# Prions passing thru predators?



## sandbur3 (Sep 24, 2005)

Now that prions have been found to exist in muscle, has anyone considered or studied the activity of prions that pass through a predator? Will the predator transport the prion greater distances and deposit prions in thier feces? Could commercial dog food pass prions thru dogs or wild carnivores and spread cwd or bse to cattle and deer?

Maybe we should be looking at what goes into dog food to protect our cattle and wild herbivores.


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## sadocf1 (Mar 10, 2002)

Excellent question- Astute Reasoning !!!!
Altho the scientific community will cry "there is no evidence" there is every reason to believe that prions can pass thru predators. If prions are found in the feces and urine of CWD positive animals they will be found in the feces and urine of predators that consume CWD infected animals, or dogs that consume commercial dog food containing ruminant protein and bone meal processed from BSE or CWD INFECTED ANIMALS. Canada does not allow any of our dog food to enter Canada.
I have wondered if perhaps scavenger birds, buzzards, eagles, crows,ravens, could be responsible for the spread of CWD. I have observed, as a practicing veterinarian, evidence that buzzards feeding on cattle that died of blackleg, apparently transmitted the disease to herds miles away w/ their droppings.
Predators infected w/ tapeworms pass the worm eggs which can be consumed by deer on contaminated vegitation, the deer becoming the secondary host.
Apparently no scientific experiments have been conducted to determine whether the urine and/or feces of predators consuming CWD infected animals
can infect CWD succeptible cervids. We must admit the possibility of environmental contamination.


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## Dave Lyons (Jun 28, 2002)

Interesting,

In fact I know the USDA trapper was trapping and or snaring coyotes, and bobcats for a study being done in MI for this very topic. I have not seen any results yet.

Dave


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## terry (Sep 13, 2002)

Detection and Localization of PrPSc in the Skeletal Muscle
Sat Mar 4, 2006 17:17
70.110.86.250


MAD COW i.e. all TSE 'FRIENDLY FIRE' GETTING SERIOUS (iCJD) Reply with quote ##################### Bovine Spongiform Encephalopathy #####################

CJD WATCH MESSAGE BOARD
TSS
Detection and Localization of PrPSc in the Skeletal Muscle
Thu Mar 2, 2006 10:40
70.110.86.250


© 2006 American Society for Investigative Pathology

Detection and Localization of PrPSc in the Skeletal Muscle of Patients with Variant, Iatrogenic, and Sporadic Forms of Creutzfeldt-Jakob Disease
Alexander H. Peden, Diane L. Ritchie, Mark W. Head and James W. Ironside
From the National Creutzfeldt-Jakob Disease Surveillance Unit and Division of Pathology, School of Molecular and Clinical Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom


Variant Creutzfeldt-Jakob disease (vCJD) differs from other human prion diseases in that the pathogenic prion protein PrPSc can be detected to a greater extent at extraneuronal sites throughout the body, principally within lymphoid tissues. However, a recent study using a high-sensitivity Western blotting technique revealed low levels of PrPSc in skeletal muscle from a quarter of Swiss patients with sporadic CJD (sCJD). This posed the question of whether PrPSc in muscle could also be detected in vCJD, sCJD, and iatrogenic (iCJD) patients from other populations. Therefore, we have used the same high-sensitivity Western blotting technique, in combination with paraffin-embedded tissue blotting, to screen for PrPSc in muscle tissue specimens taken at autopsy from 49 CJD patients in the United Kingdom. These techniques identified muscle PrPSc in 8 of 17 vCJD, 7 of 26 sCJD, and 2 of 5 iCJD patients. Paraffin-embedded tissue blotting analysis showed PrPSc in skeletal muscle in localized anatomical structures that had the morphological and immunohistochemical characteristics of nerve fibers. The detection of PrPSc in muscle tissue from all forms of CJD indicates the possible presence of infectivity in these tissues, suggesting important implications for assessing the potential risk of iatrogenic spread via contaminated surgical instruments.



http://ajp.amjpathol.org/cgi/content/abstract/168/3/927




TSS

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



BSE ALSO;


PrPSc distribution of a natural case of bovine spongiform encephalopathy


Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori- kazu Imamura, Takashi Yokoyama and Morikazu Shinagawa Priori Disease Research Center, National Institute of Animal Health, 3-1-5 Kannondai, Tsukuba 305-0856 Japan [email protected]


Abstract


Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes progressive neurodegeneration of the central nervous system. Infectivity of BSE agent is accompanied with an abnormal isoform of prion protein (PrPSc). The specified risk materials (SRM) are tissues potentially carrying BSE infectivity. The following tissues are designated as SRM in Japan: the skull including the brain and eyes but excluding the glossa and the masse- ter muscle, the vertebral column excluding the vertebrae of the tail, spinal cord, distal illeum. For a risk management step, the use of SRM in both animal feed or human food has been prohibited. However, detailed PrPSc distribution remains obscure in BSE cattle and it has caused controversies
about definitions of SRM. Therefore we have examined PrPSc distribution in a BSE cattle by Western blotting to reassess definitions of SRM. The 11th BSE case in Japan was detected in fallen stock surveillance. The carcass was stocked in the refrigerator. For the detection of PrPSc, 200 mg of tissue samples were homogenized. Following collagenase treatment, samples were digested with proteinase K. After digestion, PrPSc was precipitated by sodium phosphotungstate (PTA). The pellets were subjected to Western blotting using the standard procedure. Anti-prion protein monoclonal antibody (mAb) T2 conjugated horseradish peroxidase was used for the detection of PrPSc. PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal ganglia, sublingual ganglion, retina. In addition, PrPSc was also detected in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve). Our results suggest that the currently accepted definitions of SRM in 9/13/2005


179
Page 10 of 17



BSE cattle may need to be reexamined.


T. Kitamoto (Ed.)
PRIONS
Food and Drug Safety

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

ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004; Bovine spongiform encephalopathy (BSE) in Japan

snip...


"Furthermore, current studies into transmission of cases of BSE that are atypical or that develop in young cattle are expected to amplify the BSE prion" NO. Date conf. Farm Birth place and Date Age at diagnosis 8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23 9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21 Test results # 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology negative b = atypical BSE case c = case of BSE in a young animal b,c, No PrPSc on IHC, and no spongiform change on histology International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004. Tetsuyuki Kitamoto Professor and Chairman Department of Prion Research Tohoku University School of Medicine 2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN TEL +81-22-717-8147 FAX +81-22-717-8148 e-mail; [email protected] Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail: [email protected] ================================= 9/13/2005
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Page 11 of 17 From: TSS () Subject: Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Date: August 26, 2005 at 10:24 am PST Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Jpn. J. Infect. Dis., 56, 221-222, 2003 Laboratory and Epidemiology Communications Atypical Proteinase K-Resistant Prion Protein (PrPres) Observed in an Apparently Healthy 23-Month-Old Holstein Steer Yoshio Yamakawa*, KenÕichi Hagiwara, Kyoko Nohtomi, Yuko Nakamura, Masahiro Nishizima ,Yoshimi Higuchi1, Yuko Sato1, Tetsutaro Sata1 and the Expert Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare of Japan2 Department of Biochemistry & Cell Biology and 1Department of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640 and 2Miistry of Health, Labour and Welfare, Tokyo 100-8916 Communicated by Tetsutaro Sata (Accepted December 2, 2003) *Corresponding author: Mailing address: Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 1628640,
Japan. Tel: +81-3-5285-1111, Fax: +81-3-5285-1157, E-mail: [email protected]


Since October 18, 2001, 'bovine spongiform encephalopathy (BSE) examination for all cattle slaughtered at abattoirs in the country' has been mandated in Japan by the Ministry of Health, Labour and Welfare (MHLW). 'Plateria' ELISA-kit (Bio-Rad Laboratories, Hercules, Calif., USA) is routinely used at abattoirs for detecting proteinase K (PK)-resistant prion protein (PrPSc) in the obex region. Samples positive according to the ELISA screening are further subjected to Western blot (WB) and histologic and immunohistochemical examination (IHC) at the National Institute of Infectious Diseases (NIID) or Obihiro University. If PrPSc is detected either by WB or by IHC, the cattle are diagnosed as BSE. The diagnosis is approved by the Expert Committee for BSE Diagnosis, MHLW. From October 18, 2001 to September 30, 2003, approximately 2.5 million cattle were screened at abattoirs. A hundred and ten specimens positive according to ELISA were subjected to WB/IHC. Seven showed positive by both WB and IHC, all exhibiting the typical electrophoretic profile of a high content of the di-glycosylated molecular form of PrPSc (1-3) and the distinctive granular deposition of PrPSc in neuronal cells and neuropil of the dorsal nucleus of vagus. An ELISA-positive specimen from a 23 month-old Holstein steer slaughtered on September 29, 2003, in Ibaraki Prefecture (Ibaraki case) was sent to the NIID for confirmation. The animal was reportedly healthy before slaughter. The OD titer in ELISA was slightly higher than the 'cut-off' level given by the manufacturer. The histology showed no spongiform changes and IHC revealed no signal of PrPSc accumulation typical for BSE. However, WB analysis of the homogenate that was prepared from the obex region and used for ELISA revealed a small amount of PrPSc with an electrophoretic profile different from that of typical BSE-associated PrPSc (1-3). The characteristics were (i) low content of the di-glycosylated molecular form of PrPSc, (ii) a faster migration of the non-glycosylated form of PrPSc on SDS-PAGE, and (iii) less resistance against PK digestion as compared with an authentic PrPSc specimen derived from an 83-month-old Holstein (Wakayama case) (Fig. 1). Table 1 summarizes the relative amounts of three distinctive glycoforms (di-, mono, non-glycosylated) of PrPSc calculated by densitometric analysis of the blot shown in Fig. 1. As 2.5 mg wet weight obex-equivalent homogenate of the Ibaraki case (Fig. 1, lane 4) gave slightly stronger band intensities of PrPSc than an 8 mg wet weight obex-equivqlent homogenate of a typical BSE-affected Wakayama case (Fig. 1, lane 2), the amount of PrPSc accumulated in the Ibaraki case was calculated to be 1/500 - 1/1000 of the Wakayama case. In the Ibaraki case, the PrPSc bands were not detectable in the homogenates of the proximal surrounding region of the obex. These findings were consistent with the low OD value in ELISA, i.e., 0.2 -0.3 for the Ibaraki case versus over 3.0 for the Wakayama case. The DNA sequence of the PrP coding region of the Ibaraki case was the same as that appearing in the database (GenBank accession number: AJ298878). More recently, we encountered another case that resembled the Ibaraki case. It was a 21-monthold
Holstein steer from Hiroshima Prefecture. WB showed typical BSE-specific PrPSc deposition though IHC did not detect positive signals of PrPSc (data not shown). Though the clinical onset of BSE is usually at around 5 years of age or later, a 20-month-old case showing the clinical signs has been reported (4). Variant forms of BSE similar to our cases, i.e., with atypical histopathological and/or biochemical phenotype, have been recently reported in Italy (5) and in France (6). Such variant BSE was not associated with mutations in the prion protein (PrP) coding region as in our case (5,6). The Ministry of Agriculture, Forestry and Fisheries of Japan (MAFF) announced a ban of feeding ruminants with meat bone meal (MBM) on September 18, 2001, and a complete ban was made on October 15 of the same year. According to the recent MAFF report, the previous seven cases of BSE in Japan were cattle born in 1995 - 1996 and possibly fed with cross-contaminated feed. However, the two cattle in this report were born after the complete ban. Whether contaminated MBM was implicated in the present cases remains to be investigated.



REFERENCES Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F. (1996): Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature, 383, 685690.
Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. J.
(1997): Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature, 389, 498-501.
Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C. L., Gowland, I. and Collinge, J. (1997): The same prion strain causes vCJD and BSE. Nature, 389, 448-450.
Matravers, W., Bridgeman, J. and Smith, M.-F. (ed.)(2000): The BSE Inquiry. p. 37. vol. 16. The Stationery Office Ltd., Norwich, UK.
Casalone, C., Zanusso, G., Acutis, P. L., Crescio, M. I., Corona, C., Ferrari, S., Capobianco, R., Tagliavini, F., Monaco, S. and Caramelli, M. (2003): Identification of a novel
molecular and neuropathological BSE phenotype in Italy. International Conference on Prion Disease: from basic research to intervention concepts. Gasreig, Munhen,
October 8-10.
Bicaba, A. G., Laplanche, J. L., Ryder, S. and Baron, T. (2003): A molecular variant of bovine spongiform encephalopatie. International Conference on Prion Disease: from
basic research to intervention concepts. Gasreig, Munhen, October 8-10.
Asante, E. A., Linehan, J. M., Desbruslais, M., Joiner, S., Gowland, I., Wood, A. L., Welch, J., Hill, A. F., Lloyd, S. E., Wadsworth, J. D. F. and Collinge, J. (2002). BSE
prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J., 21, 6358-6366.
9/13/2005
Page 12 of 17 SEE SLIDES IN PDF FILE; http://www.nih.go.jp/JJID/56/221.pdf


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



AND CWD;


Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers,1* Shawn R. Browning,1* Tanya S. Seward,2 Christina J. Sigurdson,4 Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§ 1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders Brown Center on Aging, 3Department of Neurology, University of Kentucky, Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA. *These authors contributed equally to this work. Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA. Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. §To whom correspondence should be addressed: E-mail: [email protected] Prions are transmissible proteinaceous agents of mammals that cause fatal neurodegenerative diseases of the central nervous system (CNS). The presence of infectivity in skeletal muscle of experimentally infected mice raised the possibility that dietary exposure to prions might occur through meat consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious prion disease of North American cervids, is of particular concern. The emergence of CWD in an increasingly wide geographic area and the interspecies transmission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns about zoonotic transmission of CWD. To test whether skeletal muscle of diseased cervids.........SNIP....END



TSS


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## terry (Sep 13, 2002)

sandbur3 asks;

> Could commercial dog food pass prions thru dogs or wild carnivores and spread cwd or bse to cattle and deer?


indeed they can. some data for your reading;


GAH WELLS (very important statement here...TSS) 

HOUND STUDY 

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 

76 pages on hound study; 

http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf

> I thought that in Britain dogs had contracted BSE, but perhaps not. 

not so fast here; 

The spongiform changes were not pathognomonic (ie. 
conclusive proof) for prion disease, as they were atypical, 
being largely present in white matter rather than grey matter in 
the brain and spinal cord. However, Tony Scott, then head of 
electron microscopy work on TSEs, had no doubt that these 
SAFs were genuine and that these hounds therefore must have 
had a scrapie-like disease. I reviewed all the sections 
myself (original notes appended) and although the pathology 
was not typical, I could not exclude the possibility that this was 
a scrapie-like disorder, as white matter vacuolation is seen 
in TSEs and Wallerian degeneration was also present in the 
white matter of the hounds, another feature of scrapie. 

38.I reviewed the literature on hound neuropathology, and 
discovered that micrographs and descriptive neuropathology from 
papers on 'hound ataxia' mirrored those in material from 
Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had 
done much of this work, and I obtained original sections 
from hound ataxia cases from him. This enabled me provisionally to 
conclude that Robert Higgins had in all probability detected 
hound ataxia, but also that hound ataxia itself was possibly a 
TSE. Gerald Wells confirmed in 'blind' examination of single 
restricted microscopic fields that there was no distinction 
between the white matter vacuolation present in BSE and 
scrapie cases, and that occurring in hound ataxia and the hound 
survey cases. 

39.Hound ataxia had reportedly been occurring since the 1930's, 
and a known risk factor for its development was the feeding 
to hounds of downer cows, and particularly bovine offal. 
Circumstantial evidence suggests that bovine offal may also be 
causal in FSE, and TME in mink. Despite the inconclusive 
nature of the neuropathology, it was clearly evident that this 
putative canine spongiform encephalopathy merited further 
investigation. 

40.The inconclusive results in hounds were never confirmed, 
nor was the link with hound ataxia pursued. I telephoned Robert 
Higgins six years after he first sent the slides to CVL. 
I was informed that despite his submitting a yearly report to the 
CVO including the suggestion that the hound work be continued, 
no further work had been done since 1991. This was 
surprising, to say the very least. 

41.The hound work could have provided valuable evidence 
that a scrapie-like agent may have been present in cattle offal long 
before the BSE epidemic was recognised. The MAFF hound 
survey remains unpublished. 

Histopathological support to various other published 
MAFF experiments 

42.These included neuropathological examination of material 
from experiments studying the attempted transmission of BSE to 
chickens and pigs (CVL 1991) and to mice (RVC 1994). 

http://www.bseinquiry.gov.uk/witness/htm/stat067.htm 

It was thought likely that at least some, and probably all, of the cases 
in zoo animals were caused by the BSE agent. Strong support for this 
hypothesis came from the findings of Bruce and others (1994) 
( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & 
Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and 
scrapie to mice: strain variation and species barrier. Philosophical 
Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 
), who demonstrated that the pattern of variation in incubation period 
and lesion profile in six strains of mice inoculated with brain 
homogenates from an affected kudu and the nyala, was similar to that 
seen when this panel of mouse strains was inoculated with brain from 
cattle with BSE. The affected zoo bovids were all from herds that were 
exposed to feeds that were likely to have contained contaminated 
ruminant-derived protein and the zoo felids had been exposed, if only 
occasionally in some cases, to tissues from cattle unfit for human 
consumption. 

snip... 

http://www.bseinquiry.gov.uk/files/ws/s324.pdf


2005


DEFRA
Department for Environment,
Food & Rural Affairs

Area 307, London, SW1P 4PQ
Telephone: 0207 904 6000
Direct line: 0207 904 6287
E-mail: h.mcdonagh.defra.gsi.gov.uk

GTN:
FAX:

Mr T S Singeltary
P.O. Box 42
Bacliff
Texas
USA 77518

21 November 2001

Dear Mr Singeltary TSE IN HOUNDS

Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.

As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.

Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.

Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less



critical. For more details see-
http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf

As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.

Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK

You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.

I hope this is helpful

Yours sincerely 4

HUGH MCDONAGH
BSE CORRESPONDENCE SECTION


============================================
TSS


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## terry (Sep 13, 2002)

Subject: MAD MOUNTAIN LION DISEASE USA VIA CWD ? WHY NOT!
Date: September 11, 2004 at 7:57 am PST

-------- Original Message --------
Subject: Deer Tests Positive for Chronic Wasting Disease
Date: Sat, 11 Sep 2004 10:04:21 -0500
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy


Deer Tests Positive for Chronic Wasting Disease
Sep. 10, 2004

MOAB, Utah (AP) -- A mature buck deer in the La Sal Mountains east of
Moab has tested positive for chronic wasting disease, the Division of
Wildlife Resources said Friday.

Biologists believe the buck was killed by a mountain lion.

"This is the first deer to test positive for CWD in Utah this year,"
said Leslie McFarlane, a division wildlife biologist.

Last year, six of the 244 deer sampled in the La Sal Mountains tested
positive for the disease.

The DWR has collected samples from 207 animals across the state for
testing this year, and wants to collect more than 2,700 samples.

"We'll be taking samples from deer in specific units and from elk in the
Uintah Basin and southeastern Utah," McFarlane said.

A map of the units that will be sampled this year can be viewed at the
DWR's Web site http://www.wildlife.utah.gov

Results from samples that have been submitted, and information about
chronic wasting disease, are also available at the site.

Chronic wasting disease attacks the brains of infected animals, causing
them to display abnormal behavior and eventually become emaciated and
die. There is no evidence the disease can spread to people.

Once thought to exist only in the wild in northeastern Colorado and
southeastern Wyoming, the ailment has been found in wild and captive
deer and elk in Wisconsin, Kansas, Nebraska, Montana, New Mexico,
Oklahoma, South Dakota, Utah and two Canadian provinces.

(Copyright 2004 by The Associated Press. All Rights Reserved.)


http://tv.ksl.com/index.php?nid=5&sid=118740


> Biologists believe the buck was killed by a mountain lion.
>


OH, this is great, now we have the very likelyhood of TSE
via CWD transmitted to another species and on and on;


some 100+ _documented_ TSE cats of all types later...tss

on occassions, materials obtained from slaughterhouses will be derived
from sheep affected with scrapie or cattle that may be incubating BSE
for use in petfood manufacture...


http://www.bseinquiry.gov.uk/files/yb/1989/05/03007001.pdf


Meldrum's notes on pet foods and materials used


http://www.bseinquiry.gov.uk/files/yb/1989/05/16001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf


IN CONFIDENCE CJD TO CATS...


http://www.bseinquiry.gov.uk/files/yb/1989/05/18002001.pdf


Confidential BSE and __________________


http://www.bseinquiry.gov.uk/files/yb/1989/05/22012001.pdf


1st case natural FSE


http://www.bseinquiry.gov.uk/files/yb/1990/05/09002001.pdf


FSE and pharmaceuticals


http://www.bseinquiry.gov.uk/files/yb/1990/05/10005001.pdf


can't forget about the mad man and his mad cat;


Deaths of CJD man and cat linked


http://news.bbc.co.uk/1/hi/health/184558.stm


In October 1998 the simultaneous occurrence of spongiform encephalopathy
in a man and his pet cat was reported. The report from Italy noted that
the cat did not display the same clinical features as FSE cases
previously seen. Indeed, the presence of a new type of FSE was
suggested. The man was diagnosed as having sporadic CJD, and neither
case (man nor cat) appeared to be affected by a BSE-related condition.


http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html


indeed there have been 4 documented cases of TSE in Lions to date.


Lion 32 December 98 Born November 86

Lion 33 May 1999 (euthanased) Born November 81.

Lion 36 Euthanased August 2000 Born July 87. Deteriorating hind limb
ataxia.

Lion 37 Euthanased November 2001 Male, 14 years. Deteriorating hind limb
ataxia since September 2001. (Litter mate to Ref. 36.)


http://www.defra.gov.uk/animalh/bse/index.html


go to the url above, on the bar at the top, click on _statistics_, then
in middle of next page, click on _other TSEs_.

or go here;

http://www.defra.gov.uk/animalh/bse/bse-statistics/level-3-tsestat.html

and

http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html


http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf


also;

Reports on the clinical symptoms presented by these cats give a
relatively homogeneous picture: Affected cats show a lack of
coordination with an ataxia mainly of the hind limbs, they often fall
and miss their target when jumping. Fear and increased aggressiveness
against the owner and also other animals is often seen. They do not
longer tolerate to be touched (stroked) and start hiding. These
behavioural chances might be the result of a hypersensibility to touch
and noise, but also to increased fear. Excessive salivation is another
more frequently seen symptom. Cats with FSE in general show severe
behavioural disturbances, restlessness and depression, and a lack of
coat cleaning. Symptoms in large cats in general are comparable to those
in domestic cats. A report on FSE (in german) has been presented in 2001
in the Swiss FVO Magazin. A paper on the first FSE case in a domestic
cat in Switzerland is currently in press in the Journal Schweizer Archiv
für Tierheilkunde (SAT).


http://www.neurocenter-bern.ch/tse_e.shtml


TSS


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## terry (Sep 13, 2002)

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
[email protected]

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.html
===================================================

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

April 9, 2001 WARNING LETTER

01-PHI-12
CERTIFIED MAIL
RETURN RECEIPT REQUESTED

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

Tel: 215-597-4390

Dear Mr. Raymond:

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

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

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

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

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




IN TEXAS we feed our cattle 5.5 grams of potentially BSE/TSE tainted protein, and that's o.k. per the FDA;


FOR IMMEDIATE RELEASE
P01-05
January 30, 2001
Print Media: 301-827-6242
Consumer Inquiries: 888-INFO-FDA


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

Note: On Dec. 23, 2003, the U.S. Department of Agriculture reported that a cow in Washington state had tested positive for bovine spongiform encephalopathy (BSE, or mad cow disease). As a result, information on this Web page stating that no BSE cases had been found in the United States is now incorrect. However, because other information on this page continues to have value, the page will remain available for viewing.

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT


Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.


http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html


CONTINUED


----------



## terry (Sep 13, 2002)

WE know what happens to most stumbling and staggering suspect mad cows in TEXAS too. THERE tissue samples either sit up on a shelf for 7+ months waiting for everyone to forget about, OR ;


FDA Statement
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.

FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.

FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.

Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).

FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.

To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.

Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.

FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.

####


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


WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.


look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;


Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection   

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa

It is clear that the designing scientists must

also have shared Mr Bradleys surprise at the results because all the dose

levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


2

6. It also appears to me that Mr Bradleys answer (that it would take less than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise that it

could take as little of 1 gram of brain to cause BSE by the oral route within the

same species. This information did not become available until the "attack rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to ensure

that the actual result was within both a lower and an upper limit within the study

and the designing scientists would not have expected all the dose levels to trigger

infection. The dose ranges chosen by the most informed scientists at that time

ranged from 1 gram to three times one hundred grams. It is clear that the designing

scientists must have also shared Mr Bradleys surprise at the results because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]

http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm


2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml


SADLY, DEC 2005 SHOWS THAT WE STILL HAVE A SERIOUS PROBLEM WITH BSE/TSE MAD COW DISEASE FEED

GAO


GAO-06-157R FDA Feed Testing Program

October 11, 2005


SNIP...FULL TEXT 29 PAGES ;


http://www.gao.gov/new.items/d06157r.pdf


Mad Cow Disease: An Evaluation of a Small Feed Testing Program FDA Implemented in 2003 With Recommendations for Making the Program a Better Oversight Tool. GAO-06-157R, October 11

http://www.gao.gov/cgi-bin/getrpt?GAO-06-157R


CVM Update
November 2005 Update on Feed Enforcement Activities to Limit the Spread of BSE

Issued by:
FDA, Center for Veterinary Medicine,
Communications Staff, HFV-12
7519 Standish Place, Rockville, MD 20855
Telephone: (240) 276-9300 FAX: (240) 276-9115
Internet Web Site: http://www.fda.gov/cvm


http://www.fda.gov/cvm/5580.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. [[email protected]]

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

To: [email protected]

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 



TSS


----------



## terry (Sep 13, 2002)

SADOCF1 WRITES;

Apparently no scientific experiments have been conducted to determine whether the urine and/or feces of predators consuming CWD infected animals
can infect CWD succeptible cervids. We must admit the possibility of environmental contamination......
===================


something else to consider, is the Mr. Macho type great white warrior in the woods, who smears 100% bull elk/deer urine all over themselves, as a scent to attract other big game, i was concerned about this years ago and tried to warn the hunters about this route of exposure, especially if one would have a cut, i.e. inoculation. really, makes no difference to me if they smear feces all over themselves if it make them feel better, but fact is both the urine and feces carry the TSE agent, and these products are still on the market. ...tss 






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, 1, 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: [email protected] 

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


http://www.biggamehunt.net/forums/viewtopic.php?t=7603 


http://www.afia.org/Industry_News/forum.html?ShowMessage=1003 


http://www.michiganwalleye.com/forum/printthread.php?t=23313 


http://www.americansportsman.com/me...ing/deer/viewpost.asp?mb=deerhunting&post=642 






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 


TSS 

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############ 





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www.trophyshotsports.com/products.asp?cat=10 - 22k - Cached - Similar pages 
[ More results from www.trophyshotsports.com ] 


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Product Listing Scents A 100% pure cow in estrus urine with natural estrus cycle secretions. ... Place urine in scent station dispenser. Convenient "no lose" cap. ... 
www.king-cart.com/cgi-bin/ cart.cgi?store=apc&product=Scents - 36k - Cached - Similar pages 


Foggy Mountain Deer Hunting Scents & Deer Hunting Lures Bull Elk Lure Buy One Now. 100% pure Elk cow-in-heat urine that draws in ... This scent is made from gland secretions collected from bucks during the rut. ... 
www.hotdoe.com/deerlures.html - 17k - Cached - Similar pages 


Tink's Bring that big bull in close with Tink's® 6T9® Cow Elk Scent. Made from urine taken from cow ... 100% doe urine. 1 oz. Order. W6249 (83150). 1 oz Trilingual ... 
www.wellingtoninc.com/tinks/tinks1.htm - 45k - Cached - Similar pages 


Deer, Elk, Scents, Cover Scents, & Lures A natural, non-estrus urine you can use all season to mask your scent and ... 100% pure moose in heat urnine. Bull's will travel a long distance to zero in ... 
www.gamecalls.net/huntingproducts/deerlures.html - 77k - Cached - Similar pages 


Mrs. Doe Pee's Deer & Elk Urine, Lures & Scent Control Department ... DEER & ELK URINE, LURES & SCENT CONTROL DEPARTMENT by MRS.DOE PEE'S. Main Index ... There was a real advantage in using "FRESH" 100% deer urine. ... 
www.turkeyhuntingsecrets.com/ store/store-luresandscentcontroldept.htm - 45k - Cached - Similar pages 


Outdoor Super Store - Products by CODE BLUE 100% natural buck urine. Collected from a single buck deer during the rut ... World's 1st Certified natural urine cover scent. Proven effective. 1 oz. ... 
www.outdoorsuperstore.com/store/ products/doSearch~manufacturerID~CODE+BLUE.htm - 34k - Cached - Similar pages 


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CONTINUED


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## terry (Sep 13, 2002)

Research

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

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


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Whether transmission of the chronic wasting disease (CWD) prion among cervids requires direct interaction with infected animals has been unclear. We report that CWD can be transmitted to susceptible animals indirectly, from environments contaminated by excreta or decomposed carcasses. Under experimental conditions, mule deer (Odocoileus hemionus) became infected in two of three paddocks containing naturally infected deer, in two of three paddocks where infected deer carcasses had decomposed in situ &#8776;1.8 years earlier, and in one of three paddocks where infected deer had last resided 2.2 years earlier. Indirect transmission and environmental persistence of infectious prions will complicate efforts to control CWD and perhaps other animal prion diseases.



SNIP...



Discussion
Figure 

Click to view enlarged image

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

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

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

The ability of the CWD agent to persist in contaminated environments for >2 years may further increase the probability of transmission and protract epidemic dynamics (8). Because infectivity in contaminated paddocks could not be measured, neither the initial levels nor degradation rate of the CWD agent in the environment was estimable. However, the observed persistence of the CWD agent was comparable to that of the scrapie agent, which persisted in paddocks for &#8776;1 to 3 years after removal of naturally infected sheep (7). Similarities between the CWD and scrapie agents suggest that environmental persistence may be a common trait of prions. Whether persistence of the BSE prion in contaminated feed production facilities or in environments where cattle reside contributed to BSE cases in the United Kingdom after feed bans were enacted (27) remains uncertain but merits further consideration.

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

Acknowledgments

SNIP...

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


LAST, and lately, there is a study underway to test TSE in the soil;


Environ. Sci. Technol., ASAP Article 10.1021/es0516965 S0013-936X(05)01696-2 
Web Release Date: February 1, 2006 

Copyright © 2006 American Chemical Society 
Fate of Prions in Soil: Adsorption and Extraction by Electroelution of Recombinant Ovine Prion Protein from Montmorillonite and Natural Soils 

Peggy Rigou,* Human Rezaei, Jeanne Grosclaude, Siobhán Staunton, and Hervé Quiquampoix 

Virologie et Immunologie Moléculaires, INRA, F-78352 Jouy-en-Josas, France, and UMR Rhizosphère et Symbiose, INRA-ENSAM, 2 Place Pierre Viala, 34060 Montpellier Cedex 01, France 

Received for review August 26, 2005 

Revised manuscript received January 6, 2006 

Accepted January 6, 2006

Abstract:

Prions, the infectious agents thought to be responsible for transmissible spongiform encephalopathies, may contaminate soils and have been reported to persist there for years. We have studied the adsorption and desorption of a model recombinant prion protein on montmorillonite and natural soil samples in order to elucidate mechanisms of prion retention in soils. Clay minerals, such as montmorillonite, are known to be strong adsorbents for organic molecules, including proteins. Montmorillonite was found to have a large and selective adsorption capacity for both the normal and the aggregated prion protein. Adsorption occurred mainly via the N-terminal domain of the protein. Incubation with standard buffers and detergents did not desorb the full length protein from montmorillonite, emphasizing the largely irreversible trapping of prion protein by this soil constituent. An original electroelution method was developed to extract prion protein from both montmorillonite and natural soil samples, allowing quantification when coupled with rapid prion detection tests. This easy-to-perform method produced concentrated prion protein extracts and allowed detection of protein at levels as low as 0.2 ppb in natural soils. 


snip...

full text;

http://pubs.acs.org/cgi-bin/sample.cgi/esthag/asap/pdf/es0516965.pdf


TSS


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