infections in man in the form of
"new variant" Creutzfeld-Jakob disease (nvCJD).1-3 Safety for animals is
also an issue because BSE-affected cattle could possibly transmit
disease to species other than cattle, including sheep, the species that
was almost surely the unwitting source of the BSE epidemic.

The first matter to consider is the distribution of infectivity in the
bodies of infected animals. The brain (and more generally, the central
nervous system) is the primary target in all transmissible spongiform
encephalopathies (TSE), and it contains by far the highest concentration
of the infectious agent. In naturally occuring disease, infectivity may
reach levels of up to about one million lethal doses per gram of brain
tissue, whether the disease be kuru, CJD, scrapie, or BSE. The
infectious agent in BSE-infected cattle has so far been found only in
brain, spinal cord, cervical and thoracic dorsal root ganglia,
trigeminal ganglia, distal ileum, and bone marrow.4 However, the much
more widespread distribution of low levels of infectivity in human
beings with kuru or CJD, and in sheep and goats with scrapie, suggests
that caution is advisable in prematurely dismissing as harmless other
tissues of BSE-infected cattle.

A second consideration relates to the routes by which TSE infection can
occur. Decades of accumulated data, both natural and experimental, have
shown clearly that the most efficient method of infection is by direct
penetration of the central nervous system; penetration of peripheral
sites is less likely to transmit disease. Infection can also occur by
the oral route, and the ingestion of as little as 1 g of BSE brain
tissue can transmit disease to other cattle.5 Infection by the
respiratory route does not occur (an important consideration with
respect to incineration), and venereal infection either does not occur
or is too rare to be detected.

How can tissue infectivity be destroyed before disposal? The agents that
cause TSE have been known almost since their discovery to have awesome
resistance to methods that quickly and easily inactivate most other
pathogens. Irradiation, chemicals, and heat are the three commonest
inactivating techniques. Irradiation has proved entirely ineffective,
and only a handful of a long catalogue of chemicals have produced more
than modest reduction in infectivity. The most active of these are
concentrated solutions of sodium hypochlorite (bleach) or sodium
hydroxide (lye). As for heat, even though the agent shares with most
other pathogens the feature of being more effectively damaged by wet
heat than by dry heat, boiling has little effect, and steam heat under
pressure (autoclaving) at temperatures of 121ºC is not always
sterilising. To date, the most effective heat kill requires exposure of
infectious material to steam heat at 134ºC for 1 h in a porous-load
autoclave.6 Exposure to dry heat even at temperatures of up to 360ºC for
1 h may leave a small amount of residual infectivity.7 The standard
method of incineration, heating to about 1000ºC for at least several
seconds, has been assumed to achieve total sterilisation, but needs
experimental verification in the light of suggestions that rendered
tissue waste might find some useful purpose as a source of heating fuel.

Thus, TSE agents are very resistant to virtually every imaginable method
of inactivation, and those methods found to be most effective may, in
one test or another, fail to sterilise. It seems that even when most
infectious particles succumb to an inactivating process, there may
remain a small subpopulation of particles that exhibit an extraordinary
capacity to withstand inactivation, and that, with appropriate testing,
will be found to retain the ability to transmit disease. Also, almost
all available inactivation data have come from research studies done
under carefully controlled laboratory conditions, and it is always
difficult to translate these conditions to the world of commerce. Even
when the data are applied in the commercial process, the repetitive
nature of the process requires vigilance in quality control and
inspection to ensure adherence to its regulations.

The final issue that must be addressed is the "lifespan" of the
infectious agent after disposal if it has been only incompletely
inactivated beforehand. Given the extraordinary resistance of the agent
to decontamination measures, the epidemiological and experimental
evidence indicating that TSE agents may endure in nature for a long time
should come as no surprise. The first real clue to this possibility came
from the Icelandic observation that healthy sheep contracted scrapie
when they grazed on pastures that had lain unused for 3 years after
having been grazed by scrapie-infected sheep.8

Support for this observation was obtained from an experiment in which
scrapie-infected brain material was mixed with soil, placed in a
container, and then allowed to "weather" in a semi-interred state for 3
years.9 A small amount of residual infectivity was detected in the
contaminated soil, and most of the infectivity remained in the topmost
layers of soil, where the tissue had originally been placed--in other
words, there had been no significant leaching of infectivity to deeper
soil layers.

It is therefore plausible for surface or subsurface disposal of
TSE-contaminated tissue or carcasses to result in long-lasting soil
infectivity. Uncovered landfills are a favourite feeding site for
seagulls, which could disperse the infectivity.10 Other animals might do
likewise, and if the landfill site were later used for herbivore
grazing, or tilled as arable land, the potential for disease
transmission might remain. A further question concerns the risk of
contamination of the surrounding water table, or even surface
waste-water channels, by effluents and discarded solid waste from
treatment plants.

A reasonable conclusion from existing data is that there is a potential
for human infection to result from environmental contamination by
BSE-infected tissue residues. The potential cannot be quantified because
of the huge number of uncertainties and assumptions that attend each
stage of the disposal process.

On the positive side, spongiform encephalopathy can be said to be not
easily transmissible. Although the level of infectivity to which
creatures are exposed is not known, it is probably very low, since sheep
that die from scrapie, cattle that die from BSE, and human beings who
die from nvCJD represent only a small proportion of their respective
exposed populations.

Whatever risk exists is therefore extremely small, but not zero, hence
all practical steps that might reduce the risk to the smallest
acceptable level must be considered. What is practical and what is
acceptable are concepts that will be hammered out on the anvil of
politics: scientific input, such as it is, already waits in the forge. A
fairly obvious recommendation, based on the science, would be that all
material that is actually or potentially contaminated by BSE, whether
whole carcasses, rendered solids, or waste effluents, should be exposed
to lye and thoroughly incinerated under strictly inspected conditions.
Another is that the residue is buried in landfills to a depth that would
minimise any subsequent animal or human exposure, in areas that would
not intersect with any potable water-table source. Certainly, it has
been, and will continue to be, necessary in many instances to accept
less than the ideal.

Paul Brown

Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, Bethesda, MD 20892, USA

1 Will RG, Ironside JW, Zeidler M, et al. A new variant of
Creutzfeldt-Jakob disease in the UK. Lancet 1996; 347: 921-25 [PubMed].

2 Bruce M, Will RG, Ironside JW, et al. Transmissions to mice indicate
that 'new variant' CJD is caused by the BSE agent. Nature 1997: 389:
498-501.

3 Collinge J, Sidle KCL, Heads J, Ironside J, Hill AF. Molecular
analysis of prion strain variation and the aetiology of 'new variant'
CJD. Nature 1996; 383: 685-90 [PubMed].

4 Wells GAH, Hawkins SAC, Green RB, et al. Preliminary observations on
the pathogenesis of experimental bovine spongiform encephalopathy (BSE):
an update. Vet Rec 1998; 142: 103-06 [PubMed].

5 Collee JG, Bradley R. BSE: a decade on--part 2. Lancet 1997; 349:
715-21 [PubMed].

6 Taylor DM. Exposure to, and inactivation of, the unconventional agents
that cause transmissible degenerative encephalopathies. In: Baker HF,
Ridley RM, eds. Methods in molecular medicine: prion diseases. Totawa
NJ: Humana Press, 1996: 105-18.

7 Brown P, Liberski PP, Wolff A, Gajdusek DC. Resistance of scrapie
infectivity to steam autoclaving after formaldehyde fixation and limited
survival after ashing at 360°C: practical and theoretical implications,
J Infect Dis 1990; 161: 467-72 [PubMed].

8 Palsson PA. Rida (scrapie) in Iceland and its epidemiology. In:
Prusiner SB, Hadlow WJ, eds. Slow transmissible diseases of the nervous
system, vol I. New York: Academic Press, 1979: 357-66.

9 Brown P, Gajdusek DC. Survival of scrapie virus after 3 years'
interment. Lancet 1991; 337; 269-70.

10 Scrimgoeur EM, Brown P, Monaghan P. Disposal of rendered specified
offal. Vet Rec 1996; 139: 219-20 [PubMed].

http://www.thelancet.com/newlancet/sub/issues/vol351no9110/body.commenta...

snip...

88. Natural decay: Infectivity persists for a long time in the
environment. A study by Palsson in 1979 showed how scrapie was
contracted by healthy sheep, after they had grazed on
land which had previously been grazed by scrapie-infected sheep, even
though the land had lain fallow for three years before the healthy sheep
were introduced. Brown also quoted an early experiment of his own
(1991), where he had buried scrapie-infected hamster brain and found
that he could still detect substantial infectivity three years later
near where the material had been placed. 89. Potential environmental
routes of infection: Brown discusses the various possible
scenarios, including surface or subsurface deposits of TSE-contaminated
material, which would lead to a build-up of long-lasting infectivity.
Birds feeding on animal remains (such as gulls visiting landfill sites)
could disperse infectivity. Other animals could become vectors if they
later grazed on contaminated land. "A further question concerns
the risk of contamination of the surrounding water table or even surface
water channels, by effluents and discarded solid wastes from treatment
plants. A reasonable conclusion is that there is a potential for human
infection to result from environmental contamination by BSE-infected
tissue residues. The potential cannot be quantified because of the huge
numbers of uncertainties and assumptions that attend each stage of the
disposal process". These comments, from a long established authority on
TSEs, closely echo my own statements which were based on a recent
examination of all the evidence. 90. Susceptibility: It is likely that
transmissibility of the disease to humans in vivo is probably low,
because sheep that die from scrapie and cattle that die from BSE are
probably a small fraction of the exposed population. However, no
definitive data are available.

91. Recommendations for disposal procedures: Brown recommends that
material which is actually or potentially contaminated by BSE should be:
1) exposed to caustic soda; 2) thoroughly incinerated under carefully
inspected conditions; and 3) that any residue should be buried in
landfill, to a depth which would minimise any subsequent animal or
human exposure, in areas that would not intersect with any potable
water-table source.

92. This review and recommendations from Brown have particular
importance. Brown is one of the world's foremost authorities on TSEs and
is a senior researcher in the US National Institutes of Health (NIH). It
is notable that such a respected authority is forthright in
acknowledging the existence of potential risks, and in identifying the
appropriate measures necessary to safeguard public health.
Paper by SM Cousens, L Linsell, PG Smith, Dr M Chandrakumar, JW
Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will, "Geographical
distribution of variant CJD in the UK (excluding Northern Ireland)".
Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41
(02/01/99)} (J/L/353/18) examined the possibility that patients with
vCJD (variant CJD) might live closer to rendering factories than would
be expected by chance. All 26 cases of vCJD in the UK with onset up to
31 st August 1998 were studied. The incubation period of vCJD is not
known but by analogy with other human TSEs could lie within the range
5-25 years. If vCJD had arisen by exposure to rendering products, such
exposure might plausibly have occurred 8-10 years before the
onset of symptoms. The authors were able to obtain the addresses of all
rendering plants in the UK which were in production in 1988. For each
case of vCJD, the distance from the place of residence on 1st January
1998 to the nearest rendering plant was calculated

snip...

http://www.bseinquiry.gov.uk/files/ws/s019b.pdf

Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective.
based on Bown & Gajdusek, (1991), landfill and burial may be assumed to
have a reduction factor of 98% (i.e. a factor of 50) over 3 years.
CJD-infected brain-tissue remained infectious after storing at
room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is
known to remain viable after at least 30 months of desiccation (Wilson
et al, 1950). and pastures that had been grazed by scrapie-infected
sheep still appeared to be contaminated with scrapie agent three years
after they were last occupied by sheep (Palsson, 1979).

http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf

PAUL BROWN SCRAPIE SOIL TEST

http://www.bseinquiry.gov.uk/files/sc/seac07/tab03.pdf

Some unofficial information from a source on the inside looking out -

Confidential!!!!

As early as 1992-3 there had been long studies conducted on small
pastures containing scrapie infected sheep at the sheep research station
associated with the Neuropathogenesis Unit in Edinburgh, Scotland.
Whether these are documented...I don't know. But personal recounts both
heard and recorded in a daily journal indicate that leaving the pastures
free and replacing the topsoil completely at least 2 feet of thickness
each year for SEVEN years....and then when very clean (proven scrapie
free) sheep were placed on these small pastures.... the new sheep also
broke out with scrapie and passed it to offspring. I am not sure that TSE
contaminated ground could ever be free of the agent!!
A very frightening revelation!!!

----------

You can take that with however many grains of salt you wish, and
we can debate these issues all day long, but the bottom line,
this is not rocket-science, all one has to do is some
experiments and case studies. But for the life of me,
I don't know what they are waiting on?

Kind regards,

Terry S. Singeltary Sr.
Bacliff, Texas USA

More here:

http://www.bseinquiry.gov.uk/files/ws/s018.pdf

INCINERATION TEMPS

Requirements include:

a. after burning to the range of 800 to 1000*C to eliminate smell;

well heck, this is just typical public relations fear factor control.
do you actually think they would spend the extra costs for fuel,
for such extreme heat, just to eliminate smell, when they spread
manure all over your veg's. i think not. what they really meant were
any _TSE agents_.

b. Gas scrubbing to eliminate smoke -- though steam may be omitted;

c. Stacks to be fitted with grit arreaters;

snip...

1.2 Visual Imact

It is considered that the requirement for any carcase incinerator
disign would be to ensure that the operations relating to the reception,
storage and decepitation of diseased carcasses must not be publicly
visible and that any part of a carcase could not be removed or
interfered with by animals or birds.

full text;

http://www.bseinquiry.gov.uk/files/yb/1989/04/03006001.pdf

New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template
of replication

Paul Brown*, [dagger ] , Edward H. Rau [Dagger ] , Bruce K. Johnson*,
Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§

* Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, and [Dagger ] Environmental
Protection Branch, Division of Safety, Office of Research Services,
National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred
Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur
Yvette, France

Contributed by D. Carleton Gajdusek, December 22, 1999

Abstract
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References

One-gram samples from a pool of crude brain tissue from hamsters
infected with the 263K strain of hamster-adapted scrapie agent were
placed in covered quartz-glass crucibles and exposed for either 5 or 15
min to dry heat at temperatures ranging from 150°C to 1,000°C. Residual
infectivity in the treated samples was assayed by the intracerebral
inoculation of dilution series into healthy weanling hamsters, which
were observed for 10 months; disease transmissions were verified by
Western blot testing for proteinase-resistant protein in brains from
clinically positive hamsters. Unheated control tissue contained 9.9
log10LD50/g tissue; after exposure to 150°C, titers equaled or exceeded
6 log10LD50/g, and after exposure to 300°C, titers equaled or exceeded 4
log10LD50/g. Exposure to 600°C completely ashed the brain samples,
which, when reconstituted with saline to their original weights,
transmitted disease to 5 of 35 inoculated hamsters. No transmissions
occurred after exposure to 1,000°C. These results suggest that an
inorganic molecular template with a decomposition point near 600°C is
capable of nucleating the biological replication of the scrapie agent.

transmissible spongiform encephalopathy | scrapie | prion | medical
waste | incineration

Introduction
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References

The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and
chemical methods used for inactivating pathogens, including heat. It has
long been recognized, for example, that boiling is ineffective and that
higher temperatures are most efficient when combined with steam under
pressure (i.e., autoclaving). As a means of decontamination, dry heat is
used only at the extremely high temperatures achieved during
incineration, usually in excess of 600°C. It has been assumed, without
proof, that incineration totally inactivates the agents of TSE, whether
of human or animal origin. It also has been assumed that the replication
of these agents is a strictly biological process (1), although the
notion of a "virus" nucleant of an inorganic molecular cast of the
infectious [beta ] -pleated peptide also has been advanced (2). In this
paper, we address these issues by means of dry heat inactivation studies.

snip...

GUTTING DEER/ELK AND THOSE THIN GLOVES;

Distribution of prion protein in the ileal Peyer's patch of scrapie-free
lambs and lambs naturally and experimentally exposed to the scrapie agent

Ragna Heggeb'z1, Charles McL. Press1, Gjermund Gunnes1, Kai Inge Lie1,
Michael A. Tranulis2, Martha Ulvund3, Martin H. Groschup4 and Thor
Landsverk1

Department of Morphology, Genetics and Aquatic Biology1 and Department
of Biochemistry, Physiology and Nutrition2, Norwegian School of
Veterinary Science, PO Box 8146 Dep., N-0033, Oslo, Norway
Department of Sheep and Goat Research, Norwegian School of Veterinary
Science, Kyrkjevegen 332/334, 4300 Sandnes, Norway3
Federal Research Centre for Virus Diseases of Animals, Paul-Ehrlich-Str.
28, 72076 TÃbingen, Germany4

Author for correspondence: Charles Press. Fax +47 22964764. e-mail
Charles.Press@veths.no

A sensitive immunohistochemical procedure was used to investigate the
presence of prion protein (PrP) in the ileal Peyer?s patch of
PrP-genotyped lambs, including scrapie-free lambs and lambs naturally
and experimentally exposed to the scrapie agent. The tyramide signal
amplification system was used to enhance the sensitivity of conventional
immunohistochemical procedures to show that PrP was widely distributed
in the enteric nervous plexus supplying the gut wall. In scrapie-free
lambs, PrP was also detected in scattered cells in the lamina propria
and in the dome and interfollicular areas of the Peyer?s patch. In the
follicles, staining for PrP was mainly confined to the capsule and cells
associated with vascular structures in the light central zone. In lambs
naturally exposed to the scrapie agent, staining was prominent in the
dome and neck region of the follicles and was also found to be
associated with the follicle-associated epithelium. Similar observations
were made in lambs that had received a single oral dose of
scrapie-infected brain material from sheep with a homologous and
heterologous PrP genotype 1 and 5 weeks previously. These studies show
that the ileal Peyer?s patch in young sheep may be an important site of
uptake of the scrapie agent and that the biology of this major
gut-associated lymphoid tissue may influence the susceptibility to oral
infection in sheep. Furthermore, these studies suggest that homology or
heterology between PrP genotypes or the presence of PrP genotypes seldom
associated with disease does not impede uptake of PrP.
======================================================

BSE, KURU, DENTAL AND ___CUT ABRASIONS___ from gutting a deer
perhaps;

snip...

Since there was a suggestion that kuru had been transmitted
through the gums and/or gum abrasions...

snip...

http://www.bseinquiry.gov.uk/files/yb/1989/04/17005001.pdf

[PDF]BSE INQUIRY Statement of behalf of the Environment Agency ...
File Format: PDF/Adobe Acrobat - View as HTML
... his Statement of March 1998 to the BSE Inquiry ... systems subject
to regular or intermittent
contamination by rapid movement of recharge water ...
http://www.bse.org.uk/files/ws/s490.pdf

http://www.bseinquiry.gov.uk/files/ws/s490.pdf

BSE INQUIRY

Statement of behalf of the Environment Agency
Concerning Thruxted Mill
By
Mr C. P. Young
Principal Hydrogeologist, Soil Waste and Groundwater Group
WRc plc; Medmenham, Bucks

http://www.bseinquiry.gov.uk/files/ws/s490.pdf

Very important to those hunters looking for healthy
deer/elk to eat...TSS

MRC-43-00 [ ] [Text only version of this site] [Print this page]
Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH
FINDINGS RELEVANT TO CJD AND BSE

A team of researchers led by Professor John Collinge at the Medical
Research Council Prion Unit1 report today in the Proceedings of the
National Academy of Sciences, on new evidence for the existence of a
'sub-clinical' form of BSE in mice which was unknown until now.

The scientists took a closer look at what is known as the 'species
barrier' - the main protective factor which limits the ability of
prions2 to jump from one species to infect another. They found the mice
had a 'sub-clinical' form of disease where they carried high levels of
infectivity but did not develop the clinical disease during their normal
lifespan. The idea that individuals can carry a disease and show no
clinical symptoms is not new. It is commonly seen in conventional
infectious diseases.

Researchers tried to infect laboratory mice with hamster prions3 called
Sc237 and found that the mice showed no apparent signs of disease.
However, on closer inspection they found that the mice had high levels
of mouse prions in their brains. This was surprising because it has
always been assumed that hamster prions could not cause the disease in
mice, even when injected directly into the brain.

In addition the researchers showed that this new sub-clinical infection
could be easily passed on when injected into healthy mice and hamsters.

The height of the species barrier varies widely between different
combinations of animals and also varies with the type or strain of
prions. While some barriers are quite small (for instance BSE easily
infects mice), other combinations of strain and species show a seemingly
impenetrable barrier. Traditionally, the particular barrier studied here
was assumed to be robust.

Professor John Collinge said: "These results have a number of important
implications. They suggest that we should re-think how we measure
species barriers in the laboratory, and that we should not assume that
just because one species appears resistant to a strain of prions they
have been exposed to, that they do not silently carry the infection.
This research raises the possibility, which has been mentioned before,
that apparently healthy cattle could harbour, but never show signs of, BSE.

"This is a timely and unexpected result, increasing what we know about
prion disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best
to safeguard health and reduce the risk that theoretically, prion
disease could be contracted through medical and surgical procedures."

ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS
SET BY THE JOURNAL.

FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011
(OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR
PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO
TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30
ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE
MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE
DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE
ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009
(OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF
UK TIME.

NOTES FOR EDITORS

Professor Collinge is a consultant neurologist and Director of the newly
formed MRC Prion Unit based at The Imperial College School of Medicine
at St Mary's Hospital. He is also a member of the UK Government's
Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit
is was set up in 1999, and its work includes molecular genetic studies
of human prion disease and transgenic modelling of human prion diseases.

Prions are unique infectious agents that cause fatal brain diseases such
as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad
cow disease) in animals. In some circumstances prions from one species
of animals can infect another and it is clear that BSE has done this to
cause the disease variant CJD in the UK and France. It remains unclear
how large an epidemic of variant CJD will occur over the years ahead.

The strain of prion used here to infect the mice is the Sc237 strain
(also known as 263K) which infects hamsters, and until now was assumed
not to infect mice.

This research was funded by the Medical Research Council and Wellcome Trust.

The Medical Research Council (MRC) is a national organisation funded by
the UK tax-payer. Its business is medical research aimed at improving
human health; everyone stands to benefit from the outputs. The research
it supports and the scientists it trains meet the needs of the health
services, the pharmaceutical and other health-related industries and the
academic world. MRC has funded work which has led to some of the most
significant discoveries and achievements in medicine in the UK. About
half of the MRC's expenditure of £345 million is invested in over 50 of
its Institutes and Units, where it employs its own research staff. The
remaining half goes in the form of grant support and training awards to
individuals and teams in universities and medical schools.

The Wellcome Trust is the world's largest medical research charity with
a spend of some £600 million in the current financial year 1999/2000.
The Wellcome Trust supports more than 5,000 researchers, at 400
locations, in 42 different countries to promote and foster research with
the aim of improving human and animal health. As well as funding major
initiatives in the public understanding of science, the Wellcome Trust
is the country's leading supporter of research into the history of medicine.

©2002 Medical Research Council
Data Protection policy | Contact the MRC
=========================================

Subject: OPINION ON THE USE OF BURIAL FOR DEALING WITH ANIMAL CARCASSES AND OTHER ANIMAL MATERIALS THAT MIGHT CONTAIN BSE/TSE
Date: Wed, 22 Jan 2003 14:58:53 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

C:\WINNT\Profiles\bredagi.000\Desktop\Burial_OPINION_0301_OPINION_FINAL.doc
EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Directorate C - Scientific Opinions
C1 - Follow-up and dissemination of scientific opinions
OPINION ON
THE USE OF BURIAL FOR DEALING WITH ANIMAL
CARCASSES AND OTHER ANIMAL MATERIALS THAT
MIGHT CONTAIN BSE/TSE
ADOPTED BY THE
SCIENTIFIC STEERING COMMITTEE
MEETING OF 16-17 JANUARY 2003
1
OPINION
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which
safe burial of potentially TSE-infected (animal) materials can be
achieved. The details of the SSC's evaluation are provided in the
attached report. The SSC concludes as follows:
(1) The term "burial" includes a diversity of disposal conditions.
Although burial is widely used for disposal of waste the degradation
process essential for BSE/TSE infectivity reduction is very difficult to
control. The extent to which such an infectivity reduction can occur as
a consequence of burial is poorly characterised.
It would appear to be a slow process in various circumstances.
(2) A number of concerns have been identified including potential for
groundwater contamination, dispersal/transmission by
birds/animals/insects, accidental uncovering by man.
(3) In the absence of any new data the SSC confirms its previous opinion
that animal material which could possibly be contaminated with BSE/TSEs,
burial poses a risk except under highly controlled conditions (e.g.,
controlled landfill). The SSC reiterates the consideration made in its
opinion of 24-25 June 1999 on "Fallen Stock"1. The limited capacity for
destruction of animal wastes in certain countries or regions in the
first place justifies the installation of the required facilities; it
should not be used as a justification for unsafe disposal practices such
as burial. However, the SSC recognises that for certain situations or
places or for certain diseases (including animals killed and recycled or
disposed of as a measure to control notifiable diseases), the available
rendering or incinerator or disposal capacity within a region or country
could be a limiting factor in the control of a disease. Thus if hundreds
or even millions of animals need to be rendered after killing or if the
transport of a material to a rendering or disposal plant proved to be
impractical, an appropriate case by case risk assessment2 should be
carried out before deciding upon the most appropriate way of disposal.
In principle, the risk is expected to be the lower for small
incinerators3 as compared to burial. As such decisions in practice may
have to be taken at very short notice, risk management scenarios
according to various possible risks should be prepared in advance to
allow for a rapid decision when the need arises.

1 Scientific Opinion on The risks of non conventional transmissible
agents, conventional infectious agents or other hazards such as toxic
substances entering the human food or animal feed chains via raw
material from fallen stock and dead animals (including also: ruminants,
pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats,
laboratory animals and fish) or via condemned materials.
Adopted By the Scientific Steering Committee at its meeting of 24-25
June 1999. (and re-edited at its meeting of 22-23 July 1999).
2 See also the relevant sections and footnotes on risk assessment in the
report accompanying the SSC opinion of 24-25 June 1999.
3 See SSC opinion of 16-17 January 2003 on the use of small incinerators
for BSE risk reduction.
2

THE USE OF BURIAL FOR DEALING WITH CARCASSES AND OTHER MATERIALS THAT
MIGHT CONTAIN BSE/TSE
REPORT

1. MANDATE

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which
safe burial of potentially TSE-infected animal materials can be
achieved. The SSC appointed Prof.J.Bridges as rapporteur. His report was
discussed and amended by the TSE/BSE ad hoc Group at its meeting of 9
January 2003 and by the SSC at its meeting of 16-17 January 2003.

2. GENERAL CONSIDERATIONS

"Burial" covers a range of disposal situations ranging from the practice
of burying animals on farms and other premises in a relatively shallow
trench (with or without treatment such as lining) to deep disposal to a
lined and professionally managed landfill site (SSC 2001).
Buried organic material is normally decomposed by microbial and chemical
processes. However this is not a process amenable to control measures.
As noted by the SSC "Opinion on Fallen Stock" (SSC 25th June 1999) there
is little reliable information on the extent and rate of infectivity
reduction of BSE/TSEs following burial. An old paper by Brown and
Gajdusek 1991 assumed a reduction of 98% over 3 years. However it is
noted that the rate of degradation of materials following burial can
vary very considerably between sites. This is not surprising because the
degradation process is strongly influenced by factors such as water
content of the site, temperature inside the site, nature of adsorptive
"material" present etc. The previous SSC opinion noted that BSE/TSEs
appear to be resistant to degradation when stored at room temperature
over several years. It also raised concerns that mites could serve as a
vector and/or reservoir for the infected scrapie material.
Burial sites may have a thriving animal population. Uncovering of risk
material that is not deeply buried is therefore possible.
The SSC in its opinion of 28th-29th June 2001 set out a framework for
assessing the risk from different waste disposal processes. These
criteria may be applied to
burial as follows:

(1) Characterisation of the risk materials involved.

Unlike many other waste disposal options there are no technical or
economic factors that would limit the nature of the material that can be
disposed of by burial. Moreover in many cases the location of burial
sites is uncertain. The potential for transmission of BSE/TSEs for SRM
that is buried near the surface is also poorly characterised.3

(2) Risk reduction.

The extent to which the infectivity is reduced is likely to vary
substantially according to the nature of the site depth of burial
whether pre-treatment by burning or through the addition of lime is used
etc. There appears to be no scientific basis at present for the
prediction of the rate of loss of infectivity. In the absence of such
data, as a worst case, it has to be assumed that over a three-five year
period the loss of infectivity may be slight. In principle on a
well-managed fully contained landfill the risks from infective material
can approach zero. However this requires rigorous management over many
years. This is difficult to guarantee.

(3) Degree to Which the Risks can be Contained

The principal concerns are:

* Prevention of access to the SRM by animals that could result in the
transmission (directly or indirectly) of the BSE/TSE.

* Penetration of prions into the leachate/groundwater. It is noted that
on some landfill sites leachate is sprayed into the air to facilitate
oxidation of some organic components. Such a practice could in principle
lead to dispersal of BSE/TSEs. It is also noted that it is not uncommon
for landfill sites to be re-engineered to increase their stability, gas
and leachate flow and/or total capacity. If this re-engineering involved
an area where previous burial of BSE/TSE contaminated material had taken
place and additional risk could accrue. The possibility of contaminated
material being dug up in shallow and unmarked burial sites on farms etc
constitutes a considerably greater risk.

3. FURTHER INVESTIGATIONS

Research is needed on specific aspects of the behaviour of prion like
molecules in controlled landfills i.e.:

* Potential for adsorption to other material present in the waste that
might limit their mobility.

* Principal factors influencing rates of degradation.

* Effectiveness of encasement in cement in controlling/reducing the risk.

4. CONCLUSION

In the absence of new evidence the opinion of the SSC "Opinion on Fallen
Stock" (SSC 25th June 1999) must be endorsed strongly that land burial
of all animals and material derived from them for which there is a
possibility that they could incorporate BSE/TSEs poses a significant
risk. Only in exceptional circumstances where there could be a
considerable delay in implementing a safe means of disposal
should burial of such materials be considered. Guidelines should be made
available to aid on burial site selection.

http://europa.eu.int/comm/food/fs/sc/ssc/out309_en.pdf

C:\WINNT\Profiles\bredagi.000\Desktop\Burning_OPINION_0301_OPINION_FINAL.doc

EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Directorate C - Scientific Opinions
C1 - Follow-up and dissemination of scientific opinions

OPINION ON

OPEN BURNING OF POTENTIALLY TSE-INFECTED ANIMAL
MATERIALS

ADOPTED BY THE
SCIENTIFIC STEERING COMMITTEE
AT ITS MEETING OF 16-17 JANUARY 2003

2
OPINION

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which
safe burning of potentially TSE-infected (animal) materials can be
achieved. The details of the SSC's evaluation are provided in the
attached report. The SSC concludes as follows:

(1) "Burning" covers a wide variety of combustion conditions. This
opinion is concerned with the process of open burning e.g. bonfires.

(2) There are serious concerns regarding the use of open burning for the
destruction of pathogen contaminated animal waste, particularly for
waste which may be contaminated with relatively heat stable pathogens.
Issues include: the potentially very high variability of the pathogen
inactivation, the nature of the gaseous and particulate emissions, and
the risks from the residual ash.

(3) The SSC recommends that open burning is only considered for pathogen
destruction under exceptional circumstances following a specific risk
assessment. In the case of animal waste possibly contaminated with
BSE/TSE in view of the uncertainty of the risk open burning should be
considered a risk. Suitable monitoring methods for TSE contamination of
both air and ash are needed. Protocols for safe burning in emergency
situations need to be established. The SSC reiterates the consideration
made in its opinion of 24-25 June 1999 on "Fallen Stock"1. The limited
capacity for destruction of animal wastes in certain countries or
regions in the first place justifies the installation of the required
facilities; it should not be used as a justification for unsafe disposal
practices such as burial. However, the SSC recognises that for certain
situations or places or for certain diseases (including animals
killed and recycled or disposed of as a measure to control notifiable
diseases), the available rendering or incinerator or disposal capacity
within a region or country could be a limiting factor in the control of
a disease. Thus if hundreds or even millions of animals need to be
rendered after killing or if the transport of a material to a rendering
or disposal plant proved to be impractical, an appropriate case by case
risk assessment2 should be carried out before deciding upon the most
appropriate way of disposal. In principle, the risk is expected to be
the lower for small incinerators3 as compared to open burning. As
such decisions in practice may have to be taken at very short notice,
risk management scenarios according to various possible risks should be
prepared in advance to allow for a rapid decision when the need arises.
1 Scientific Opinion on The risks of non conventional transmissible
agents, conventional infectious agents or other hazards such as toxic
substances entering the human food or animal feed chains via raw
material from fallen stock and dead animals (including also: ruminants,
pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats,
laboratory animals and fish) or via condemned materials.
Adopted By the Scientific Steering Committee at its meeting of 24-25
June 1999. (and re-edited at its meeting of 22-23 July 1999).
2 See also the relevant sections and footnotes on risk assessment in the
report accompanying the SSC opinion of 24-25 June 1999.
3 See SSC opinion of 16-17 January 2003 on the use of small incinerators
for BSE risk reduction.
3

OPEN BURNING OF POTENTIALLY TSE-INFECTED ANIMAL MATERIALS
REPORT

1. MANDATE

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to advice on the examples of conditions under which
safe burning of potentially TSE-infected animal materials can be
achieved. The SSC appointed Prof.J.Bridges as rapporteur. His report was
discussed and amended by the TSE/BSE ad hoc Group at its meeting of 9
January 2003 and by the SSC at its meeting of 16-17 January 2003.

2. GENERAL CONSIDERATIONS

Burning is a combustion process to which a range of control measures may
be applied to contain emissions and to ensure the completeness of the
degradation process for organic matter. Depending on the source (waste)
material the burning process may or may not require addition of other
energy sources. Incineration/pyrolysis are contained combustion
processes are contained combustion processes and therefore have the
potential for a high level of control.
(However see opinion on small incinerators). At the other end of the
control spectrum is open burning; such as bonfires.
Typically combustion of animal waste requires the addition of a high
calorific fuel in order to initiate (and for some materials to sustain)
the process. It is recognised that open burning of animal waste is a
very cheap and convenient method of disposal. However uncontained
burning has a number of problems in terms of the potential risks involved:

(1) In the open burning situation a range of temperatures will be
encountered. It is difficult therefore to ensure complete combustion of
the animal waste. If the waste is contaminated with pathogens there will
remain considerable uncertainty as to the degree of their inactivation.

(2) Gaseous and particulate emissions to the atmosphere will occur and
consequently worker and public exposure is likely. There is very little
data to indicate whether or not some pathogens could be dispersed to air
as a consequence of open burning.

(3) The supporting/secondary fuel may be a source of contamination
itself. For example in the recent foot and mouth disease outbreak in the
UK timbers were used at some sites that were heavily contaminated with
pentachlorophenol.

(4) The residual ash must be considered to be a risk source. Its safe
disposal needs to be assured (see opinion on small incinerators) to
prevent human and animal contact and protect from groundwater
contamination. While careful selection of burning sites can reduce the
risks open burning should only be considered in emergency situations.
For each such emergency situation a specific risk assessment should be
conducted which must include the risk 4 from the pathogen of immediate
concern but also other pathogens that might be present.

3. RISK ASSESSMENT OF OPEN BURNING FOR BSE

The SSC, at its meeting of 28th-29th June 2001, recommended "a framework
for the assessment of the risk from different options for the safe
disposal or use of meat and bone meal (MBM) and other products which
might be contaminated with TSEs and other materials. Applying the
framework to the practice of open burning, the following conclusions can
be drawn:

3.1. Nature of the materials handled
Potentially a wide variety of materials can be used provided suitable
secondary fuel is available. The burning process is very simple in
principle and difficult in practice to regulate effectively.

3.2. Risk reduction due to open burning There is no reliable data to
indicate the extent of risk reduction that could be achieved by open
burning. It is reasonable however to assume that overall it
will be rather less effective in reducing the infectivity of BSE/TSE
than wellconducted incineration. Moreover the reproducibility of the
risk reduction is likely to be very variable even at a single location.

3.3. Airborne emissions and residue ash The composition of airborne
emissions and residue ash is rarely monitored. From a risk assessment
viewpoint particular attention needs to be given to the potential for
the airborne dispersal of relatively heat stable pathogens as a
consequence of open burning. In the absence of reliable data both
airborne emissions and residual ash must be considered to constitute a
significant risk if animal waste that might be contaminated with TSEs is
being burnt.

4. FURTHER INVESTIGATION

Research is needed particularly on:
* The potential for airborne dispersal of relatively heat stable pathogens.
* Methodologies to improve the efficacy of the combustion process to
ensure the inactivation of pathogen contaminated animal waste.

5. CONCLUSION

Open burning potentially represents a significant risk where the animal
waste has the possibility of being contaminated with BSEs/TSEs. Suitable
monitoring methods for TSE contamination of both air and ash are needed.
Protocols for safe burning in emergency situations need to be established.

http://europa.eu.int/comm/food/fs/sc/ssc/out310_en.pdf

C:\WINNT\Profiles\bredagi.000\Desktop\Incinerator_OPINION_0301_FINAL.doc

EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL

Directorate C - Scientific Opinions
C1 - Follow-up and dissemination of scientific opinions
OPINION ON

THE USE OF SMALL INCINERATORS FOR BSE RISK REDUCTION

SCIENTIFIC STEERING COMMITTEE
MEETING OF 16-17 JANUARY 2003

2
OPINION
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to (i) evaluate a risk assessment1 prepared for the
UK's Spongiform Encephalopathy Advisory Committee (SEAC), on the
potential risk arising from the use of small incinerators to dispose of
specified risk materials and (ii) to advise on the safety
with regard to TSE risks of the use of such small incinerators.

The details of the SSC's evaluation are provided in the attached report.
The SSC concludes as follows:

(i) The SSC, at its meeting of 28th -29th June 2001, recommended "a
framework for the assessment of the risk from different options for the
safe disposal or use of meat and bone meal (MBM) and other products
which might be contaminated with TSEs and other materials." This
framework comprised five components:

(1) Identification and characterisation of the risk materials involved,
the possible means for their transmission and potential at risk groups.

(2) The risk reduction achieved by the particular process.

(3) The degree to which the risks can be contained under both normal and
emergency operating conditions. This inevitably includes consideration
of the effectiveness of control measures.

(4) Identification of interdependent processes for example transport,
storage, loading of any TSE related risk materials.

(5) The intended end-use of the products for example disposal, recycling
etc. The risk assessment prepared for SEAC focuses on the risks involved
steps 1 and 2 in respect of BSE/TSEs only and is based on a visit to 10
incinerators out of a total of 263 in the UK of which 60% had after
burners. The risk assessment is also using a number of assumptions and
data that may be valid for certain incinerator types under certain
conditions, but are not necessarily applicable either for all types of
materials to be disposed of, or to the whole range of types of small
incinerators in use the EU and the UK.

(ii) Small incinerators are widely used to meet the needs of local
communities. These incinerators vary greatly in their design, nature of
use and performance characteristics and the quality of their management.
As a consequence of this variability there are many uncertainties in
identifying risks posed by small incinerators that are used to treat SRM
materials and each type should eventually receive its own assessment.
Also, general operating and control criteria should be established for

1 DNV Consulting (Det Norske Veritas), 2001. Risk assessment of SRM
incinerators. Prepared for the UK Ministry of Agriculture, Fisheries and
Food. Revision 2 of the Draft report, February 2001. 24
pages. 3

Potential risk sources arising from the incineration process include:
gaseous emissions and residual ash. Research is currently ongoing
mimicking incineration of TSE-infected brain tissue to assess the
infectivity clearance level under various scenarios2. However, there are
no final reported measurements that enable the risk to be assessed from
either the emissions or the ash from small incinerators. It has
been argued that the protein content of the ash is a reasonable
surrogate measure of the degree of risk deduction caused by the
incineration process. This assumption is questionable in view of the
resistance to heat of prions as compared to other proteins. Protein
measurements in ash are however probably a useful general
measure of the overall efficiency and reproducibility of the
incineration process. Results in the aforementioned report1 indicate a
large degree of variability in performance among the small incinerators
in the UK that have been evaluated. It is anticipated that small
incinerators, used by other Member States will also show a
considerable variation in performance. In evaluating the risk of small
incinerators, consideration should be given to the risk of potential
contamination of the ash and of the gaseous emissions.
In the absence of generally accepted and enforced performance standards
for small incinerators handling SRMs each such facility therefore needs
to be the subject of a specific risk assessment. The SSC considers that
the standards set up by the new Waste Incinerator Directive (2000/76/EC)
and in its opinion of June 1999 on waste disposal should serve as
guidance. In the absence of reliable data on the possible residual
infectivity of the ash, it should be disposed of, i.e., in controlled
landfills as described in the SSC opinion of June 1999 on safe disposal
of waste. The SSC finally wishes to emphasise the need for suitable
monitoring methods in order that risks can be assessed readily for
individual types of small incinerators.
2 P.Brown, pers.comm., December 2002. Publication in progress.4

THE USE OF SMALL INCINERATORS FOR BSE RISK REDUCTION
REPORT

1. MANDATE

On 17 May 2002, the Scientific Steering Committee (SSC) was invited by
Commission Services to (i) evaluate a risk assessment3 prepared for the
UK's Spongiform Encephalopathy Advisory Committee (SEAC), on the
potential risk arising from the use of small incinerators to dispose of
specified risk materials and (ii) to advise on the safety with regard to
TSE risks of the use of such small incinerators.

The SSC appointed Prof. J. Bridges as rapporteur. His report was discussed
and amended by the TSE/BSE ad hoc Group at its meeting of 9 January 2003
and by the SSC at its meeting of 16-17 January 2003.

2. CURRENT LEGISLATIVE FRAMEWORK

Until 2000, small incinerators were exempt from the emission limits set
by the EC for MSW and hazardous waste incinerators with throughputs
greater than 50 kg/hour. An "incineration plant" is defined by the new
Incineration of Waste Directive (2000/76/EC) as "any stationary or
mobile technical equipment dedicated to the thermal treatment of waste
with or without recovery of the combustion heat generated". This
definition would appear to exclude open burning of waste. The
new Directive, which must be transposed into the legislation of each
Member State by December 2002, replaces a range of previous directives
on incineration. It applies to all new incinerator installations from
December 28th 2002 and all existing installations from December 28th
2005. The principal aim of the Directive is to prevent and/or limit
negative environmental effects due to emissions into air, soil,
surface and ground water and the resulting risks to human health from
the incineration and co-incineration of waste. It covers many aspects
from a requirement for afterburners to airborne emission limits and
criteria for the composition of residual ash. Previous EC legislation
has exempted small incinerators (i.e. those operating at less than 50 kg
per hour). The Waste Incinerator Directive (WID) (2000) allows such
small incinerators to be exempt from licensing at the national level
however they will still be subjected to the same onerous
requirements of the WID as larger incinerators.

In the UK it is proposed that in future incinerators dealing with
non-hazardous waste but with a throughput of less than 1 tonne per hour
will be regulated by local authorities whereas those with a larger
throughput will be regulated by the national authority. It is possible
that different regulatory mechanisms may result in differences in the
rigour with which the new standards are enforced. The position
on the disposal of animal waste is complicated. Animal carcass
incineration use not covered by the WID and therefore the existing
regulatory framework (90/66/EEC which covers animal and public health
requirements to ensure destruction of pathogens) will continue to be
applied. A new Animal By-Products Regulation

3 DNV Consulting (Det Norske Veritas), 2001. Risk assessment of SRM
incinerators. Prepared for the UK Ministry of Agriculture, Fisheries and
Food. Revision 2 of the Draft report, February 2001. 24
pages.
5

(ABPR) will apply in Member States during the first part of 2003. The
relationship to WID has been included in the ABPR. It is important that
it does not result in less strict standards being applied for animal
carcass incineration. In contrast to whole carcasses WID will apply to
the burning of meat and bone meal, tallow or other material (even if
they burn animal carcasses too). Additional specific directives will
continue to apply to waste that could be contaminated with BSE/TSEs.
(96/449/EC)

3. CURRENT USE OF SMALL INCINERATORS TO DISPOSE OF ANIMAL WASTE
Small incinerators are used for a variety of purposes and in a range of
locations among Member States. Many are located alongside small
abattoirs, knackers, hunt kennels, or laboratories. Thus they meet the
needs of relatively small communities. Across Member States these small
incinerators include a variety of designs and operating conditions (as
indicated above in principle they will probably be required
to meet specific standards for emissions and for the composition of the
residual ash by December 28th 2005).
In the UK there are indications (see DNV Report 2001) that a
considerable quantity of SRM which would have previously been sent for
rendering is now being incinerated directly in small incinerators. Thus

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3. CURRENT USE OF SMALL INCINERATORS TO DISPOSE OF ANIMAL WASTE
Small incinerators are used for a variety of purposes and in a range of
locations among Member States. Many are located alongside small
abattoirs, knackers, hunt kennels, or laboratories. Thus they meet the
needs of relatively small communities. Across Member States these small
incinerators include a variety of designs and operating conditions (as
indicated above in principle they will probably be required
to meet specific standards for emissions and for the composition of the
residual ash by December 28th 2005).
In the UK there are indications (see DNV Report 2001) that a
considerable quantity of SRM which would have previously been sent for
rendering is now being incinerated directly in small incinerators. Thus
evaluation of the risks from such incinerators is of increasing importance.

4. RISK ASSESSMENT FOR SMALL INCINERATORS

The SSC, at its meeting of 28th -29th June 2001, recommended "a
framework for the assessment of the risk from different options for the
safe disposal or use of meat and bone meal (MBM) and other products
which might be contaminated with TSEs and other materials.
This framework comprised five components:

(1) Identification and characterisation of the risk materials involved,
the possible means for their transmission and potential at risk groups.

(2) The risk reduction achieved by the particular process.

(3) The degree to which the risks can be contained under both normal and
emergency operating conditions. This inevitably includes consideration
of the effectiveness of control measures.

(4) Identification of interdependent processes for example transport,
storage, loading of any TSE related risk materials.

(5) The intended end-use of the products for example disposal, recycling
etc. Recently a report has been prepared by DNV consulting (2001) for
the UK Ministry of Agriculture, Fisheries and Food (now known as DEFRA)
that assesses the risks from small incinerators in the UK that receive
SRMs. This report focuses on the risks involved steps 1 and 2 in respect
of BSE/TSEs only. 10 incinerators out of a total of 263 in the UK were
visited of which 60% had after burners.

(1) Nature of the materials handled.

The DNV report 2001 starts with the assumption that "the materials
incinerated at small abattoirs will be mainly SRM and bones from animals
that are fit for human consumption. It may also include material from
animals failed by meat inspectors. The likelihood of there being an animal
6 with significant BSE infectivity is very small and certainly much less
than for the fallen stock handled by hunt kennels and knackers4. For
this reason the study has concentrated on the latter type of operation".
The Report notes that "the material handled by both knacker and hunt
kennels is highly variable and difficult to characterise". In terms of
input the key factors to consider are:

* The number of adult bovines processed and the proportion of these
carcasses that are likely to be infected.

* The extent of infectivity (in terms of human oral Infectious Units)
that may occur (average and worst case).

In the DNV (2001) risk assessment only the BSE risk from processing
bovine SRMs was considered. For quantitative risk assessment purposes
the mean value of the oral ID50 for cattle was taken as 0.1 gram. A
range of values was taken to cover uncertainty in the inter-species
barrier from 104 to 1 (as recommended by the SSC 2000). In order to
assess the likelihood that a particular carcass could be infected, UK
and Swiss monitoring data was used. An incidence rate based on Prionics
test findings of between 0.013 and 0.0025 was calculated. The DNV Report
notes that prevalence rates are progressively reducing from these
1998/99 figures. Finally the report concludes that the SRM from an
infected bovine could contribute 700 Infectious Units.

(2) Risk reduction due to incineration

Once a carcass/SRM has been introduced into a small incinerator there
are two main sources for the potential release of BSE infectivity

(a) Airborne emissions
(b) Residual ash

There is no direct data on the TSE levels that may occur in those two
media. The SSC however is aware of currently ongoing heat studies
mimicking various incineration conditions and scenarios and aiming at
assessing the TSE clearance efficacy of these processes (P.Brown,
pers.comm., 16.01.03) on both the residual ash and the trapped emission
gases. In the absence of final data from such experiments for individual
(small) incinerator types, the DNV Report (2001) assumes that
measurement of the total protein content of ash is a relevant surrogate
for BSE/TSE material. Protein content is a useful indicator of the
general performance of an incinerator. However it is much more
problematic whether it is also a valid marker for possible BSE/TSE
contamination as it known that BSE/TSE are relatively heat resistant as
compared to other proteins. Failure to detect certain amino acids
present in prions is encouraging but the sensitivity limits
for amino acids are relatively poor for reassurance purposes. Equally
important, the data provided in the DNV report shows moderate split sample
4 It may be mentioned that this assumption may be valid for the UK as a
whole, but note necessarily for all other Member States. 7
variation but often substantial inter sampling variation (up to 600
fold). This indicates a wide span of performance standards among the
small SRM incinerators in the UK and most likely across the whole of the
EU. Typically performance was substantially poorer than is the case for
larger incinerators. Unburned material is not uncommonly noted in the
ash from small incinerators. If the reduction in protein content due to
incineration is accepted as a valid indicator, typical infectivity
reduction can be calculated to be of the order of 1600 (DNV Report
2001). Incinerators are known to emit particulate matter from their
stacks. Larger incinerators have much higher stacks to facilitate
disposal of emissions, they also have gas cleaning equipment to minimise
the emission of particulate matter, metals and acidic gases. Small
incinerators generally do not have any gas cleaning equipment. It can be
speculated (as in the DNV Report 2001) that unburned materials (and
therefore potentially infections is much less likely to be emitted in
the form of particulate matter than burnt material.
Nonetheless there is no data to support this assumption.

(3) Other considerations.

(a) Disposal of ash.

In the case of small incinerators ash is often dispersed of locally to a
trench, which is typically neither lined, nor is the residue buried
deeply. In contrast for larger incinerators in the UK ash is normally
disposed of to a contained landfill. The risk from disposal to a trench
is difficult to gauge in the absence of reliable data on the possible
infectivity of the ash.

(b) Management factors.

Almost inevitably the level of expertise available for the management
of small incinerators is highly variable because few such facilities can
afford to employ specialists in incineration. This is also likely to be
often the case for the inspectors as well. While such considerations
cannot formally be taken into account in a risk assessment, they are
not the less relevant factors that need to be considered in assessing
the risk from a particular plant.

(c) Benchmarking.

The DNV 2001 risk assessment relies greatly on the assumption that
BSE/TSE contaminated material is very unlikely to be processed.
The Report seeks to compare the risks from a small incinerator with
that from large SRM incinerators which the author had assessed
previously (DNV, 1997). It identifies that the risk is four-five -fold
less from a typical small incinerator because the scale of activities is
much lower. However it is noted that the amount of experimental
data to back this conclusion is extremely limited and does not take
into account either risks from the residual ash or any consequences of
a substantially lower stack height limiting the dilution of the emitted
particulate and gaseous matter. 8

5. FURTHER INVESTIGATIONS

In view of the uncertainty regarding the risks due to BSE/TSE
contamination of the fly and bottom ash and airborne emissions it is
recommended that further research is conducted to identify the residual
risks (along with attendant uncertainties) from the burial of ash
(without further treatment,) in uncontained sites. It is essential that
suitable monitoring methods are developed.

6. LITERATURE

EC (European Commission), 1999. Opinion on The risks of non conventional
transmissible agents, conventional infectious agents or other hazards
such as toxic substances entering the human food or animal feed chains
via raw material from fallen stock and dead animals (including also:
ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals,
cats, laboratory animals and fish) or via condemned materials. Adopted
By the Scientific Steering Committee at its meeting of 24-25 June 1999
and re-edited at its meeting of 22-23 July 1999. DNV Consulting (Det
Norske Veritas), 1997. Risks from disposing of BSE infected cattle in
animal carcass incinerators. Report prepared for the UK Environment
Agency. DNV Consulting (Det Norske Veritas), 2001. Risk assessment of
SRM incinerators. Prepared for the UK Ministry of Agriculture, Fisheries
and Food. Revision 2 of the Draft report, February 2001. 24 pages.
SEAC (Spongiform Encephalopathy Advisory Committee, UK), 2001. Public
summary of the SEAC meeting of 25 April 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out311_en.pdf

TSS

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Environmental Sources of Prion Transmission in Mule Deer
Michael W. Miller,* Elizabeth S. Williams,† N. Thompson Hobbs,‡ and Lisa L. Wolfe*
*Colorado Division of Wildlife, Fort Collins, Colorado, USA; †University of Wyoming, Laramie, Wyoming, USA; and ‡Colorado State University, Fort Collins, Colorado, USA

Suggested citation for this article: Miller MW, Williams ES, Hobbs NT, Wolfe LL. Environmental sources of prion transmission in mule deer. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm

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Whether transmission of the chronic wasting disease (CWD) prion among cervids requires direct interaction with infected animals has been unclear. We report that CWD can be transmitted to susceptible animals indirectly, from environments contaminated by excreta or decomposed carcasses. Under experimental conditions, mule deer (Odocoileus hemionus) became infected in two of three paddocks containing naturally infected deer, in two of three paddocks where infected deer carcasses had decomposed in situ ≈1.8 years earlier, and in one of three paddocks where infected deer had last resided 2.2 years earlier. Indirect transmission and environmental persistence of infectious prions will complicate efforts to control CWD and perhaps other animal prion diseases.

Controlling and possibly eradicating animal prion diseases (1) are goals shared by the international community (2,3). However, progress toward eliminating prion diseases from food-producing animals worldwide has been hampered by incomplete knowledge about transmission and environmental persistence of these novel proteinaceous pathogens. Two prion diseases, scrapie of sheep and goats (4-8) and chronic wasting disease (CWD) of deer (Odocoileus spp.) and elk (Cervus elaphus nelsoni) (9-14), are particularly difficult to control because both are contagious among susceptible hosts. In contrast, bovine spongiform encephalopathy (BSE) does not appear to be contagious in cattle, but epidemics are sustained artificially through exposure to feed contaminated with infected bovine tissues (15); whether BSE in sheep is contagious remains undetermined (16). Both infected animals and environments apparently contaminated with the causative agent contribute to scrapie epidemics (4,6,8), and under some conditions, scrapie agents may persist in contaminated environments for years (7). Similarly, CWD is transmitted in the presence of infected mule deer (O. hemionus) (10), and circumstantial evidence exists for transmission from environments contaminated with the CWD agent (9,11,14). CWD epidemics do not appear to have been perpetuated by exposure to contaminated feed, but because ingestion of brain tissue can transmit CWD experimentally to deer (11,17), decomposed carcasses could serve as sources of infection in the environment.

Environmental sources of CWD infection represent potential obstacles to control in natural and captive settings. To investigate their role in transmission of this disease, we compared three potential sources of infection: infected live deer, decomposed infected deer carcasses, and an environment contaminated with residual excreta from infected deer.

Materials and Methods
We conducted a replicated experiment to compare CWD transmission from three infection sources: naturally infected captive mule deer (one infected deer/paddock), carcasses from naturally infected captive mule deer that had decomposed in situ ≈1.8 years earlier (one carcass/paddock), or undisturbed paddock environments where infected mule deer had last resided 2.2 years earlier. Each exposure source was replicated in three separate paddocks; two clean paddocks served as unexposed controls. Control paddocks and paddocks where live infected deer were added or where carcasses decomposed were constructed specifically for this experiment; these paddocks had never housed captive deer or elk and had been closed to access by free-ranging cervids for ≈17 years. Because clinical courses varied in naturally infected deer that served as sources of direct exposure, actual exposure periods varied from 0.75 year (replicate 3) to 1 year (replicate 1). Excreta-contaminated paddocks previously held 19 mule deer that had been orally inoculated during a 2-year pathogenesis study (11) that ended 2.2 years before our study began (≈3.8 infected deer x years of excreta/paddock, assuming equal distribution) but that had not held deer or elk in the interim. All three carcasses were from mule deer euthanized in end-stage clinical CWD. They had been left to decompose in intact form except for the removal of small pieces of brainstem used to confirm CWD infection; only the skeletal remains of carcasses were present at the start of the study.

Experimental animals included 31 free-ranging mule deer from two donor populations distant to endemic CWD foci. Experimental animals were captured from the grounds of the Rocky Mountain Arsenal National Wildlife Refuge (n = 17) and the U.S. Air Force Academy (n = 14), Colorado. We assumed that all experimental animals were free from CWD when they were introduced into the experiment, and surveillance data provided evidence that deer obtained from these herds were uninfected before exposure. Surveillance for CWD in the source populations (10,18) showed 0 positive cases in a sample of 210 adult deer from the refuge and 0 positive cases in a sample of 65 adult deer from the academy.

We used these data to estimate the probability that infection could have been caused by transmission from animals from the source herds. To do so, we estimated one-sided, exact 99% binomial confidence intervals (BCI) on the proportion of each population that could be positive for CWD (refuge = 0–0.022, academy = 0–0.068). We then used the upper limit of this interval to estimate the maximum prevalence,, that could be reasonably expected in each of the source populations, given the inability to detect infections through surveillance. To assess whether observed results were likely due to preexisting infections, we treated each replicate (i.e., paddock) as an independent binomial experiment because the conditions in one paddock had no opportunity to influence the events in another paddock. Thus, for each replicate where infection occurred, we calculated the probability of at least one positive (i.e., "success") given the number of animals introduced to that replicate from the source population (i.e., "trials"), on the assumption that the probability of drawing a positive from the source population was . When two replicates within an exposure category showed infections, we estimated the probability that cases in both replicates resulted from introducing infected animals (and not from our experiment) as the product of the individual replicate probabilities.

We captured deer during March and May 2002 and transported them to the Colorado Division of Wildlife's Foothills Wildlife Research Facility, where they were confined in outdoor paddocks of ≈800 m2 (three replicate paddocks/exposure route, three deer/paddock); four deer were held in the two clean paddocks as unexposed controls. Each replicate of exposure paddocks was initially stocked with three mule deer. Shortly after arrival, one deer was moved to a different paddock within the same exposure condition to resolve social strife, and four fawns were born into three other paddocks; these changes are reflected in denominators in the Table. The distribution of prion protein genotype at codon 225 (serine [S]/phenylalanine [F] [19]) did not differ (Fisher exact test p = 0.6) among the four groups (three exposure groups + control).

Deer were fed alfalfa hay and a pelleted supplement; diets contained no animal protein or other animal byproducts. Individual paddocks and exposure blocks were physically segregated to prevent cross-transmission within and among exposure categories; dedicated clothing and equipment were used to minimize potential cross-contamination, but other potential fomites, like small mammals, birds, and insects, could not be controlled. However, transmission by routes such as these would be consistent with hypothesized transmission from environmental sources rather than direct animal-to-animal contact. After the animals had undergone ≈1 year of exposure to respective sources of infection, we obtained biopsied tonsil specimens from each participant deer and conducted an immunohistochemical analysis using anti-PrP MAb 99/97.6.1 (20,21). Upon detecting >1 infected deer in a paddock, we removed all inhabitants of that paddock and confirmed CWD infection in animals with positive biopsy results (20). Study protocols were reviewed and approved by the Colorado Division of Wildlife Animal Care and Use Committee.

Results
Mule deer exposed to contaminated environments or to infected deer contracted CWD (Table). None of the unexposed deer were infected. One or more introduced deer became infected in two of three paddocks containing a naturally infected deer, in two of three paddocks containing a decomposed deer carcass, and in one of three paddocks contaminated with residual deer excreta (Table) within 1 year of exposure. Infected deer included unrelated animals from both donor herds (2/17, 3/14; Fisher exact test p = 0.64), as well as one of four fawns born during the study. Males (4/16) and females (2/15) were infected at equivalent rates (Fisher exact test p = 0.65); similarly, deer of all three codon 225 genotypes (SS = 6/26, SF = 0/7, FF = 0/2) were infected at equivalent rates (Fisher exact test p = 0.52). Deer with positive biopsy results appeared healthy and did not show signs of CWD, consistent with early (<1 year in duration) infections (11,17).

On the basis of prior data from surveillance of source populations, our results were not likely explained by the null hypothesis of infections introduced from the source populations (p = 0.036 for academy source deer and p < 0.0001 for refuge source deer). The probability of prior infection accounting for our results in the pattern observed (Table) was p < 0.0013 for the infected animal exposure, p < 0.037 for the carcass exposure, p < 0.064 for the excreta exposure, and overall p ≈ 0.000003 for the observed results arising from preexisting infections. Because these probabilities were based on one-sided, upper 99% BCIs, we can conservatively reject the null hypothesis of infection arising from the source populations. The only remaining possibility is that infections arose from experimental exposures that included environments harboring the infectious agent from excreta or decomposed carcasses.

Discussion
Figure

Click to view enlarged image

Figure. Green forage growing at the site where a deer carcass infected with chronic wasting disease had decomposed...

Prions cannot be directly demonstrated in excreta or soil. However, CWD infection–specific protease-resistant prion protein (PrPCWD) accumulates in gut-associated lymphoid tissues (e.g., tonsils, Peyer patches, and mesenteric lymph nodes) of infected mule deer (11,17,22), which implicates alimentary shedding of the CWD agent in both feces and saliva (10,11,17). Because PrPCWD becomes progressively abundant in nervous system and lymphoid tissues through the disease course (11), carcasses of deer succumbing to CWD also likely harbor considerable infectivity and thus serve as foci of infection. We could not determine the precise mechanism for CWD transmission in excreta-contaminated paddocks, but foraging and soil consumption seemed most plausible. Deer did not actively consume decomposed carcass remains, but they did forage in the immediate vicinity of carcass sites where a likely nutrient flush (23) produced lush vegetation (Figure).

Our findings show that environmental sources of infectivity may contribute to CWD epidemics and illustrate the potential complexity of such epidemics in natural populations. The relative importance of different routes of infection from the environment cannot be discerned from our experiment, but each could play a role in sustaining natural epidemics. Although confinement likely exaggerated transmission probabilities, conditions simulated by this experiment do arise in the wild. Mule deer live in established home ranges and show strong fidelity to historic home ranges (24-26). As a result of such behavior, encounters with contaminated environments will occur more frequently than if deer movements were random. Feces and carcass remains are routinely encountered on native ranges, thus representing natural opportunities for exposure. Social behavior of deer, particularly their tendency to concentrate and become sedentary on their winter range, also may increase the probability of coming into contact with sources of infection in their environment.

The ability of the CWD agent to persist in contaminated environments for >2 years may further increase the probability of transmission and protract epidemic dynamics (8). Because infectivity in contaminated paddocks could not be measured, neither the initial levels nor degradation rate of the CWD agent in the environment was estimable. However, the observed persistence of the CWD agent was comparable to that of the scrapie agent, which persisted in paddocks for ≈1 to 3 years after removal of naturally infected sheep (7). Similarities between the CWD and scrapie agents suggest that environmental persistence may be a common trait of prions. Whether persistence of the BSE prion in contaminated feed production facilities or in environments where cattle reside contributed to BSE cases in the United Kingdom after feed bans were enacted (27) remains uncertain but merits further consideration.

Indirect transmission and environmental persistence of prions will complicate efforts to control CWD and perhaps other animal prion diseases. Historically, control strategies for animal prion diseases have focused on infected live animals as the primary source of infection. Although live deer and elk represent the most plausible mechanism for geographic spread of CWD, our data show that environmental sources could contribute to maintaining and prolonging local epidemics, even when all infected animals are eliminated. Moreover, the efficacy of various culling strategies as control measures depends in part on the rates at which the CWD agent is added to and lost from the environment. Consequently, these dynamics and their implications for disease management need to be more completely understood.

Acknowledgments
We thank T. Baker, T. Davis, P. Jeager, and others for assisting in field work, animal care, and laboratory aspects of this study; K. Cramer, J. Jewell, and M. Conner for providing genotype data and analyses; J. Hoeting, M. Samuel, and two anonymous reviewers for providing helpful comments on earlier drafts of our paper.

Our work was supported by the Colorado Division of Wildlife, the University of Wyoming, and National Science Foundation–National Institutes of Health Grant DEB-0091961.

Dr. Miller is a wildlife veterinarian with the Wildlife Research Center, Colorado Division of Wildlife. His research has focused on the ecology and management of infectious diseases in free-ranging wildlife.

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Sigurdson CJ, Williams ES, Miller MW, Spraker TR, O'Rourke KI, Hoover EA. Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus). J Gen Virol. 1999;80:2757-64.
Colorado Division of Wildlife. Prevalence and distribution of chronic wasting disease in Colorado 2002-2003 [monograph on the Internet]. 2003 Aug [cited 2003 Sep 4]. Available from: http://wildlife.state.co.us/cwd/pdf/prevalencesummary8-031.pdf
Brayton KA, O'Rourke KI, Lyda AK, Miller MW, Knowles Jr DP. A processed pseudogene contributes to apparent mule deer prion gene heterogeneity. Gene. 2004;326:167-73.
Miller MW, Williams ES. Detecting PrPCWD in mule deer by immunohistochemistry of lymphoid tissues. Vet Rec. 2002;151:610-2.
Wolfe LL, Conner MM, Baker TH, Dreitz VJ, Burnham KP, Williams ES, et al. Evaluation of antemortem sampling to estimate chronic wasting disease prevalence in free-ranging mule deer. J Wildl Manage. 2002;66:564-73.
Spraker TR, Zink RN, Cummings BA, Wild MA, Miller MW, O'Rourke KI. Comparison of histological lesions and immunohistochemical staining of protease resistant prion protein in a naturally occurring spongiform encephalopathy of free-ranging mule deer (Odocoileus hemionus) with those of chronic wasting disease of captive mule deer. Vet Pathol. 2002;39:110-9.
Towne EG. Prairie vegetation and soil nutrient responses to ungulate carcasses. Oecologia. 2000;122:232-9.
Conner MM, Miller MW. Movement patterns and spatial epidemiology of prion disease in mule deer population units. Ecological Applications. 2004;14: in press.
Kufeld RC, Bowden DC, Schrupp DL. Distribution and movements of female mule deer in the Rocky Mountain foothills. J Wildl Manage. 1989;53:871-7.
Mackie RJ. Mule deer habitat. In: Gerlach D, Atwater S, Schnell J, editors. Deer. Mechanicsburg (PA): Stackpole Books; 1994. p. 286-96.
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Table. Chronic wasting disease arising in mule deer exposed to environments contaminated by residual excreta, carcasses, or other infected deer

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

Replicate
Exposure source
Unexposed

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

Infected deer
Infected carcass
Residual excreta

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

1
1/4a
0/3
1/3
0/2

2
0/2
2/4
0/3
0/2

3
1/4
1/5
0/3
NAb

Total
2/10
3/12
1/9
0/4

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

aNumber positive/number exposed (not including infected source deer).
bNot applicable; controls included only two replicate paddocks.

http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm

tss

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Posts: 230
WHO IS THIS 'HOLE IN THE FENCE GANG'

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

Subject: HOLE IN THE FENCE MAD DEER MAKE GREAT ESCAPE TO INFECT OTHERS (who is the hole in the fence gang?)
Date: January 21, 2006 at 2:04 pm PST
Wildlife officials find only 4 deer on infected game farm

PLOVER, Wis. Sharpshooters killed only four deer at a central Wisconsin game preserve where a number of animals were found to have chronic wasting disease.

State officials had expected to find as many as 40 deer there.

They plan to meet with the preserve's owner for clues as to why so few deer were found in an enclosure where a hole found in a fence prompted concern that some deer escaped.

Sharpshooters had killed 76 deer in breeding pens on Tuesday and four additional deer about a week ago.

Authorities, though, were especially interested in the 40 or so bucks they believed were at Stan Hall's shooting preserve near Plover.

Before sharpshooters arrived, 20 of Hall's deer tested positive for chronic wasting disease.

Copyright 2006 Associated Press. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.

http://www.wbay.com/Global/story.asp?S=4392308

Posted January 18, 2006

State kills CWD-infected herds at Almond preserve

Eradication planned before recent breach in fence

By Heather Clark
Journal staff

ALMOND -- An Almond deer hunting preserve under watch for having deer test positive for chronic wasting disease in the past is being eradicated.

State officials began the task of killing the breeding and hunting herds at Buckhorn Flats, 9403 Third St., on Tuesday, closing off neighboring roads for safety purposes during the shootings.

The Portage County Sheriff's Department was called out about 6 a.m. Tuesday at the request of the state Department of Agriculture, Trade and Consumer Protection (DATCP) to block off Second Avenue from Third Street to Highway J as a safety measure during the shootings, officials said.

The roads were re-opened to through traffic just before 11 a.m.

The killings were planned prior to the recent concern that diseased deer escaped the preserve.

Preserve owner Stan Hill discovered the fence had been cut open and food placed near the opening to bait the deer. When notified, the DATCP closed off the opening and the state Department of Natural Resources was called in. About 40 deer had been known to roam the 59 acres of fenced-in preserve.

Portage County Sher-iff's Department's investigation into that criminal damage continues.

DNR sharpshooters and other personnel remained on site until Monday afternoon, having laid bait for deer near the damaged area of the fence. During that time, four deer were killed coming back to the fenced area, said Alan Crossley, the DNR's chronic wasting disease project leader.

The group left when the DATCP said it was arriving for the scheduled eradication, and Crossley was not sure when they would return.

"Whether those are deer from inside the pen is going to be hard to know, but we felt that was the first place that made the most sense for us to set up and shoot," he said, adding that samples from those two does and two fawns are in the process of being tested.

"The remaining question is OK, is there anything we should do in the short term to try to get additional samples, and that would likely involve working with local landowners," he said.

Hill had been fighting a July 2003 order that the livestock be killed after deer from the preserve were found to have the disease. An agreement between Hill and the state and federal agriculture agencies was reached in December.

Hill's property is about 70 acres, 59 of which are in the fenced-in preserve and another fenced portion contains a breeding herd.

The breeding herd, which was closed off in a different but nearby pen, was comprised of 79 does, fawns and yearling bucks at Hill's last count. DATCP found three dead when they arrived Tuesday, which is not uncommon, said Donna Gilson, communication specialist with the state DATCP. They killed the remaining 76. The carcasses have been transported to the state's testing facility, where samples will be sent to Iowa for CWD testing. Results will take about three weeks, she said.

"We will have people in and out for the next several days," Gilson said. "Killing the hunting preserve herd is a much more complex operation because they are over a larger area, so that will take some time."

The DNR had been surveying wild deer through hunter registration in the past, and given the recent preserve breach, that likely will continue, Crossley said. But should the decision be made to continue killing wild deer outside of the preserve, it would be done in agreement with individual neighboring property owners, he said.

The killings over the weekend were set up on a neighboring property with that landowner's permission, he said.

Hill will be paid up to a maximum of $4,500 per animal from state and federal funds, Gilson said.

http://www.wausaudailyherald.com/apps/pbcs.dll/article?AID=/20060118/SPJ...

TSS

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