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CWD aka mad deer/elk disease i.e. TSE update 2005

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...

Colorado Division of Wildlife (DOW) has detected CWD in deer in two new game management units (GMU’s)

12/29/2005
Division of Wildlife

CWD detected in Units 109 and 84
~ Late Season Hunters Encouraged to Submit Heads for Testing ~

The Colorado Division of Wildlife (DOW) has detected chronic wasting disease (CWD) in deer in two new game management units (GMU’s) where it was not previously detected in eastern Colorado. The new units are GMU 109 north of Burlington and GMU 84 west of Pueblo.

One animal was reported to the DOW by a landowner west of Bonny Reservoir. It was in poor physical condition at the time of death. The second animal, in GMU 84, was a road kill picked up by DOW personnel west of Pueblo on Highway 96.

Tissues from both animals were submitted to Colorado State University’s Veterinary Diagnostics Laboratory and both had positive test results.

In addition, two more deer harvested by hunters at Fort Carson in GMU 591 this year tested positive for CWD.

Some late hunting seasons in Colorado continue through the end of January, and all successful hunters are encouraged to submit their animals for testing. In some units, including Fort Carson, the DOW has waived CWD testing fees encourage more hunters to have their animals tested.

So far this year over 5,000 elk, 6,000 deer and 133 moose had been tested in Colorado. Elk submissions by hunters were down about 15 percent despite an increase in over the counter license sales of about eight percent, suggesting hunter interest in testing is waning or harvest was down or both.

Chronic Wasting Disease affects the brains of deer, elk and moose. Brain tissue of infected animals degenerates causing weight loss, abnormal behavior and eventually, death.

For more information about CWD, log onto: http://wildlife.state.co.us/cwd/index.asp

http://wildlife.state.co.us/news/press.asp?pressid=3725

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...

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

http://neurology.thelancet.com Published online October 31, 2005

Coexistence of multiple PrPSc types in individuals with

Creutzfeldt-Jakob disease

Magdalini Polymenidou, Katharina Stoeck, Markus Glatzel, Martin Vey, Anne Bellon, and Adriano Aguzzi

Summary

Background The molecular typing of sporadic Creutzfeldt-Jakob disease (CJD) is based on the size and glycoform

ratio of protease-resistant prion protein (PrPSc), and on PRNP haplotype. On digestion with proteinase K, type 1 and

type 2 PrPSc display unglycosylated core fragments of 21 kDa and 19 kDa, resulting from cleavage around amino

acids 82 and 97, respectively.

Methods We generated anti-PrP monoclonal antibodies to epitopes immediately preceding the differential proteinase

K cleavage sites. These antibodies, which were designated POM2 and POM12, recognise type 1, but not type 2, PrPSc.

Findings We studied 114 brain samples from 70 patients with sporadic CJD and three patients with variant CJD.

Every patient classified as CJD type 2, and all variant CJD patients, showed POM2/POM12 reactivity in the

cerebellum and other PrPSc-rich brain areas, with a typical PrPSc type 1 migration pattern.

Interpretation The regular coexistence of multiple PrPSc types in patients with CJD casts doubts on the validity of

electrophoretic PrPSc mobilities as surrogates for prion strains, and questions the rational basis of current CJD

classifications.

snip...

The above results set the existing CJD classifications

into debate and introduce interesting questions about

human CJD types. For example, do human prion types

exist in a dynamic equilibrium in the brains of affected

individuals? Do they coexist in most or even all CJD

cases? Is the biochemically identified PrPSc type simply

the dominant type, and not the only PrPSc species?

http://neurology.thelancet.com Published online October 31, 2005

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

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

New Mexico Department of Game and Fish
Media contact: Dan Williams, (505) 476-8004
Public contact: (505) 476-8000
dan.williams@state.nm.us

FOR IMMEDIATE RELEASE, DEC. 9, 2005:

TWO NEW MEXICO ELK TEST POSITIVE FOR CHRONIC WASTING DISEASE

SANTA FE - Two elk killed in the southern Sacramento Mountains of southeast
New Mexico have tested positive for chronic wasting disease (CWD), the
Department of Game and Fish announced. The animals were the first elk in New
Mexico to test positive for CWD since the disease was first discovered in
mule deer in 2002.

Both CWD-afflicted elk were killed in an area 10 to 15 miles southeast of
Cloudcroft in Game Management Unit 34, the same general area where the
state's most recent case of CWD was detected in a mule deer. One of the
elk - a mature male -- was taken Oct. 3 by a hunter and showed no symptoms
of the disease. The other elk - a yearling female -- was in very poor
condition and unable to stand when a Department of Game and Fish
conservation officer found it Oct. 1. Testing and verification of the
samples required about two months. Future testing is expected to occur more
quickly as the Department of Game and Fish and the Veterinary Diagnostic
Services in the New Mexico Department of Agriculture further implement
recently achieved in-state CWD testing capabilities.

"The range in which the disease is found appears to be expanding, so finding
it in more animals in that area is not surprising," said Kerry Mower, the
Department's lead wildlife disease biologist. "But it is disappointing to
find our first cases of CWD in free-ranging elk."

Brain stem samples from the two elk were among more than 100 taken from deer
and elk in Unit 34 this year and sent to the Veterinary Diagnostic Services
Laboratory in Albuquerque. The Albuquerque laboratory's "presumptive
positive" samples from the two elk were confirmed as CWD-positive by the
National Veterinary Services Laboratory in Ames, Iowa.

"We will continue our efforts to monitor the disease by actively testing
animals in Units 34 and 19," Mower said. "We also encourage all hunters
statewide to submit their animals for testing." The Department personally
informs hunters if the tests are positive. Hunters will be able to see the
complete list of test results as they become available on the Department Web
site, http://www.wildlife.state.nm.us .

This season, hunters who kill animals in a "Control Area" of Unit 34 are
required to submit their animals for testing and observe special regulations
affecting which body parts of a deer or elk can be removed from the unit.
Hunting seasons continue in that area into January.

Chronic wasting disease is a fatal neurological illness that afflicts deer,
elk and moose. There is no evidence of CWD being transmitted to humans or
livestock. The disease causes animals to become emaciated, display abnormal
behavior and lose control of bodily functions. To date, it has been found in
captive and wild deer, elk and moose in eight states and two Canadian
provinces.

The origin of CWD in New Mexico is unknown. It has been found in 12 wild
deer and two wild elk since 2002, when the disease was first discovered east
of Las Cruces. All of the CWD-positive deer and elk in New Mexico were from
the southern Sacramento Mountains southeast of Cloudcroft and areas
surrounding the Organ Mountains near Las Cruces.

For more information about CWD in New Mexico, including special regulations
and how hunters can assist in research and prevention, visit the Department
Web site at http://www.wildlife.state.nm.us . More information about CWD also can
be found on the Chronic Wasting Disease Alliance site at http://www.cwd-info.org/
or on the Colorado Division of Wildlife site at
http://wildlife.state.co.us/.

###

http://www.wildlife.state.nm.us/publications/press_releases/documents/10...
delk.htm

CWD CONTROL MAP NM

http://www.wildlife.state.nm.us/documents/cwdcontrolmap.pdf

TSS
----- Original Message -----
From: "ProMED-mail"
To:
Sent: Tuesday, June 28, 2005 11:32 AM
Subject: PRO/AH/EDR> Chronic wasting disease, cervids - USA (NM)

> CHRONIC WASTING DISEASE, CERVIDS - USA (NEW MEXICO)
> ***************************************************
> A ProMED-mail post
>
> ProMED-mail is a program of the
> International Society for Infectious Diseases
>
>
> Date: 24 Jun 2005
> From: Terry S. Singeltary Sr.
> Source: New Mexico Wildlife News, Mon, 27 Jun 2005 [edited]
>
>
>
> 2 Mule Deer Test Positive For Chronic Wasting Disease
> ---------------------------------------------------
> 2 mule deer captured in the Organ Mountains as part of an ongoing
> research project near White Sands Missile Range have tested positive
> for chronic wasting disease (CWD), a fatal neurological disease that
> attacks the brains of infected deer and elk, the Department of Game
> and Fish announced.
>
> The number of confirmed CWD cases in New Mexico now stands at 11
> since 2002, when the disease was first confirmed in a deer found near
> the eastern foothills of the Organ Mountains. All 11 CWD-infected
> deer were found in the same general area of southern New Mexico. The
> origin of the disease in New Mexico remains unknown. The carcasses of
> the infected deer will be incinerated, said Kerry Mower, the
> Department's lead wildlife disease biologist.
>
> Mower said the most recent CWD-positive deer showed no obvious
> physical signs of having the disease. They were captured in April
> 2005 and tested as part of a 3-year-old research project studying
> deer population dynamics in southern New Mexico. More than 140 deer
> have been captured alive and tested for the study, in which
> researchers hope to find the cause of a 10-year decline in the area
> deer population. Study participants include the Department of Game
> and Fish, the U.S. Army at White Sands Missile Range and Fort Bliss,
> Bureau of Land Management, U.S. Geological Survey at New Mexico State
> University, and San Andres National Wildlife Refuge.
>
> Hunters can assist the Department in its CWD research and prevention
> efforts by bringing their fresh, legally harvested deer or elk head
> to an area office, where officers will remove the brain stem for
> testing. Participants will be eligible for drawings for an oryx hunt
> on White Sands Missile Range and a trophy elk hunt on the Valle
> Vidal. For more information about the drawing and chronic wasting
> disease, visit the Department web site at
>
>
> See map:
>
>
> --
> ProMED-mail
>
>
> [Members are strongly encouraged to view the NM CWD map at the URL
> below. In 2004 they tested 997 deer, each shown. These recent deer
> are clustered with the others just to the east of Las Cruces in
> southern New Mexico. The absence of cases elsewhere in the state at
> this level of surveillance increases one's confidence in the reality
> of this specific high-risk area. The origin of their infection is
> still obscure.
>
> The New Mexico CWD website is:
>
>
> Unfortunately, other than their admirable map, they have not been
> updated since 14 Jun 2004.
>
> The site being close to Texas and to Mexico has spawned speculation,
> but as yet without foundation. In the past 3 years Texas has tested
> some 9103 deer out of a target population estimate of 3 917 926, all
> negative. For details of the Texas Chronic Wasting Management Plan,
> go to:
>
> or the Texas Animal Health Commission CWD website:
>
> - Mod.MHJ]
>
> [see also:
> 2003
> ----
> Chronic wasting disease, cervids - USA (NM) (02) 20030217.0414
> Chronic wasting disease, cervids - USA (NM) 20030207.0328
> 2002
> ----
> Chronic wasting disease, cervids - USA (New Mexico) (02) 20020620.4548
> Chronic wasting disease, cervids - USA (New Mexico) 20020619.4535]
> ...............................................lm/mhj/pg/lm
>
>
> *##########################################################*
> ************************************************************
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#################### https://lists.aegee.org/bse-l.html ####################

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

HUMAN TSE USA 2005

Animal Prion Diseases Relevant to Humans (unknown types?)
Thu Oct 27, 2005 12:05
71.248.128.109

About Human Prion Diseases /
Animal Prion Diseases Relevant to Humans

Bovine Spongiform Encephalopathy (BSE) is a prion disease of cattle. Since 1986, when BSE was recognized, over 180,000 cattle in the UK have developed the disease, and approximately one to three million are likely to have been infected with the BSE agent, most of which were slaughtered for human consumption before developing signs of the disease. The origin of the first case of BSE is unknown, but the epidemic was caused by the recycling of processed waste parts of cattle, some of which were infected with the BSE agent and given to other cattle in feed. Control measures have resulted in the consistent decline of the epidemic in the UK since 1992. Infected cattle and feed exported from the UK have resulted in smaller epidemics in other European countries, where control measures were applied later.

Compelling evidence indicates that BSE can be transmitted to humans through the consumption of prion contaminated meat. BSE-infected individuals eventually develop vCJD with an incubation time believed to be on average 10 years. As of November 2004, three cases of BSE have been reported in North America. One had been imported to Canada from the UK, one was grown in Canada, and one discovered in the USA but of Canadian origin. There has been only one case of vCJD reported in the USA, but the patient most likely acquired the disease in the United Kingdom. If current control measures intended to protect public and animal health are well enforced, the cattle epidemic should be largely under control and any remaining risk to humans through beef consumption should be very small. (For more details see Smith et al. British Medical Bulletin, 66: 185. 2003.)

Chronic Wasting Disease (CWD) is a prion disease of elk and deer, both free range and in captivity. CWD is endemic in areas of Colorado, Wyoming, and Nebraska, but new foci of this disease have been detected in Nebraska, South Dakota, New Mexico, Wisconsin, Mississippi Kansas, Oklahoma, Minnesota, Montana, and Canada. Since there are an estimated 22 million elk and deer in the USA and a large number of hunters who consume elk and deer meat, there is the possibility that CWD can be transmitted from elk and deer to humans. As of November 2004, the NPDPSC has examined 26 hunters with a suspected prion disease. However, all of them appeared to have either typical sporadic or familial forms of the disease. The NPDPSC coordinates with the Centers for Disease Control and state health departments to monitor cases from CWD-endemic areas. Furthermore, it is doing experimental research on CWD transmissibility using animal models. (For details see Sigurdson et al. British Medical Bulletin. 66: 199. 2003 and Belay et al. Emerging Infectious Diseases. 10(6): 977. 2004.)

http://www.cjdsurveillance.com/abouthpd-animal.html

SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2004. SPORADIC CJD CASES TRIPLED, and that is with a human TSE surveillance system that is terrible flawed. in 1997 cases of the _reported_ cases of cjd were at 54, to 163 _reported_ cases in 2004. see stats here;

p.s. please note the 47 PENDING CASES to Sept. 2005

p.s. please note the 2005 Prion D. total 120(8) 8=includes 51 type pending, 1 TYPE UNKNOWN ???

p.s. please note sporadic CJD 2002(1) 1=3 TYPE UNKNOWN???

p.s. please note 2004 prion disease (6) 6=7 TYPE UNKNOWN???

http://www.cjdsurveillance.com/resources-casereport.html

CWD TO HUMANS = sCJD ???

AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.

snip...

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf

ATYPICAL TSEs in USA CATTLE AND SHEEP ?

http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf

Infected and Source Flocks

As of August 31, 2005, there were 115 scrapie infected and source flocks (figure 3). There were 3 new infected and source flocks reported in August (Figure 4) with a total of 148 flocks reported for FY 2005 (Figure 5). The total infected and source flocks that have been released in FY 2005 are 102 (Figure 6), with 5 flocks released in August. The ratio of infected and source flocks released to newly infected and source flocks for FY 2005 = 0.69 :
1. In addition, as of August 31, 2005, 574 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 122 were RSSS cases (Figure 7). This includes 55 newly confirmed cases in August 2005 (Figure 8). Fifteen cases of scrapie in goats have been reported since 1990 (Figure 9). The last goat case was reported in May 2005.

snip...

full text ;

http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report...

CHRONIC WASTING DISEASE UPDATE 2005 (03)
****************************************
A ProMED-mail post

ProMED-mail, a program of the
International Society for Infectious Diseases

Sponsored in part by Elsevier, publisher of
The Lancet Infectious Diseases

[1]
Date 18 Oct 2005
From: Terry S Singeltary Sr
Source: Utah Division of Wildlife Resources [edited]

2 buck deer taken during this year's Utah muzzleloader hunt have tested
positive for chronic wasting disease (CWD), the Division of Wildlife
Resources announced on 17 Oct 2005.

The 1st deer was a yearling buck taken near the south end of Flaming Gorge
Reservoir. This is the 1st CWD positive deer found in Daggett County. Other
CWD positive deer have been found in the past just 20 miles to the south,
near Vernal. The 2nd deer to test positive was a mature buck taken on the
LaSal Mountains in south eastern Utah.

Both of the hunters who took the deer have been notified that their animals
tested positive for CWD. "We've tested approximately 450 deer and elk so
far this year, and these are the only animals that have tested positive for
CWD," said Leslie McFarlane, wildlife disease specialist for the DWR.
"Nearly all of the testing has been completed on samples collected during
the archery and muzzleloader hunts. We expect to collect nearly 2000
samples during the rifle deer hunt that starts this weekend."

The Utah Veterinary Diagnostic Laboratory in Logan is testing the samples
for the DWR. The latest finds bring to 20 the number of deer that have
tested positive for CWD since the disease was first found in Utah in
February 2003. 14 of the 20 deer have come from the LaSal Mountain area,
where DWR biologists estimate about 2 per cent of the deer have the disease.

Of the remaining deer, 4 came from the Vernal area, 1 was taken near the
south end of Flaming Gorge, and one was killed near Fountain Green in
central Utah.

CWD is fatal to deer and elk that contract it. However, according to the
World Health Organization, "There is currently no evidence that CWD in
cervidae (deer and elk) is transmitted to humans."

******
[2]
Date: 18 Oct 2005
From: Terry S Singeltary Sr
Source: Utah Division of Wildlife Resources [edited]

Division of Wildlife Resources (DWR) personnel are in the process of
monitoring the presence and prevalence of chronic wasting disease (CWD) in
the State of Utah. A small number of deer harvested in the state have
tested positive for CWD during the past 4 years. Sportsmen participating in
the general season rifle hunt, which opens 22 Oct 2005, are encouraged to
participate in this disease monitoring effort.

Testing for the disease is done by removing the lymph nodes from the throat
of the deer. The abnormal prions (proteins) indicative of CWD tend to
accumulate in these lymph node tissues. Lymph node samples from each deer
sampled are sent to a laboratory in Logan and hunters can learn whether the
deer has tested positive for CWD within 4 weeks.

Currently, there is no evidence to suggest that the disease can be
transmitted to humans by eating or handling meat of infected animals.
However, it is advised that hunters avoid consumption and direct contact
with brain tissues, spinal fluids, and lymph nodes.

DWR personnel will be taking disease samples from deer harvested throughout
the south eastern region. Hunters may encounter officers in the field or at
check stations. Hunters who are not contacted and have questions regarding
CWD can contact the Price DWR office at (435) 636-0260 during business
hours, or (435) 820-8921 during non-business hours.

******
[3]
Date: 18 Nov 2005
From: Terry S Singeltary Sr
Source: New Hampshire State Wildlife, 9 Nov 2005 [edited]

Officials from the New Hampshire Fish and Game Department announced today
that 2 hunters have been cited for illegally importing whole deer from New
York State, a state where chronic wasting disease (CWD) has been detected.
The 2 deer were confiscated and destroyed as part of ongoing attempts to
protect New Hampshire's deer and moose populations from the threat of CWD,
a disease -- fatal to some members of the deer family -- that is found in
16 US states and Canadian provinces.

"The threat posed by CWD to New Hampshire's deer herd is of serious concern
to us," said Lee Perry, Fish and Game's executive director. "Hunters who
hunt out of state need to abide by the rules, which are designed to allow
people to bring their deer back to New Hampshire without putting the
state's herd at risk." The confiscated deer from New York, not yet
butchered, were incinerated to destroy any potentially contagious material.

Current NH regulations allow for the importation into New Hampshire of only
deboned meat, antlers, upper canine teeth, and/or hides or capes with no
part of the head attached of deer and elk, from the 16 states and provinces
where CWD has been confirmed. These include Alberta, Canada; Colorado;
Illinois; Kansas; Minnesota; Montana; Nebraska; New Mexico; New York;
Oklahoma; Saskatchewan, Canada; South Dakota; Utah; Wisconsin; West
Virginia (the newest addition to the list), and Wyoming.

Antlers attached to skull caps or canine teeth must have all soft tissue
removed. More information on CWD is found on pages 6 and 60 of the current
New Hampshire Hunting Digest or [go to the URL above and click here] for
New Hampshire-related questions and answers about CWD.

A CWD monitoring and testing program for wild deer has been conducted in
New Hampshire by Fish and Game biologists since 2002. There is no evidence
that this disease exists in the New Hampshire deer herd, and the rules and
testing program are designed to prevent exposure via infected animals being
imported from other areas.

CWD is a contagious neurological disease that is fatal to deer, moose, elk,
and other members of the cervid (deer) family. It is classified as a
transmissible spongiform encephalopathy or TSE, and it attacks the brains
of infected animals, resulting in their becoming emaciated, exhibiting
abnormal behavior and eventually dying.

State officials remind hunters and others who enjoy eating venison that CWD
is a wildlife management issue, not a public health issue. There is no
evidence that CWD is linked to disease in humans.

--
ProMED-mail

[In states where CWD is present, it would not be unexpected to find it
during the hunting season. Many states have a hunter surveillance program.
Most often the harvested animal is taken to a station where samples are
collected for testing for CWD.

Clearly NH is being very diligent in its efforts to keep CWD out of the
state. However, there is no mention that these animals were tested for the
disease.

It is believed that infected deer from other states transported into NY for
taxidermy work introduced the disease into NY. The taxidermist in NY did
not dispose of the deer offal in the recommended manner, but rather spread
it around the fence line, thus giving curious captive and wild deer
opportunity to come into contact with the intestines of the infected deer.
Since prions are believed to be presented to the neurological system
through the intestines, and cervidae are curious animals that taste what is
new in their environment, it is possible this was the method of
introduction of the disease to NY.

For hunters hunting outside of their home state, it appropriate to know the
regulations regarding bringing carcasses home. - Mod.TG]

[see also:
Chronic wasting disease, moose - USA (CO) 20050930.2865
Chronic wasting disease, cervids - Canada (AB) 20050907.2650
Chronic wasting disease - USA (WV) 20050904.2615
Chronic wasting disease, cervids - Canada (SK) 20050706.1917
Chronic wasting disease, cervids - USA (NM) 20050628.1827
Chronic wasting disease, cervids - USA (NY)(05) 20050505.1241
Chronic wasting disease, cervids - USA (NY)(04) 20050428.1187
Chronic wasting disease, cervids - USA (NY) (03): human exposure 20050409.1028
Chronic wasting disease, cervids - USA (NY)(02) 20050402.0952
Chronic wasting disease, cervids - USA (NY) 20050331.0932
Chronic wasting disease update 2005 (02) 20050201.0346
Chronic wasting disease update 2005 20050131.0337]

...............tg/pg/sh

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From: TSS ()
Subject: CWD SPREADING IN WYOMING ! what about scrapieTSE and bseTSE ?
Date: November 29, 2005 at 10:35 am PST

From: TSS ()
Subject: CWD SPREADING IN WYOMING !
Date: November 29, 2005 at 9:41 am PST

CWD DETECTED IN NEW HUNT AREA NEAR NEWCASTLE

11/18/2005

CASPER - A white-tailed deer harvested in Hunt Area 9 near Newcastle has tested positive for chronic wasting disease. The disease had not previously been found in deer Hunt Area 9.

The deer was harvested on a ranch southeast of Newcastle in early October. The area is open to hunting for doe and fawn deer until Nov. 30 with 200 doe/fawn licenses, according to Wyoming Game and Fish Department regulations.

“It’s not a surprise that CWD was found in Hunt Area 9,” said Scott Edberg, wildlife supervisor for the Game and Fish’s Casper Region. “The disease has previously been found in the same drainage about 18 miles downstream in South Dakota, and across (U.S.) highway 16 in Hunt Area 6.”

Hunt Area 9 borders the Wyoming/South Dakota state line. Edberg said area landowners are cooperating with CWD research efforts by allowing hunters to harvest antlerless deer and submit them for testing.

The Game and Fish will continue to collect as many samples as possible from deer harvested in the area and killed by vehicles on adjacent highways. CWD surveillance sampling stations will be set up at the Old Mill in Newcastle and at C&A Meats in Sundance Nov. 18-20 from 9 a.m. to 5 p.m.

“We encourage all hunters harvesting deer in northeast Wyoming to stop by a surveillance sampling station and have their animal tested,” Edberg said. Collecting additional samples will help the Game and Fish understand how widespread the disease is in the area.

In addition to the positive test in Deer Area 9, a third deer has tested positive for CWD in Hunt Area 8, southwest of Upton. Although Hunt Area 8 is considered an endemic area (the disease has already been documented in this area), there have been only two positives per year since 2003. The most recent positive sample was from a white-tailed deer. The previous positives were from mule deer.

CWD is a fatal neurological disease that has been diagnosed in wild deer, elk and moose. Animals show no apparent signs of illness throughout much of the course of the disease. In terminal stages of CWD, animals typically are emaciated and display abnormal behavior.

There is no confirmed link between CWD and any human illness.

For more information on chronic wasting disease visit the Game and Fish Web site at http://gf.state.wy.us.

(contact: Robin Kepple (307) 473-3400)

-WGFD-

http://gf.state.wy.us/services/news/pressreleases/05/11/18/051118_3.asp

CWD FOUND IN NEW AREA IN BIG HORN BASIN

10/28/2005

THERMOPOLIS – Two mature mule deer bucks harvested in hunt area 127 immediately northwest of Thermopolis have tested positive for chronic wasting disease (CWD), a fatal brain disease that can affect all members of Wyoming’s deer family. CWD had not previously been detected in this area.

Worland Wildlife Biologist Bart Kroger collected lymph nodes from the deer Oct. 17 as part of the Wyoming Game and Fish Department’s CWD surveillance effort. Both samples were tested at the department’s laboratory in Laramie and tested positive for CWD.

CWD testing is a two-pronged approach, according to Cody Region Wildlife Management Coordinator Kevin Hurley. “The first test is an immunologic test called the ELISA. When a sample tests positive, it is termed a ‘presumptive positive’ until the results from a second IHC (immunohistochemistry) test is known,” Hurley said. “In nearly every case, when the ELISA turns up a presumptive positive, it is confirmed positive by the IHC.”

The two samples from area 127 tested positive for first the ELISA test and then the IHC test on Oct. 28.

In an effort to manage the spread of CWD and to understand how widespread it might be in an area, the department considers taking aggressive actions when cases are found in new areas. In this case, Game and Fish Deputy Director Gregg Arthur has instructed personnel in the Cody region to remove up to 50 deer within a five-mile radius of where the area 127 deer were harvested.

“I have asked our Cody personnel to move forward and collect additional samples. This action is consistent with the best science and the department’s CWD Management Plan,” Arthur said. He added that surveillance in other states has shown that it may be possible to slow down the spread of CWD if new cases of CWD are identified early.

According to Arthur, the additional sampling serves three purposes. First, it allows the Game and Fish to determine the prevalence of CWD in an area. Secondly, it may eliminate CWD in an area and prevent its spread to other areas. And thirdly, it may allow the Game and Fish to locate an area of infection that it can manage aggressively.

“Should more positives turn up, we will expand our efforts,” Arthur said.

The Game and Fish will conduct the removal harvesting both adult males and females between Oct. 27 and mid-November during daytime and nighttime hours. Research has demonstrated that samples taken from adult males and adult females are more likely to indicate if CWD is present than taking samples from younger-aged animals.

All of the animals collected will be field dressed and held in cold storage until the absence or presence of CWD in each is known. The meat from deer testing negative will be donated to individuals and families in need. Carcasses testing positive will be disposed of in an approved landfill in accordance with the Game and Fish CWD transportation regulation.

CWD is a fatal neurological disease that has been diagnosed in wild deer and elk in 10 states and two Canadian provinces. Animals show no apparent signs of illness throughout much of disease course. In terminal stages of CWD, animals typically are emaciated and display abnormal behavior.

There is no confirmed link between CWD and any human illness.

For more information on chronic wasting disease visit the Game and Fish Web site http://gf.state.wy.us

(contact: Dennie Hammer or Kevin Hurley (307) 527-7125)

-WGFD-

http://gf.state.wy.us/services/news/pressreleases/05/10/28/051028_1.asp

CWD FOUND IN DEER AND ELK IN NEW AREA SOUTH OF LARAMIE

10/21/2005

LARAMIE – The first deer and elk to test positive for chronic wasting disease in deer hunt area 77 and elk hunt area 8 south of Laramie were discovered this hunting season by the Wyoming State Veterinary Laboratory and Game and Fish Department.

The discovery was not surprising because CWD has been confirmed in all surrounding hunt areas in both Wyoming and Colorado, according to Bob Lanka, Game and Fish wildlife management coordinator in Laramie.

Both animals testing positive south of Laramie were hunter-killed adult females. The deer was taken on Jelm Mountain Oct. 2 and the elk on Boulder Ridge very near the Colorado border Oct. 3.

“Even though we expected CWD to show up in this area at some time, it is still a little disappointing when we have to add another hunt area to the list of positive areas,” Lanka said.

Hank Edwards, wildlife disease specialist in charge of testing and mapping CWD data, reports his crew has examined the lymph nodes from 1,800 hunter-harvested deer and elk this fall for CWD and expects to test a total of over 4,000 samples this year. No other new area hunt areas in Wyoming have been discovered with CWD this fall.

CWD is a communicable disease of the deer family caused by an abnormal protein or prion. There is no evidence that CWD can infect humans.

As tests are completed the Game and Fish will keep the public informed of any other cases of CWD found in new hunt areas.

(contact: Michelle Zitek (307) 745-4046)

-WGFD-

http://gf.state.wy.us/services/news/pressreleases/05/10/21/051021_2.asp

9/8/2005 DRAFT

WYOMING GAME AND FISH DEPARTMENT

CHRONIC WASTING DISEASE MANAGEMENT PLAN

August 19, 2005

EXECUTIVE SUMMARY

• It is the purpose of this plan to provide flexible and adaptable direction for management of Chronic Wasting Disease (CWD).

• The plan will be reviewed and updated as the CWD situation in Wyoming changes and additional information becomes available.

• The plan consists of four components: Disease Management, Applied Research, Public Information, and Funding.

• Based upon the known epidemiology of CWD in free-ranging deer and elk, eradication currently is not a justified or realistic disease management objective.

• The WGFD will work to minimize the spread of CWD and coordinate CWD management with other state and federal agencies.

• The WGFD will conduct surveillance to determine spatial distribution and prevalence of CWD, and coordinate CWD research with other state and federal agencies.

• The WGFD will provide timely, complete, and accurate information about CWD.

• Although there are concerns or perceptions by some people that CWD could be a livestock or human health threat, there currently is no credible supporting evidence; consequently, this plan addresses CWD as a disease of deer and elk.

• The WGFD will continue to work cooperatively with the Wyoming Department of Public Health and other human health organizations worldwide to monitor current research on CWD and human health and to provide up-to-date information to the public.

• Many very expensive CWD management, research, and public outreach activities are driven by the consideration of CWD as an international disease of concern; therefore, federal funding is appropriate for complete implementation of this plan.

INTRODUCTION

snip...

http://gf.state.wy.us/downloads/pdf/CWD2005Plan8-19-05.pdf

WHAT WILL cwdCJD LOOK LIKE IN HUMANS IN WYOMING ???

Subject: Interspecies Transmission of Chronic Wasting Disease Prions to
Squirrel Monkeys (Saimiri sciureus)
Date: October 19, 2005 at 8:33 am PST

0022-538X/05/$08.00+0 doi:10.1128/JVI.79.21.13794-13796.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Interspecies Transmission of Chronic Wasting Disease Prions to Squirrel
Monkeys (Saimiri sciureus)
Richard F. Marsh,1, Anthony E. Kincaid,2 Richard A. Bessen,3 and Jason C.
Bartz4*
Department of Animal Health and Biomedical Sciences, University of
Wisconsin, Madison 53706,1 Department of Physical Therapy,2 Department of
Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska
68178,4 Department of Veterinary Molecular Biology, Montana State
University, Bozeman, Montana 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.

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

* 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.

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

Journal of Virology, November 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.

http://jvi.asm.org/cgi/content/abstract/79/21/13794maxtoshow=&HITS=10&hi...

SCRAPIE IN WYOMING

Wyoming State Veterinary Laboratory Newsletter Vol 3(#2):July, 2002

Wyoming State Veterinary Laboratory

1174 Snowy Range Road, Laramie, WY 82070

TEL: (800) 442-8331 FAX: (307) 721-2051

http://wyovet.uwyo.edu/

University of Wyoming

snip...

Scrapie in Wyoming

Scrapie infected flocks are being detected at the rate of about one per month in

Wyoming. Live animal testing reveals that classical signs of scrapie (pruritis; severe weight loss)

are not always present. In fact, we have detected several cases of scrapie in completely

asymptomatic sheep. Practitioners should include scrapie as a rule-out whenever a progressive,

debilitating illness is noted in 3 -5 year old sheep, particularly black-face breeds. Please recall

that goats can be infected with scrapie, too.

Wyoming requires that live scrapie suspects be reported. The USDA, in collaboration

with the Wyoming State Veterinary Laboratory and other state diagnostic laboratories, is doing

research on scrapie infected sheep and goats. This research requires numerous tissues be

collected from live suspects (e.g. eyelid biopsy, blood for genetic testing) or that freshly

harvested tissues (e.g. placentomes, gut lymph nodes) be collected at necropsy. Indemnity is

paid for live scrapie suspects. The USDA will provide reasonable transportation costs for

clinically suspect sheep. Live suspects should be transported to Wyoming State Veterinary

Laboratory for necropsy and collection of samples for the USDA.

Please report live clinical scrapie suspects to USDA @ 772-2186 or WLSB @ 777-7515.

John Duncan

http://wyovet.uwyo.edu/WSVL/archives/V3i2.pdf

http://www.aphis.usda.gov/vs/nahps/scrapie/yearly_report/figure06.gif

http://www.aphis.usda.gov/vs/nahps/scrapie/yearly_report/figure07.gif

1 goat scrapie case Wyoming

http://www.aphis.usda.gov/vs/nahps/scrapie/yearly_report/figure09.gif

RSSS postive samples

http://www.aphis.usda.gov/vs/nahps/scrapie/yearly_report/figure13.gif

BSE TESTING WYOMING ???

http://www.aphis.usda.gov/lpa/issues/bse/surveillance/figure4f.html

http://www.aphis.usda.gov/lpa/issues/bse/surveillance/figure5f.html

http://www.aphis.usda.gov/lpa/issues/bse/surveillance/figure6f.html

http://www.aphis.usda.gov/lpa/issues/bse/surveillance/06bse_descriptionf...

http://www.fda.gov/ohrms/dockets/ac/04/slides/4019S1_2.ppt

http://www.fsis.usda.gov/PPT/BSE_APHIS_Surveillance_alt/index.asp

12/10/76
AGRICULTURAL RESEARCH COUNCIL
REPORT OF THE ADVISORY COMMITTE ON SCRAPIE
Office Note
CHAIRMAN: PROFESSOR PETER WILDY

snip...

A The Present Position with respect to Scrapie
A] The Problem

Scrapie is a natural disease of sheep and goats. It is a slow
and inexorably progressive degenerative disorder of the nervous system
and it ia fatal. It is enzootic in the United Kingdom but not in all
countries.

The field problem has been reviewed by a MAFF working group
(ARC 35/77). It is difficult to assess the incidence in Britain for
a variety of reasons but the disease causes serious financial loss;
it is estimated that it cost Swaledale breeders alone $l.7 M during
the five years 1971-1975. A further inestimable loss arises from the
closure of certain export markets, in particular those of the United
States, to British sheep.

It is clear that scrapie in sheep is important commercially and
for that reason alone effective measures to control it should be
devised as quickly as possible.

Recently the question has again been brought up as to whether
scrapie is transmissible to man. This has followed reports that the
disease has been transmitted to primates. One particularly lurid
speculation (Gajdusek 1977) conjectures that the agents of scrapie,
kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of
mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed
for human or animal food at slaughter or rendering plants" (ARC 84/77)"
The problem is emphasised by the finding that some strains of scrapie
produce lesions identical to the once which characterise the human
dementias"

Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety
of laboratory personnel requires prompt attention. Second, action
such as the "scorched meat" policy of USDA makes the solution of the
acrapie problem urgent if the sheep industry is not to suffer
grievously.

snip...

76/10.12/4.6

http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf

Infected and Source Flocks

As of August 31, 2005, there were 115 scrapie infected and source flocks (figure 3). There were 3 new infected and source flocks reported in August (Figure 4) with a total of 148 flocks repor

Offline
Joined: 01/01/2006
Posts: 230
CWD aka mad deer/elk disease i.e. TSE update 2005

Infected and Source Flocks

As of August 31, 2005, there were 115 scrapie infected and source flocks (figure 3). There were 3 new infected and source flocks reported in August (Figure 4) with a total of 148 flocks reported for FY 2005 (Figure 5). The total infected and source flocks that have been released in FY 2005 are 102 (Figure 6), with 5 flocks released in August. The ratio of infected and source flocks released to newly infected and source flocks for FY 2005 = 0.69 :
1. In addition, as of August 31, 2005, 574 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 122 were RSSS cases (Figure 7). This includes 55 newly confirmed cases in August 2005 (Figure 8). Fifteen cases of scrapie in goats have been reported since 1990 (Figure 9). The last goat case was reported in May 2005.

snip...

full text ;

http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report...

[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle

03-025IFA
03-025IFA-2
Terry S. Singeltary

Page 1 of 17

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

Sent: Thursday, September 08, 2005 6:17 PM

To: fsis.regulationscomments@fsis.usda.gov

Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements

for the Disposition of Non-Ambulatory Disabled Cattle

Greetings FSIS,

I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and

Requirements for the Disposition of Non-Ambulatory Disabled Cattle

THE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled Cattle

Broken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;

snip...FULL TEXT ;

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf

SRM Guidance Material
FSIS provides assistance to inspection program personnel in performing their verification activities as outlined in the interim final rule issued to amend 9 CFR 310.22(a)(3) of its regulations for the removal, segregation, and disposition of specified risk materials (SRMs).
Photograph 1 - Basic anatomical features to help determine the location of the most distal point of the distal ileum portion of the small intestine. (PDF only)
http://www.fsis.usda.gov/PDF/TSC_SRM_Cecum_Ileum.pdf
Photograph 2 - View of the ileocecal junction. (PDF only)
http://www.fsis.usda.gov/PDF/TSC_SRM_Ileocecal_Junction.pdf
Photograph 3 - View the uncoiling and trimming of the distal ileum proximal to the ileocecal junction. (PDF only)
http://www.fsis.usda.gov/PDF/TSC_SRM_Trimmed_Uncoiled_Ileum.pdf

BSE Guidance Material
Using Dentition to Age Cattle
Despite individual differences, when the age of an animal is not known, examination of the teeth serves as the best and most practical method of age determination.
Information and diagrams on the acceptable removal of tonsils from cattle for purposes of 9 CFR 310.22.
Visual diagrams and information provided in support of FSIS Notice 50-04

http://www.fsis.usda.gov/About_FSIS/Technical_Service_Center/index.asp

http://www.usda.gov/Newsroom/0264.04.html

http://www.usda.gov/Newsroom/0273.04.html

http://www.usda.gov/Newsroom/0289.04.html

Greetings,

i am trying to refrain in the new year, from having any opinion at all, one of a few of my new years resolutions. just go with the flow i suppose. the wife is estatic about it, her mom and dad have a bet. i even plan to expand this into my ongoing search for answers into TSE. so if i become boring, it's because i have no opinion on anything,
i will say nothing. it's going to be a quiet 2006. the betting lines are open at;
1-800-dontgiva ;-)

however, i suppose it does not hurt to ponder. i only ponder why they have ignored there own science there at USDA for all these years ;

Section
Title
File Format
Updated
Complete Manual The Complete BSE Surveillance Manual pdf 9.3mb 10/01/04 What's New Changes from the previous version html 17kb
10/01/04

Title Page
Contents

pdf 30kb
pdf 32kb
10/01/04
08/24/04
Procedure Manual Procedure Manual for BSE Surveillance pdf 420kb 10/01/04 Appendix A Procedures for investigations and
surveillance of targeted cattle for bovine spongiform encephalopathy (BSE) pdf 1.14mb 08/24/04 Appendix B BSE Surveillance Plan pdf 67kb 08/24/04 Appendix C State-level Surveillance Plan Templates pdf 80kb 08/24/04 Appendix D Sampling Job Aid pdf 1.6mb 08/24/04 Appendix E Taking a Quality Sample pdf 346kb 08/24/04 Appendix F AVIC Directory pdf 27kb 09/09/04 Appendix G Forms pdf 953kb 08/24/04 Appendix H Barcodes pdf 99kb 08/24/04 Appendix I Determining the Age of the Cattle pdf 888kb 08/24/04 Appendix J Background on BSE pdf 31kb 08/24/04 Appendix K FSIS Documents pdf 1.3mb 08/24/04 Appendix L Outreach Materials pdf 357kb 08/24/04 Appendix M Veterinary Services Memorandum NO. 580.4 – Procedures for Investigating a Suspected Foreign Animal Disease/Emerging Disease Incident (FAD/EDI) pdf 2.4mb 08/24/04

http://www.aphis.usda.gov/vs/nvsl/BSE/specimencollectionbse.htm

[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle

03-025IFA
03-025IFA-2
Terry S. Singeltary

Page 1 of 17

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

Sent: Thursday, September 08, 2005 6:17 PM

To: fsis.regulationscomments@fsis.usda.gov

Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements

for the Disposition of Non-Ambulatory Disabled Cattle

Greetings FSIS,

I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and

Requirements for the Disposition of Non-Ambulatory Disabled Cattle

THE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled Cattle

Broken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;

snip...FULL TEXT ;

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf

Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)

USA BSE RED BOOK

> October 1998
>
> BSE Red Book 2.1-36
>

> 7.2.1.7 Laboratory Coordination--The Laboratory Coordination Officer
> will advise the READE(3 Director concerning laboratory capabilities and
> appropriate laboratory examinations to be conducted to provide needed
> results as rapidly as possible. This individual will assist with
> interpretation of results.

> BSE Red Book 2.1-39
>
> 7.6 Depopulation Procedures
>
> Under no
> circumstances may BSE suspects be sent fo slaughhter or rendering.

snip...

> BSE Red Book 2.1-40
>
> 7.7 Disposal
> Under no circumstances may BSE suspects be sent to slaughter or
> rendering. Notify FDA, CVM if you suspect that the carcass of a
> BSE-confirmed animal has moved to rendering or animal feed
> manufacturing. Field personel should arrange for the carcass to be
> transported to and examined by a qualified veterinary pathologist or
> field veterinary medical officer. After the pathologic examination has
> been completed and the necessary diagnostic specimens have been
> obtained, field personnel should arrange for disposal of the carcass.
> Before a method of disposal is selected, there are many factors that
> must be considered, and often other State and Federal agencies must be
> consulted. The environmental and legal impacts of the operation must be
> considered. Upon recommendation of the State or Federal agencies, VS may
> consider other disposal methods.
>
snip...

> 7.7.3 Rendering
> Because BSE is spread by rendered animal protein, BSE-suspect and
> confirmed carcasses must not be rendered, unless the rendered material
> is incinerated. Notify FDA, CVM if you suspect that dead BSE animals or
> carcasses have moved to rendering or animal feed manufacturing.
>

snip...

> 7.10.11 Prevention--Suspects and animals confirmed to have BSE must not
> be rendered. Producers, feed mills, and rendering establishments should
> adhere to U.S. State and local rendering policies and FDA regulations
> concerning the feeding of rendered animal protein to ruminants.

snip...

If additional tests do suggest a
presumptive diagnosis of BSE, an NVSL pathologist will hand carry the
sample to the United Kingdom for confirmation. It is at this critical
point, when NVSL suggests a diagnosis of BSE and is preparing to send
the sample to the United Kingdom, that this BSE Response Plan is
initiated. The Plan begins the preliminary notification from NVSL to
APHIS. Preliminary Notification The director of NVSL is responsible for
immediately notifying the APHIS, Veterinary Services (VS) deputy
administrator when tests suggest a presumptive diagnosis of BSE. Once
NVSL has made a presumptive diagnosis of BSE, APHIS and FSIS field
activities will also be initiated. APHIS will receive notification
(either confirming or not confirming NVSL's diagnosis) from the United
Kingdom anywhere between 24 and 96 hours. (The international animal
health community has recognized the United Kingdom's Central Veterinary
Laboratory {CVL} as the world's reference laboratory for diagnosing BSE.
Other countries, including Belgium, France, Ireland, Luxembourg, the
Netherlands, Portugal, and Switzerland, have all sent samples to this
lab to confirm their first case of BSE).

snip...

https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000...

FOR IMMEDIATE RELEASE
Statement
May 4, 2004
Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA

Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed. ...

http://www.fda.gov/bbs/topics/news/2004/NEW01061.html

Statement by Chief Veterinary Medical Officer John Clifford Animal and Plant Health Inspection Service Regarding Non-Definitive BSE Test Results
July 27, 2005

snip...

The veterinarian treated the sample with a preservative, which readies it for testing using the immunohistochemistry (IHC) test —an internationally recognized confirmatory test for BSE. Neither the rapid screening test nor the Western blot confirmatory test can be conducted on a sample that has been preserved.

snip...

I would note that the sample was taken in April, at which time the protocols allowed for a preservative to be used (protocols changed in June 2005). The sample was not submitted to us until last week, because the veterinarian set aside the sample after preserving it and simply forgot to send it in.

http://www.aphis.usda.gov/lpa/news/2005/07/bsestatement_vs.html

"Earlier this week, USDA's Office of the Inspector General (OIG), which has been partnering with the Animal and Plant Health Inspection Service, the Food Safety and Inspection Service, and the Agricultural Research Service by impartially reviewing BSE-related activities and making recommendations for improvement, recommended that all three of these samples be subjected to a second internationally recognized confirmatory test, the OIE-recognized SAF immunoblot test, often referred to as the Western blot test. We received final results a short time ago. Of the three samples, two were negative, but the third came back reactive.

"Because of the conflicting results on the IHC and Western blot tests, a sample from this animal will be sent to the OIE-recognized reference laboratory for BSE in Weybridge, England. USDA will also be conducting further testing, which will take several days to complete.

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2005/06/0206.xml

"Each was then followed up with an IHC test. Each confirmatory IHC test was negative. The Inspector General, in reviewing our surveillance system that we have in place, decided to retest with a second confirmatory test which is called the Western Blot. We have received test results showing a positive on one animal for the Western Blot.

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2005/06/0207.xml

ONE YEAR LATER, not 24 to 96 hours (this is what i call mad cow market timing)

STATEMENT BY DR. JOHN CLIFFORD REGARDING FURTHER ANALYSIS OF BSE TEST RESULTS IN WEYBRIDGE, ENGLAND
June 16, 2005

"Today, an official with USDA's National Veterinary Services Laboratory departed for Weybridge, England, hand-carrying samples for further testing.

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2005/06/0218.xml

"So let me start first with the test results. As you are aware, last November we had an inconclusive report from a rapid screening test. USDA then conducted two IHC confirmatory tests, and both came out negative. A few weeks ago an additional confirmatory test was conducted, and that test is referred to as the Western blot test.

"On June 10 I learned that test was reactive and shared those results at that time.

"We now have the test results from the lab in Weybridge, England, as well as the results from additional testing in our own lab, and again I am here today to share those results with you.

"The results confirm the presence of BSE in this animal, an animal that was blocked from entering the food supply thanks to the firewalls that are in place. It is critically important to note that this animal was identified as a high risk animal. A sample was taken, and the carcass was incinerated.

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2005/06/0233.xml

06/09/05
BSE Roundtable Discussion Transcript

http://www.aphis.usda.gov/lpa/issues/bse/BSE_roundtable_6_9_05.pdf

NOW, let us look at another BSE ROUNDTABLE DISCUSSION by USDA et al in the year 2003, please note the BSE science on IHC testing then, and then compare to now, and then ponder those other 9,200 cattle of the infamous June 2004 BSE cover-up program, that did not have rapid testing or WB, just IHC, the lease likely to find BSE/TSE ;

USDA 2003

We have to be careful that we don't get so set in the way we do things that
we forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain
stem and we're looking in only one area. In Norway, they were doing a
project and looking at cases of Scrapie, and they found this where they did
not find lesions or PRP in the area of the obex. They found it in the
cerebellum and the cerebrum. It's a good lesson for us. Ames had to go
back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got
away from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS
.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking
only at the brainstem. We may be missing certain things if we confine
ourselves to one area.

snip.............

Dr. Detwiler: It seems a good idea, but I'm not aware of it.
Another important thing to get across to the public is that the negatives
do not guarantee absence of infectivity. The animal could be early in the
disease and the incubation period. Even sample collection is so important.
If you're not collecting the right area of the brain in sheep, or if
collecting lymphoreticular tissue, and you don't get a good biopsy, you
could miss the area with the PRP in it and come up with a negative test.
There's a new, unusual form of Scrapie that's been detected in Norway. We
have to be careful that we don't get so set in the way we do things that we
forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain
stem and we're looking in only one area. In Norway, they were doing a
project and looking at cases of Scrapie, and they found this where they did
not find lesions or PRP in the area of the obex. They found it in the
cerebellum and the cerebrum. It's a good lesson for us. Ames had to go
back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got
away from it. They've recently gone back.

Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS
.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking
only at the brainstem. We may be missing certain things if we confine
ourselves to one area.

snip...

FULL TEXT;

Completely Edited Version
PRION ROUNDTABLE

Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado

2005

National Veterinary Services Laboratory (NVSL) Immunohistochemistry (IHC) Testing Summary

The BSE enhanced surveillance program involves the use of a rapid screening test, followed by confirmatory testing for any samples that come back "inconclusive." The weekly summary below captures all rapid tests conducted as part of the enhanced surveillance effort. It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200 routine IHC tests on samples that did not first undergo rapid testing.

http://www.aphis.usda.gov/lpa/issues/bse_testing/test_results.html

Office of Inspector General OIG

Semiannual Report to Congress FY - 2005 - First Half

snip...

Stopping BSE at the Border—USDA Needs To

Strengthen Controls Over Canadian Beef Imports

Following the detection of a Canadian cow with bovine

spongiform encephalopathy (BSE or “mad cow disease”)

in May 2003, we examined the Animal and Plant Health

Inspection Service’s (APHIS) oversight of the importation

of beef products from Canada. Following requests from

four U.S. Senators, we began several reviews in June

2004 to explore whether USDA did not follow appropriate

safety measures, beginning sometime in the fall of 2003,

in allowing expanded Canadian beef imports into the

United States.

After the initial halt of imports, in August 2003 the

Secretary announced a list of low-risk products that would

be allowed from Canada. APHIS also allowed an

expansion in the type of Canadian facilities that could

produce items for export to the United States. The

gradual expansion occurred because agency employees

included products similar to those on the published lowrisk

list, but APHIS did not communicate this broadly.

As a result, from August 2003 to April 2004, APHIS issued

permits for products with questionable eligibility. Contrary

to publicly stated policy, the agency allowed the import of

products from Canadian facilities that produced both

eligible and ineligible products, increasing the possibility

that higher-risk product could be inadvertently imported.

APHIS also issued permits to allow the import of more

than 63,000 pounds of beef cheek meat with questionable

eligibility because the agency did not establish a clear

definition for “boneless beef.” Further, we found that

FSIS did not always communicate effectively about the

eligibility status of beef cheek meat, specifically to import

inspectors. In addition, APHIS issued 1,155 permits for

the importation of ruminant (e.g., cow, goat) products

from Canada without ensuring that the agency had an

appropriate system of internal controls to manage the

process for a suddenly overwhelming volume of requests.

From May through September 2004, we identified more

than 42,000 pounds of product with questionable

eligibility.

APHIS generally agreed to institute procedures for

communicating changes in policy and monitoring the

consistency between agency practice and publicly stated

policy, as well as to strengthen controls and finalize

procedures to issue and monitor permits. FSIS generally

agreed to implement controls to communicate the specific

eligibility of product when its eligibility status changes and

to implement an edit check in its import information

system to identify ineligible product. (Audit Report No.

33601-1-Hy, APHIS Oversight of the Importation of Beef

Products from Canada)

snip...

Restaurant Owner Sentenced for Smuggling Beef

from Japan, Importation of Which Is Prohibited Due

to Disease Concerns

In January 2005, a Los Angeles restaurant owner was

placed on probation for 60 months, to include 800 hours

of community service, after he pled guilty to smuggling

beef from Japan. Under 9 Code of Federal Regulations

(C.F.R.) § 94, beef from Japan is a prohibited product

for United States importation due to disease. On two

occasions in 2001 and 2002, inspectors in Anchorage,

Alaska, intercepted shipments sent from Japan that

were manifested as “book,” but upon inspection by

USDA and the United States Customs Service, were

found to contain approximately 25 kilograms of beef

inside a Styrofoam ice chest. Both shipments were

addressed to the restaurant owner. Shipping records

showed that the restaurant owner had received 13

shipments manifested as “book” from the same sender

in Japan in 2001 and 2002. All but one of the shipments

were in the same weight range as the two intercepted

shipments. The shipper and the restaurant owner were

subsequently indicted for various charges including

conspiracy and smuggling. An arrest warrant was

issued for the shipper, who is still in Japan.

http://www.usda.gov/oig/webdocs/SarcFirstHalf05.pdf

Working Group Report on

the Assessment of the Geographical BSE-Risk (GBR) of

CANADA

2004

snip...

- 2 -

2. EXTERNAL CHALLENGES

2.1 Import of cattle from BSE-Risk2 countries

An overview of the data on live cattle imports is presented in table 1 and is based on

data as provided in the country dossier (CD) and corresponding data on relevant exports

as available from BSE risk countries that exported to Canada. Only data from risk

periods are indicated, i.e. those periods when exports from a BSE risk country already

represented an external challenge, according to the SSC opinion on the GBR (SSC July

2000 and updated January 2002).

• According to the CD, 231 cattle were imported from UK during the years 1980 to

1990 and no cattle imports from UK were recorded after 1990.

• According to Eurostat, altogether 198 cattle have been imported from the UK during

the years 1980 to 1990, Additionally 500 were recorded in 1993; this import is

1 For the purpose of the GBR assessment the abbreviation "MBM" refers to rendering products, in particular

the commodities Meat and Bone Meal as such; Meat Meal; Bone Meal; and Greaves. With regard to imports

it refers to the customs code 230110 "flours, meals and pellets, made from meat or offal, not fit for human

2 BSE-Risk countries are all countries already assessed as GBR III or IV or with at least one confirmed

Annex to the EFSA Scientific Report (2004) 2, 1-14 on the Assessment of the

Geographical BSE Risk of Canada

- 3 -

mentioned in Eurostat and the updated UK export statistic as male calves, but not

mentioned in the original UK export statistics. According to the CD, detailed

investigations were carried out and it is very unlikely that the 500 calves have been

imported. Therefore, they were not taken into account.

• According to the CD, in 1990 all cattle imported from UK and Ireland since 1982

were placed in a monitoring program.

• Following the occurrence of the BSE index case in 1993 (imported from UK in 1987

at the age of 6 months), an attempt was made to trace all other cattle imported from

UK between 1982 and 1990.

• Of the 231 cattle imported from the UK between 1980 and 1990, 108 animals had

been slaughtered and 9 had died. From the remaining, 37 were exported, 76 were

sent to incineration and one was buried; these were not entering the rendering system

and therefore not taken into account.

• According to the CD, 16 cattle were imported from Ireland (according to Eurostat

20), of which 9 were slaughtered, 3 died. The remaining 4 were incinerated and did

therefore not enter the rendering system. According to the CD, the 6 animals which

were imported in 1990 according to Eurostat, were never imported.

• Moreover 22 cattle have been imported from Japan (through USA), of which 4 were

exported (excluded from the table) and 14 were destroyed and therefore not entering

the rendering system, 4 were slaughtered.

• Of 28 imported bovines from Denmark, 1 was destroyed and 1 was exported. Of the

19 buffalos imported in 2000, 1 was incinerated and the others were ordered to be

destroyed.

• Additionally in total 264 cattle according to the CD (276 according to other sources)

were imported from Austria, France, Germany, Hungary, Italy, The Netherlands and

Switzerland.

• The numbers imported according to the CD and Eurostat are very similar. Some

discrepancies in the year of import can be explained by an extended quarantine;

therefore it is likely that imports according to Eurostat in 1980 and imports

according to the CD in 1981 are referring to the same animals.

• Additionally, between 16.000 and 340.000 bovines have annually been imported

from US, almost all are steers and heifers. In total, between 1981 and 2003,

according to the CD more than 2.3 million, according to other sources 1.5 million

cattle have been imported.

• According to the CD, feeder/slaughter cattle represent typically more than 90% of

the imported cattle from the USA; therefore, only 10% of the imported cattle have

been taken into account.

snip...

Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the

Geographical BSE Risk of Canada

2.2 Import of MBM or MBM-containing feedstuffs from BSE-Risk

countries

An overview of the data on MBM imports is presented in table 2 and is based on data

provided in the country dossier (CD) and corresponding data on relevant exports as

available from BSE risk countries that exported to Canada. Only data from risk periods

are indicated, i.e. those periods when exports from a BSE risk country already

represented an external challenge, according to the SSC opinion on the GBR (SSC, July

2000 and updated January 2002).

According to the CD, no imports of MBM took place from UK since 1978 (initially

because of FMD regulations).

• According to Eurostat data, Canada imported 149 tons MBM from the UK in the

period of 1993 to 2001. According to up-dated MBM statistics from UK (August

2001) no mammalian MBM was exported to Canada from 1993 – 1996. As it was

illegal to export mammalian meat meal, bone meal and MBM from UK since

27/03/1996, exports indicated after that date should only have included nonmammalian

MBM. Therefore, these imports were not taken into account.

• According to the CD, imports of MBM have taken place from Denmark, Germany,

France, Japan and US.

• According to Eurostat Canada imported MBM from Denmark, Belgium, France and

Ireland.

• According to the CD further investigations concluded that all imported MBM from

Denmark consisted of pork and poultry origin and was directly imported for

aquaculture, the imported MBM from France was feather meal, the imported MBM

from Germany was poultry meal for aquaculture and the imported MBM from

Belgium was haemoglobin; therefore these imports were not taken into account.

• The main imports of MBM were of US origin, according to the CD around 250.000

tons, according to other sources around 310.000 tons between 1988 and 2003.

snip...

2.3 Overall assessment of the external challenge

The level of the external challenge that has to be met by the BSE/cattle system is

estimated according to the guidance given by the SSC in its final opinion on the GBR of

July 2000 (as updated in January 2002).

Live cattle imports:

In total the country imported according to the CD more than 2.3 million, according to

other data 1.5 million live cattle from BSE risk countries, of which 231 (CD)

respectively 698 (other sources) came from the UK. The numbers shown in table 1 are

the raw import figures and are not reflecting the adjusted imports for the assessment of

the external challenge. Broken down to 5 year periods the resulting external challenge is

as given in table 3. This assessment takes into account the different aspects discussed

above that allow to assume that certain imported cattle did not enter the domestic

BSE/cattle system, i.e. were not rendered into feed. In the case of Canada, the 500 cattle

imported from UK according to Eurostat were not taken into account and it is assumed

that all incinerated, buried, exported animals and the animals still alive did not enter the

rendering system and were therefore excluded from the external challenge.

MBM imports:

In total the country imported according to the CD around 300.000 tons, according to

other sources nearly 360.000 tons of MBM from BSE risk countries, of which 149 tons

came from the UK. The majority consisted of MBM imported from the US. The

numbers shown in table 2 are the raw import figures and are not reflecting the adjusted

imports for the assessment of the external challenge. Broken down to 5 year periods the

resulting external challenge is as given in table 3. This assessment takes into account

the different aspects discussed above that allow to assume that certain imported MBM

did not enter the domestic BSE/cattle system or did not represent an external challenge

for other reasons. As it was illegal to export mammalian meat meal, bone meal and

MBM from UK since 27/03/1996, exports indicated after that date should only have

included non-mammalian MBM. In the case of Canada all imported MBM from UK,

Germany, Belgium, Denmark and France was not taken into account.

snip...

3. STABILITY

3.1 Overall appreciation of the ability to avoid recycling of BSE

infectivity, should it enter processing

Feeding

The annual Canadian production of MBM is approximately 575,000 tons of which

approx. 40,000 tons are exported each year, mainly to USA.

Use of MBM in cattle feed

• Before the feed ban, dairy cattle received supplementary feed containing MBM

during their productive life (maximum 200-400 g MBM per day). Beef cattle in the

western part of the country do not usually receive complementary feed. Beef cattle

in the eastern part receive normally no supplement protein but the calves could have

access to creep feeds containing MBM, after weaning the ratios may have contained

supplemental protein containing MBM (100-400 g per day).

• According to the CD, MBM is mainly fed to pigs and poultry and included in pet

food.

• According to the CD, only a proportion of dairy cattle may have received MBM.

Feed bans

• Before 1997, there was no legal restriction to include MBM into cattle feed.

• An MBM-ban was introduced in August 1997; it is forbidden since to feed

mammalian MBM to ruminants except if of pure porcine, equine and non

mammalian origin, i.e. in practice a ruminant-to-ruminant ban (RMBM-ban).

Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the

Geographical BSE Risk of Canada

- 9 -

Potential for cross-contamination and measures taken against

• Cross-contamination in the about 600 feed mills is assumed to be possible as long as

cattle and pig feed is produced in the same production lines, and premises.

• Cross-contamination during transport is possible, particularly if the same trucks are

used for transporting ruminant MBM (RMBM) and non-ruminant MBM (porcine or

poultry MBM which still might be included into cattle feed) or for transporting

pig/poultry feed and cattle feed.

• On-farm cross-contamination is regarded to be possible.

• Cross-contamination of cattle feed with RMBM can not be excluded. Hence, as

reasonable worst case scenario, it has to be assumed that cattle, in particular dairy

cattle, can still be exposed to RMBM and hence to BSE-infectivity, should it enter

the feed chain.

Control of Feed bans and cross-contamination

• With the introduction of the RMBM ban (1997) the feed mills (approximately 600)

were checked for compliance with the ban, including good manufacturing practices

(GMP) and record keeping, i.e. the separation in production of MBM containing

ruminant material (RMBM) from non-ruminant MBM.

• The feed mills had previously – since 1983 – been regularly checked in relation to

production of medicated feed.

• No examinations are performed to assess cross-contamination with RMBM of the

protein (e.g. non ruminant MBM) that enters cattle feed. Differentiation would

anyway be difficult.

Rendering

Raw material used for rendering

• Ruminant material is rendered together with material from other species, but

according to the CD only in the production of MBM prohibited for use in ruminant

feeds.

• Slaughter by-products, including specified risk material (SRM) and fallen stock are

rendered.

• The country expert estimated that 20% of the rendering plants, processing 20% of

the total amount of raw material, are connected to slaughterhouses. Their raw

material is more than 98 % animal waste from these slaughterhouses while less than

2 % is fallen stock. No estimation was given for the remaining 80% of the rendering

capacity.

• There are 32 rendering plants of which 3 are processing blood exclusively.

Rendering processes

• The rendering systems (parameters) were specified for 6 plants producing mixed

MBM, none of these fulfilled the 133/20/3 standard. Of these, 5 have dedicated

facilities to produce products for use in ruminant feed and products not permitted for

use in ruminant feed.

• The remaining plants process porcine or poultry material exclusively.

SRM and fallen stock

• There is an SRM ban for human food in place since 2003.

Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the

Geographical BSE Risk of Canada

- 10 -

• However, SRM are rendered together with other slaughter waste and fallen stock.

However, according to the CD, MBM with SRM is not permitted to be fed to

ruminants.

Conclusion on the ability to avoid recycling

• Between 1980 and 1997 the Canadian system would not have been able to avoid

recycling of the BSE-agent to any measurable extent. If the BSE-agent was

introduced into the feed chain, it could have reached cattle.

• Since 1997 this ability gradually improved with the introduction of the ruminant

MBM ban and its implementation.

• Since cross-contamination cannot be excluded, and as SRM is still rendered by

processes unable to significantly reduce BSE-infectivity, the system is still unable to

avoid recycling of BSE-infectivity already present in the system or incoming.

3.2 Overall appreciation of the ability to identify BSE-cases and to

eliminate animals at risk of being infected before they are processed

Cattle population structure

• Cattle population: 12.15 Million in 1988 increasing to 14.6 Million in 2001;

• Of the total cattle population, 2.2 million are dairy cattle and 12.4 million are beef.

• The cattle population above 24 months of age: approx. 6.0 Million.

• Of the approximately 2.2 Million dairy cattle 2 Million are located in the two eastern

provinces Ontario and Quebec.

• Mixed farming (cattle and mono-gastric species) is usually not practiced; the

country expert estimated the proportion of mixed farming to be less than 1%.

• Individual regions traditionally have ID systems under provincial authorities. Brand

inspectors are present when cattle are assembled. It is estimated by the Canadians

that the level of a national, uniform ID for cattle is less than 10%; most of those

individual pedigree animals. Mandatory ID for the milk-fed veal sector was

implemented in Quebec in 1996, but does not contain information on the herd of

origin. An agreement of the relevant industries to develop a national cattle ID and

trace back strategy was reached on 1 May 1998 (starting in 2001).Since 2002, a

national identification program is existing. Al cattle leaving any farm premises must

be uniquely identified by ear tag.

BSE surveillance

• BSE was made notifiable in 1990.

• Every cow over one year of age exhibiting central nervous system signs suggestive

of BSE submitted to a laboratory or presented at an abattoir is subjected to a BSE

laboratory diagnostic test (histology and over the past years also PrPSc-based

laboratory tests).

• In addition, cattle submitted for rabies examination and found rabies negative are

examined for BSE. Samples are prepared immediately upon arrival to the federal

laboratory responsible for the rabies diagnostic for possible later BSE examination,

i.e. formalin fixation.

• Since the 1940’s, a rabies control program has been in place, where farmers,

veterinarians and the general public are well educated about this neurological

Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the

Geographical BSE Risk of Canada

- 11 -

disease. In 1990, when BSE was made notifiable, this awareness was extended to

suspicions of BSE.

• Since 1993 the number of brains examined per year did exceed the number

recommended by OIE (300 - 336 for countries with a cattle population over 24

months of age of 5.0 to 7.0 Million) in all years, except in 1995 (table 4).

year 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003

samples 225 645 426 269 454 759 940 895 1´020 1´581 3´377 3´361

Table 4: Number of bovine brains annually examined for CNS diseases, including BSE.

• According to the CD approx. 98% of the examined cattle were older than 24 months

and approx. 90% exhibited neurological symptoms. Although the identification

system of Canada does not document the birth date or age of the animals, according

to the CD, examination of the dentition is used to ascertain the maturity of the

animals.

• The list of neurological differential diagnoses for the 754 brains examined in 1997

included encephalitis (70 cases), encephalomalacia (19), hemophilus (7),

hemorrhage (2), listeriosis (38), meningoencephalitis (36), rabies (22), tumors (2),

other conditions (135) and no significant findings (423).

• Compensation is paid for suspect BSE cases as well as for animals ordered to be

destroyed (90-95% of market value with a maximum of 2,500 Can$ per cow).

• Diagnostic criteria developed in the United Kingdom are followed at ADRI,

Nepean. According to the very detailed protocol for the collection, fixation and

submission of Bovine Spongiform Encephalopathy (BSE) specimens at abattoirs

under inspection by the Canadian Food Inspection Agency, the specimen shall be

shipped to National Center for Foreign Animal Disease, Winnipeg, Manitoba.

• In 2003, around 3000 animals from risk populations have been tested.

• According to the CD, it is aimed to test a minimum of 8000 risk animals (animals

with clinical signs consistent with BSE, downer cows, animals died on farm animals

diseased or euthanized because of serious illness) in 2004 and then continue to

progressively increase the level of testing to 30,000.

• In May 2003, Canada reported its first case of domestic BSE. A second case was

detected in the US on 23 December 2003 and traced back to Canadian origin. Both

were born before the feed ban and originated from Western Canada.

3.3 Overall assessment of the stability

For the overall assessment of the stability, the impact of the three main stability factors

(i.e. feeding, rendering and SRM-removal) and of the additional stability factor,

surveillance, has to be estimated. Again, the guidance provided by the SSC in its

opinion on the GBR of July 2000 (as updated January 2002) is applied.

Feeding

Until 1997, it was legally possible to feed ruminant MBM to cattle and a certain fraction of

cattle feed (for calves and dairy cattle) is assumed to have contained MBM. Therefore

feeding was "Not OK". In August 1997 a ruminant MBM ban was introduced but feeding

of non-ruminant MBM to cattle remained legal as well as feeding of ruminant MBM to

non-ruminant animals. This makes control of the feed ban very difficult because laboratory

differentiation between ruminant and non ruminant MBM is difficult if not impossible.

Annex to the EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the

Geographical BSE Risk of Canada

Due to the highly specialised production system in Canada, various mammalian MBM

streams can be separated. Such a feed ban would therefore be assessed as "reasonably

OK", for all regions where this highly specialised system exists. However, several areas

in Canada do have mixed farming and mixed feed mills, and in such regions, an RMBM

ban would not suffice. Additionally, official controls for cattle feeds to control for the

compliance with the ban were not started until the end of 2003. Thus, for the whole

country, the assessment of the feeding after 1997 remains "Not OK".

Rendering

The rendering industry is operating with processes that are not known to reduce infectivity.

It is therefore concluded that the rendering was and is "Not OK".

SRM-removal

SRM and fallen stock were and are rendered for feed. Therefore SRM-removal is assessed

as "Not OK"

snip...

4.2 Risk that BSE infectivity entered processing

A certain risk that BSE-infected cattle entered processing in Canada, and were at least

partly rendered for feed, occurred in the early 1990s when cattle imported from UK in

the mid 80s could have been slaughtered. This risk continued to exist, and grew

significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached

processing. Given the low stability of the system, the risk increased over the years with

continued imports of cattle and MBM from BSE risk countries.

4.3 Risk that BSE infectivity was recycled and propagated

A risk that BSE-infectivity was recycled and propagated exists since a processing risk

first appeared; i.e. in the early 90s. Until today this risk persists and increases fast

because of the extremely unstable BSE/cattle system in Canada.

5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK

5.1 The current GBR as function of the past stability and challenge

The current geographical BSE-risk (GBR) level is III, i.e. it is confirmed at a lower level

that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.

This assessment deviates from the previous assessment (SSC opinion, 2000) because at

that time several exporting countries were not considered a potential risk.

snip...

full text;

http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/s...

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA)
Publication date: 20 August 2004
Adopted July 2004 (Question N° EFSA-Q-2003-083)

Report

Summary
Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.

The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.

http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/5...

SUMMARY

Summary of Scientific Report
http://www.efsa.eu.int
1 of 1
Scientific Report of the European Food Safety Authority
on the Assessment of the Geographical BSE-Risk (GBR) of
United States of America (USA)
Question N° EFSA-Q-2003-083
Adopted July 2004
Summary of scientific report
The European Food Safety Authority and its Scientific Expert Working Group on the
Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR)
were asked by the European Commission (EC) to provide an up-to-date scientific report on
the GBR in the United States of America, i.e. the likelihood of the presence of one or more
cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific
report addresses the GBR of USA as assessed in 2004 based on data covering the period
1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in
the middle of the eighties. These cattle imported in the mid eighties could have been rendered
in the late eighties and therefore led to an internal challenge in the early nineties. It is possible
that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to
an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk
countries were slaughtered or died and were processed (partly) into feed, together with some
imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when
domestic cattle, infected by imported MBM, reached processing. Given the low stability of
the system, the risk increased over the years with continued imports of cattle and MBM from
BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed
that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as
there are no significant changes in rendering or feeding, the stability remains extremely/very
unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the
BSE-agent persistently increases.
Key words: BSE, geographical risk assessment, GBR, USA, third countries

http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/5...

REPORT (6 PAGES)

snip...

EFSA Scientific Report (2004) 3, 1-6 on the Assessment of the Geographical BSE Risk of
Conclusions
The European Food Safety Authority concludes:
1. The BSE agent was probably imported into USA and could have reached domestic
cattle in the middle of the eighties. This cattle imported in the mid eighties could have
been rendered in the late eighties and therefore led to an internal challenge in the early
nineties. It is possible that meat and bone meal (MBM) imported into the USA
reached domestic cattle and lead to an internal challenge in the early nineties.
2. A processing risk developed in the late 80s/early 90s when cattle imports from BSE
risk countries were slaughtered or died and were processed (partly) into feed, together
with some imports of MBM. This risk continued to exist, and grew significantly in the
mid 90’s when domestic cattle, infected by imported MBM, reached processing.
Given the low stability of the system, the risk increased over the years with continued
imports of cattle and MBM from BSE risk countries.
3. The current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed
that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
4. This assessment deviates from the previous assessment (SSC opinion, 2000) because
at that time several exporting countries were not considered a potential risk.
5. It is also worth noting that the current GBR conclusions are not dependent on the large
exchange of imports between USA and Canada. External challenge due to exports to
the USA from European countries varied from moderate to high. These challenges
indicate that it was likely that BSE infectivity was introduced into the North American
continent.
6. EFSA and its Scientific Expert Working group on GBR are concerned that the
available information was not confirmed by inspection missions as performed by the
Food and Veterinary office (FVO – DG SANCO) in Member States and other third
countries. They recommend including, as far as feasible, BSE-related aspects in
future inspection missions.
Expected development of the GBR
As long as there are no significant changes in rendering or feeding, the stability remains
extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically)
infected with the BSE-agent persistently increases.
A table summarising the reasons for the current assessment is given in the table below

snip...

http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/5...

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of Mexico
Last updated: 08 September 2004
Adopted July 2004 (Question N° EFSA-Q-2003-083)

Report

http://www.efsa.eu.int
3 of 6
Conclusions
The European Food Safety Authority concludes:
1. The BSE agent was probably imported into Mexico and could have reached domestic
cattle. These cattle imported could have been rendered and therefore led to an internal
EFSA Scientific Report (2004) 4, 1-6 on the Assessment of the Geographical BSE Risk of
challenge in the mid to late 1990’s. It is possible that imported MBM into Mexico
reached domestic cattle and leads to an internal challenge around 1993.
2. It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’
MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late
1990s). The high level of external challenge is maintained throughout the reference
period, and the system has not been made stable. Thus it is likely that BSE infectivity
was recycled and propagated from approximately 1993. The risk has since grown
consistently due to a maintained internal and external challenge and lack of a stable
system.
3. The current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed
that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
4. EFSA and its Scientific Expert Working group on GBR are concerned that the
available information was not confirmed by inspection missions as performed by the
Food and Veterinary office (FVO – DG SANCO) in Member States and other third
countries. They recommend including, as far as feasible, BSE-related aspects in
future inspection missions.

http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/5...

Summary

Summary of Scientific Report
http://www.efsa.eu.int
1 of 2
Scientific Report of the European Food Safety Authority
on the Assessment of the Geographical BSE-Risk (GBR) of
MEXICO
Question N° EFSA-Q-2003-083
Adopted July 2004
SUMMARY OF SCIENTIFIC REPORT
The European Food Safety Authority and its Scientific Expert Working Group on the
Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR)
were asked by the European Commission (EC) to provide an up-to-date scientific report on
the GBR in Mexico, i.e. the likelihood of the presence of one or more cattle being infected
with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the
GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into Mexico and could have reached domestic cattle.
These cattle imported could have been rendered and therefore led to an internal challenge in
the mid to late 1990s. It is possible that imported meat and bone meal (MBM) into Mexico
reached domestic cattle and leads to an internal challenge around 1993.
It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’ MBM
(1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late 1990s). The
high level of external challenge is maintained throughout the reference period, and the system
has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated
from approximately 1993. The risk has since grown consistently due to a maintained internal
and external challenge and lack of a stable system.
EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely
but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSEagent.
The GBR is likely to increase due to continued internal and external challenge, coupled
with a very unstable system.
Key words: BSE, geographical risk assessment, GBR, Mexico, third countries
Summary of Scientific Report
http://www.efsa.eu.int
2 of 2

http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/5...

Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in Mexico, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003.

The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal challenge in the mid to late 1990s. It is possible that imported meat and bone meal (MBM) into Mexico reached domestic cattle and leads to an internal challenge around 1993.

It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’ MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system.

EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. The GBR is likely to increase due to continued internal and external challenge, coupled with a very unstable system.

http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/5...

ONE YEAR PREVIOUSLY ;

From: Terry S. Singeltary Sr. [flounder@wt.net]
Sent: Tuesday, July 29, 2003 1:03 PM
To: fdadockets@oc.fda.gov
Cc: ggraber@cvm.fda.gov; Linda.Grassie@fda.gov; BSE-L
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

Greetings FDA,

snip...

PLUS, if the USA continues to flagrantly ignore the _documented_ science to date about the known TSEs in the USA (let alone the undocumented TSEs in cattle), it is my opinion, every other Country that is dealing with BSE/TSE should boycott the USA and demand that the SSC reclassify the USA BSE GBR II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the SSC to _flounder_ any longer on this issue, should also be regarded with great suspicion as well. NOT to leave out the OIE and it's terribly flawed system of disease surveillance. the OIE should make a move on CWD in the USA, and make a risk assessment on this as a threat to human health. the OIE should also change the mathematical formula for testing of disease. this (in my opinion and others) is terribly flawed as well. to think that a sample survey of 400 or so cattle in a population of 100 million, to think this will find anything, especially after seeing how many TSE tests it took Italy and other Countries to find 1 case of BSE (1 million rapid TSE test in less than 2 years, to find 102 BSE cases), should be proof enough to make drastic changes of this system. the OIE criteria for BSE Country classification and it's interpretation is very problematic. a text that is suppose to give guidelines, but is not understandable, cannot be considered satisfactory. the OIE told me 2 years ago that they were concerned with CWD, but said any changes might take years. well, two years have come and gone, and no change in relations with CWD as a human health risk. if we wait for politics and science to finally make this connection, we very well may die before any decisions
or changes are made. this is not acceptable. we must take the politics and the industry out of any final decisions of the Scientific community. this has been the problem from day one with this environmental man made death sentence. some of you may think i am exaggerating, but you only have to see it once, you only have to watch a loved one die from this one time, and you will never forget, OR forgive...yes, i am still very angry... but the transmission studies DO NOT lie, only the politicians and the industry do... and they are still lying to this day...TSS

http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt

TSS

Offline
Joined: 01/01/2006
Posts: 230
CWD aka mad deer/elk disease i.e. TSE update 2005

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

http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm

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

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

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

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

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

Science 14 October 2005:Vol. 310. no. 5746, pp. 324 - 326DOI: 10.1126/science.1118829

Reports

Coincident Scrapie Infection and Nephritis Lead to Urinary Prion Excretion

Harald Seeger,1* Mathias Heikenwalder,1* Nicolas Zeller,1 Jan Kranich,1 Petra Schwarz,1 Ariana Gaspert,2 Burkhardt Seifert,3 Gino Miele,1 Adriano Aguzzi1

Prion infectivity is typically restricted to the central nervous and lymphatic systems of infected hosts, but chronic inflammation can expand the distribution of prions. We tested whether chronic inflammatory kidney disorders would trigger excretion of prion infectivity into urine. Urinary proteins from scrapie-infected mice with lymphocytic nephritis induced scrapie upon inoculation into noninfected indicator mice. Prionuria was found in presymptomatic scrapie-infected and in sick mice, whereas neither prionuria nor urinary PrPSc was detectable in prion-infected wild-type or PrPC-overexpressing mice, or in nephritic mice inoculated with noninfectious brain. Thus, urine may provide a vector for horizontal prion transmission, and inflammation of excretory organs may influence prion spread.

snip...

How do prions enter the urine? Upon extrarenalreplication, blood-borne prions may beexcreted by a defective filtration apparatus.Alternatively, prions may be produced locallyand excreted during leukocyturia. Althoughprionemia occurs in many paradigms ofperipheral prion pathogenesis (15, 16), thelatter hypothesis appears more likely, becauseprionuria was invariably associated with localprion replication within kidneys.Urine from one CJD patient was reported toelicit prion disease in mice (17, 18), but not inprimates (19). Perhaps unrecognized nephriticconditions may underlie these discrepantobservations. Inflammation-associated prionuriamay also contribute to horizontal transmissionamong sheep, deer, and elk, whose high efficiencyof lateral transmission is not understood.References and Notes...snip...end

1 Institute of Neuropathology, University Hospital of Zürich, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland.2 Institute of Clinical Pathology, University Hospital of Zürich, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland.3 Institute of Biostatistics, University of Zürich, Sumatrastrasse 30, CH-8006 Zürich, Switzerland. * These authors contributed equally to this work. To whom correspondence should be addressed. E-mail: adriano@pathol.unizh.ch

http://www.sciencemag.org/cgi/content/abstract/310/5746/324

what about those 'deer scents' of 100% urine', and the prion that is
found in urine, why not just pass the prion with the urine to other deer...

Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is
made from Estrus urine collected at the peak of the rut, blended with
Fresh Doe Urine for an extremely effective buck enticer. Use pre-rut
before the does come into heat. Use during full rut when bucks are most
active. Use during post-rut when bucks are still actively looking for
does. 1 oz.

http://www.gamecalls.net/huntingproducts/deerlures.html

ELK SCENT/SPRAY BOTTLE * Works anytime of the year * 100 % Cow
Elk-in-Heat urine (2oz.) * Economical - mix with water in spray mist
bottle * Use wind to your advantage

Product Code WP-ESB $9.95

http://www.elkinc.com/Scent.asp

prions in urine?

[PDF] A URINE TEST FOR THE IN-VIVO DIAGNOSIS OF PRION DISEASES

http://www.sigov.si/vurs/PDF/diagnoastika-bse-urin.pdf

WHAT WILL cwdCJD LOOK LIKE IN HUMANS IN WYOMING ???

Subject: Interspecies Transmission of Chronic Wasting Disease Prions to
Squirrel Monkeys (Saimiri sciureus)
Date: October 19, 2005 at 8:33 am PST

0022-538X/05/$08.00+0 doi:10.1128/JVI.79.21.13794-13796.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Interspecies Transmission of Chronic Wasting Disease Prions to Squirrel
Monkeys (Saimiri sciureus)
Richard F. Marsh,1, Anthony E. Kincaid,2 Richard A. Bessen,3 and Jason C.
Bartz4*
Department of Animal Health and Biomedical Sciences, University of
Wisconsin, Madison 53706,1 Department of Physical Therapy,2 Department of
Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska
68178,4 Department of Veterinary Molecular Biology, Montana State
University, Bozeman, Montana 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.

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

* 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.

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

Journal of Virology, November 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.

http://jvi.asm.org/cgi/content/abstract/79/21/13794maxtoshow=&HITS=10&hi...

kind regards,
terry

Offline
Joined: 01/01/2006
Posts: 230
CWD aka mad deer/elk disease i.e. TSE update 2005

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

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

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

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

snip...

_animal protein_

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

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

snip...

_animal protein_

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

Ingredients

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

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

MORE ANIMAL PROTEIN PRODUCTS FOR DEER

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

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

Ingredients

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

FEEDING DIRECTIONS
Feed as Creep Feed with Normal Diet

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

INGREDIENTS

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

DIRECTIONS FOR USE

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

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

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

April 9, 2001 WARNING LETTER

01-PHI-12
CERTIFIED MAIL
RETURN RECEIPT REQUESTED

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

Tel: 215-597-4390

Dear Mr. Raymond:

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

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

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

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

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

Gerald Wells: Report of the Visit to USA, April-May 1989

snip...

The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...

snip...

It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...

snip...

3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...

snip...

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

To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

•Department of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

ABSTRACT
Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in
England.

INTRODUCTION

Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough
and Burger who demonstrated that the disease was transmissible with a long incubation
period, and that affected mink had a spongiform encephalopathy similar to that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965).
Because of the similarity between TME and scrapie, and the subsequent finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was
concluded that TME most likely resulted from feeding mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time provided
evidence that they may be different. Epidemiologic studies on previous incidences of
TME indicated that the incubation periods in field cases were between six months and
one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be
transmitted to mink in less than one year.
To investigate the possibility that TME may be caused by a (particular strain of
scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie
agent, including their sheep or goat sources, were inoculated into a total of 61 mink.
Only one mink developed a progressive neurologic disease after an incubation period of
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused
by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent
from an unidentified source.

OBSERVATIONS AND RESULTS

A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were "acting funny", and some had died. At this time, we
visited the farm and found that approximately 10% of all adult mink were showing
typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over
their _backs like squirrels. These signs were followed by progressive deterioration of
neurologic function beginning with locomoior incoordination, long periods of somnolence
in which the affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over the past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy
cattle and a few horses. Sheep had never been fed.

Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after incubation
periods of four months. To investigate the possible involvement of cattle in this disease
cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally
with a brain suspension from affected mink. Each developed a fatal spongiform
encephalopathy after incubation periods of 18 and 19 months.

DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle and
we have alerted bovine practitioners that there may exist an as yet unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new
bovine spongiform encephalopathy has recently been reported in England (Wells et al.,
1987), and investigators are presently studying its transmissibility and possible
relationship to scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be
confused with rabies in the United Stales and not be diagnosed. Presently, brains from
cattle in the United States which are suspected of rabies infection are only tested with
anti-rabies virus antibody and are not examined histopathologically for lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no agent-
specific proteins or nucleic acids identified for these transmissible neuropathogens, one
means of distinguishing them is by animal passage and selection of the biotype which
grows best in a particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral
backpassage of the experimental bovine agent resulted in incubations of only four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine passage.
Mink fed infected bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.

ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United
States Department of Agriculture. The authors also wish to acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.

REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.

MARSH

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

In Confidence - Perceptions of unconventional slow virus diseases
of animals in the USA - APRIL-MAY 1989 - G A H Wells

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

IT ain't pretty, but it's the truth as I KNOW it , to date. now you do to. ...

kind regards,
terry

Offline
Joined: 01/01/2006
Posts: 230
16 NEW CASES CWD ILLINOIS NEW CASES FOUND IN THE NORTH

Subject: ILLINOIS FINDS 16 MORE CASES OF CWD WITH New cases found in Northern Illinois
Date: January 10, 2006 at 11:57 am PST

FOR IMMEDIATE RELEASE
January 9, 2006

DEER SEASON SAMPLING FINDS ADDITIONAL EVIDENCE OF CHRONIC WASTING DISEASE
New cases found in Northern Illinois

SPRINGFIELD, IL. – Sixteen additional cases of chronic wasting disease (CWD) have been detected in northern Illinois through sampling of hunter-harvested deer during the state’s 2005-06 deer seasons. The new cases include two deer taken by hunters in Ogle County, the first time CWD has been detected there.

“The Department of Natural Resources continues intensive sampling for CWD as part of our effort to slow the spread of the disease in our wild deer herd,” said Paul Shelton, manager of the IDNR Forest Wildlife Program. “We appreciate the support of hunters who continue to voluntarily allow us to take tissue samples from their deer to test for the disease. The sampling, testing and surveillance is extremely important as we deal with CWD.”

Chronic wasting disease was first discovered in Illinois in November 2002 and to date Illinois has detected 112 positive cases.

The disease had been confined in northern Illinois in Boone, Winnebago, McHenry and northern DeKalb until the two new cases were detected in nearby Ogle County this winter.

“We were somewhat surprised to find these two cases in Ogle County because no cases had been detected there previously despite very intensive sampling,” Shelton said. “We’ve sampled nearly 2,000 deer in Ogle County since 2003 and these are the only two cases we have found there to date. We are still awaiting the results of approximately 350 other samples from Ogle County taken this fall.”

Illinois biologists have collected samples from more than 2,500 deer in seven northern Illinois counties so far during the 2005-06 firearm and archery deer seasons and from suspect animals reported to the IDNR.

Hunters in Boone, Winnebago and McHenry counties a portion of DeKalb County north of the East-West Tollway will participate in a CWD Deer Season Jan. 13-15 to help control deer densities and the spread of chronic wasting disease. Hunters with unfilled 2005 firearm, muzzleloader or archery deer permits valid for one of the open counties may use those to hunt. Hunters using unfilled permits from the 2005 firearm, muzzleloader or archery season may take deer appropriate for that permit (antlerless-only or either-sex). Special CWD season permits were also issued previously. Check stations will be manned in the four counties and successful hunters who submit samples for CWD testing will be provided with an additional permit valid for the remainder of the season.

Confirmed CWD cases by county:
Boone-53
Winnebago-42
McHenry-9
Dekalb-6
Ogle-2

Check station locations for the CWD Deer Season:

Boone County - Boone County Fairgrounds, Rt. 76 and Business Rt. 20, Belvidere.
DeKalb County - Potawatomi Woods Forest Preserve, 32199 Kirkland Rd.(one-quarter mile north of Rt. 72), Kirkland.
McHenry County - Sportsman’s Choice, intersection of Routes 14 and 47, Woodstock.
Winnebago County - Rock Cut State Park, 6425 Hart Rd. (one mile east of Perryville Rd. on Hart Rd.), Loves Park.

While not thought to be contagious to humans or livestock, CWD is known to spread from animal to animal among deer and elk. The disease affects the brain of the infected animal, causing it to become emaciated, display abnormal behavior, lose coordination and eventually die.

Illinois expanded its chronic wasting disease surveillance effort in 2002 following the discovery of CWD in neighboring Wisconsin. For updated information about CWD, check the IDNR web site at: http://dnr.state.il.us/cwd. Hunters who participated in the CWD sampling can check the status of their deer at this site. Hunters who provided samples from deer that test positive are notified by the IDNR.

###

http://dnr.state.il.us/pubaffairs/2006/Jan/cwd.htm

http://dnr.state.il.us/cwd/map.pdf

TSS

Offline
Joined: 01/01/2006
Posts: 230
Transmission of Elk and Deer Prions to Transgenic Mice

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

Transmission of Elk and Deer Prions to Transgenic Mice
--------------------------------------------------------------------------------

Journal of Virology, September 2006, p. 9104-9114, Vol. 80, No. 18
0022-538X/06/$08.00+0 doi:10.1128/JVI.00098-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Transmission of Elk and Deer Prions to Transgenic Mice
Gültekin Tamgüney,1 Kurt Giles,1,2 Essia Bouzamondo-Bernstein,3 Patrick J. Bosque,1,2, Michael W. Miller,4 Jiri Safar,1,2 Stephen J. DeArmond,1,3 and Stanley B. Prusiner1,2,5*
Institute for Neurodegenerative Diseases,1 Departments of Neurology,2 Pathology,3 Biochemistry and Biophysics, University of California, San Francisco, California,5 Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, Colorado4

Received 13 January 2006/ Accepted 21 June 2006

Chronic wasting disease (CWD) is a fatal prion disease in deer and elk. Unique among the prion diseases, it is transmitted among captive and free-ranging animals. To facilitate studies of the biology of CWD prions, we generated five lines of transgenic (Tg) mice expressing prion protein (PrP) from Rocky Mountain elk (Cervus elaphus nelsoni), denoted Tg(ElkPrP), and two lines of Tg mice expressing PrP common to white-tailed deer (Odocoileus virginianus) and mule deer (Odocoileus hemionus), denoted Tg(DePrP). None of the Tg(ElkPrP) or Tg(DePrP) mice exhibited spontaneous neurologic dysfunction at more than 600 days of age. Brain samples from CWD-positive elk, white-tailed deer, and mule deer produced disease in Tg(ElkPrP) mice between 180 and 200 days after inoculation and in Tg(DePrP) mice between 300 and 400 days. One of eight cervid brain inocula transmitted disease to Tg(MoPrP)4053 mice overexpressing wild-type mouse PrP-A in 540 days. Neuropathologic analysis revealed abundant PrP amyloid plaques in the brains of ill mice. Brain homogenates from symptomatic Tg(ElkPrP) mice produced disease in 120 to 190 days in Tg(ElkPrP) mice. In contrast to the Tg(ElkPrP) and Tg(DePrP) mice, Tg mice overexpressing human, bovine, or ovine PrP did not develop prion disease after inoculation with CWD prions from among nine different isolates after >500 days. These findings suggest that CWD prions from elk, mule deer, and white-tailed deer can be readily transmitted among these three cervid species.

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

* Corresponding author. Mailing address: Institute for Neurodegenerative Diseases, 513 Parnassus Ave., HSE-774, University of California, San Francisco, CA 94143-0518. Phone: (415) 476-4482. Fax: (415) 476-8386. E-mail: stanley@ind.ucsf.edu .

Supplemental material for this article may be found at http://jvi.asm.org/.

Present address: Department of Neurology, University of Colorado Health Sciences Center, Denver, CO 80262.

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

Journal of Virology, September 2006, p. 9104-9114, Vol. 80, No. 18
0022-538X/06/$08.00+0 doi:10.1128/JVI.00098-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

http://jvi.asm.org/cgi/content/abstract/80/18/9104

TSS

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

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)

http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf

[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk
Materials for Human Food and Requirement for the Disposition of
Non-Ambulatory Disabled Cattle

03-025IFA
03-025IFA-2
Terry S. Singeltary

9/13/2005

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf

TSS

Offline
Joined: 01/01/2006
Posts: 230
Re: CWD aka mad deer/elk disease i.e. TSE update 2005

Thursday, June 03, 2010

Prion Strain Mutation and Selection John Collinge

Science Journal MEDICINE

http://www.sciencemag.org SCIENCE VOL 328 28 MAY 2010

see full text ;

http://chronic-wasting-disease.blogspot.com/2010/06/prion-strain-mutatio...

Friday, May 14, 2010

Prion Strain Mutation Determined by Prion Protein Conformational Compatibility and Primary Structure

Published Online May 13, 2010 Science DOI: 10.1126/science.1187107 Science Express Index

http://www.sciencemag.org/cgi/content/abstract/science.1187107

see full text and more here ;

http://chronic-wasting-disease.blogspot.com/2010/05/prion-strain-mutatio...

>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.She left 6 Kids and a Husband.The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.-

Physician Discharge Summary, Parkland Hospital, Dallas Texas

Admit Date: 12/29/2009 Discharge Date: 1/20/2010 Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General Neurology Team

Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence.She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers.

The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically. Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.

http://www.recordandoalinda.com/index.php?option=com_content&view=articl...

>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<

Monday, March 29, 2010

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas

http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo...

CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER

http://cjdtexas.blogspot.com/2010/03/cjd-texas-38-year-old-female-worked...

YOU can be assured they are squirming behind closed doors, and that they are doing there best to squirm right out of this one. they will come up with something, international travel long ago, or some strange PRNP mutation that they might say like sporadic ffi ??? or a case of atypical case of inherited Creutzfeldt-Jakob disease (CJD) ??? they will make up something. but it will be anything but BSE related here in the USA, in my opinion. sporadic FFI, or sporadic GSS, or sporadic inherited CJD is an oxymoron. it's either familial or not. or even this new novel human disease known as Protease-Sensitive Prionopathy (PSPr), they might come up with that. if they cannot do this, it will be an occupational TSE infection, whether they want to admit it or not. ...TSS

14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America

update October 2009

T. Singeltary

Bacliff, TX, USA

Background:

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

Methods:

12 years independent research of available data

Results:

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

Conclusion:

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf

International Society for Infectious Diseases Web: http://www.isid.org

Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***

http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-...

my comments to PLosone here ;

http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi...

Friday, February 05, 2010

New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review

http://vcjd.blogspot.com/2010/02/new-variant-creutzfelt-jakob-disease.html

Sunday, February 14, 2010

[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)

http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard...

http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transm...

Wednesday, March 31, 2010

Atypical BSE in Cattle

http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position...

http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-huma...

Saturday, June 5, 2010

Research Project: Transmissible Spongiform Encephalopathies: Identification of atypical scrapie in Canadian sheep

http://nor-98.blogspot.com/2010/06/research-project-transmissible.html

Transmissible Spongiform Encephalopathy

http://transmissiblespongiformencephalopathy.blogspot.com/

Monday, April 5, 2010

Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010

http://madcowfeed.blogspot.com/2010/04/update-on-feed-enforcement-activi...

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net

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