# Susceptibility of Domestic Cats to CWD Infection



## terry (Sep 13, 2002)

Monday, August 8, 2011 


Susceptibility of Domestic Cats to CWD Infection


http://felinespongiformencephalopat...8/susceptibility-of-domestic-cats-to-cwd.html




TSS


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## Michihunter (Jan 8, 2003)

Although this is interesting, I'm not quite sure how this would effect anything. We already know that several species are capable of obtaining the disease but only a few are capable of transmitting it. It appears as though cats only fall into the former category.


BTW- Thanks for the continued updates Terry. You are definitely responsible for a great portion of my knowledge regarding these matters.


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## terry (Sep 13, 2002)

Michihunter said:


> Although this is interesting, I'm not quite sure how this would effect anything. We already know that several species are capable of obtaining the disease but only a few are capable of transmitting it. It appears as though cats only fall into the former category.
> 
> 
> BTW- Thanks for the continued updates Terry. You are definitely responsible for a great portion of my knowledge regarding these matters.




Hello Michihunter, 

in my opinion, this has the potential to be another factor in the spreading of CWD. please see why here ;



CWD, FELINE, HUNTING, DIET

Hunting and diet

A successful generalist predator, the cougar will eat any animal it can catch, from insects to large ungulates (over 500 kg). Like all cats, it is an obligate carnivore, feeding only on meat. The mean weight of vertebrate prey (MWVP) was positively correlated (r=0.875) with puma body weight and inversely correlated (r=-0.836) with food niche breadth in all America. In general, MWVP was lower in areas closer to the Equator.[3] Its most important prey species are various deer species, particularly in North America; mule deer, white-tailed deer, elk, and even large moose are taken by the cat. Other species such as Bighorn Sheep, wild horses of Arizona, domestic horses, and domestic livestock such as cattle and sheep are also primary food bases in many areas.[38] A survey of North America research found 68% of prey items were ungulates, especially deer. Only the Florida Panther showed variation, often preferring feral hogs and armadillos.[3]

Shown eating. Cougars are ambush predators, feeding mostly on deer and other mammals. Investigation in Yellowstone National Park showed that elk, followed by mule deer, were the cougar's primary targets; the prey base is shared with the park's gray wolves, with whom the cougar competes for resources.[39] Another study on winter kills (NovemberApril) in Alberta showed that ungulates accounted for greater than 99% of the cougar diet. Learned, individual prey recognition was observed, as some cougars rarely killed bighorn sheep, while others relied heavily on the species.[40]

http://en.wikipedia.org/


Oral.22:

Transmission and Pathogenesis of Chronic Wasting Disease in Cervid and Non-Cervid Species

Edward Hoover, Candace K. Mathiason, Nicholas J. Haley, Timothy D. Kurt, Davis M. Seelig, Amy V. Nalls, Mark D. Zabel, Glenn C. Telling Department of Microbiology, Immunology, and Pathology; Colorado State University; Fort Collins, CO; Department of Microbiology, Immunology and Molecular Genetics and Neurology; University of Kentucky Medical Center; Lexington, KY USA Presenting author

Now recognized in 18 states in the US, two Canadian provinces, and one Asian country, efficient horizontal transmission is a signature trait of chronic wasting disease (CWD) of cervids. The facile spread of CWD appears linked to the prion/host relationship facilitating efficient mucosal uptake, peripheral lymphoreticular amplification, and horizontal dissemination exploiting excretory tissues and their products. In addition, recent studies suggest the likelihood of early life mother to offspring transmission. Growing evidence from studies of cervid CWD exposure by natural routes indicate that the incubation period for overt infection detection and disease onset (if any) may be much longer than originally thought. Whether non-cervid species (including humans) may be susceptible to CWD infection and/or act as reservoirs for infection in nature remains unknown. In vitro and in vivo studies of the CWD species barrier indicate the potential for a host range extending beyond cervid species, although no evidence for this has thus far been detected in nature. Interestingly, rodent and mustelid species sympatric with free ranging cervids have been shown susceptible to CWD prions and such trans-species infection broadens the host range/strain characteristics of CWD prions. While the origins of CWD remain unknown, the relationship between sheep scrapie and CWD and the existence of multiple CWD prion strains/quasispecies remain interesting and merit further investigation.

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

Oral.26: Minor Oral Lesions Facilitate CWD Infection

Nathaniel D. Denkers,1, Glenn C. Telling2 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Kentuckty; Lexington, KY USA Presenting author; Email: [email protected]

Purpose: While the exact mechanisms of chronic wasting disease (CWD) prion transmission, entry, and trafficking remain incompletely elucidated, transmission by exposure of the oral and/or nasal mucous membranes seems certain. As part of foraging, cervids likely experience minor lesions in the oral mucous membranes; these could have impact on susceptibility to prion entry and subsequent infection. To explore this potential co-factor, we used cervid PrP transgenic mice to assess whether or not micro-abrasions to the tongue may enhance susceptibility to oral CWD infection and whether or not infectious CWD PrPCWD could be detected immediately after exposure.

Methods: Two sets of FVB mice transgenically expressing the normal cervid PrPC protein [Tg(CerPrP-E226)5037+/-], with or without abrasions on the lingual mucosa, were inoculated orally with 10µl of a 10% w/v brain homogenate from either CWD-positive or negative deer. Abrasions were created by lightly scratching the dorsal lingual epithelium with a 27g needle. Cohorts were sacrificed at either early [0, 1, and 4 h post inoculation (pi)] or late [3, 12, and 24 months pi] time points or when signs of neurologic disease were observed. Tongue, lymphoid tissue, and the brain were assessed by western blotting and tyramide signal amplification (TSA) immunohistochemistry to detect the CWD abnormal prion protein (PrPCWD).

Results: Between 296 and 515 dpi, 9 of the 9 CWD-inoculated mice with lingual lesions developed clinical signs of neurologic dysfunction mandating euthanasia. Only the brain in all nine mice was positive for PrPCWD by western blot and TSA immunohistochemistry. Conversely, all mice without oral lesions remained asymptomatic for >700 dpi and no evidence of PrPCWD was detected in these mice terminally. Moreover, no evidence of PrPCWD could be detected when the micro-abrasion sites were examined at 0, 1, or 4 h after oral exposure or at any pre-terminal time point thereafter.

Conclusions: Micro-abrasions to the lingual surface substantially facilitated CWD transmission, suggesting that minor oral mucosal lesions may be a significant co-factor facilitating infection in foraging cervids or other species.

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

Oral.27: Identification of PrPCWD in the Salivary Gland Epithelium of White-Tailed Deer: Novel Insights Into Mechanisms of CWD Horizontal Transmission

Davis Seelig,1, Gary Mason,1 Glenn Telling2 and Edward Hoover1

1Colorado State University; Fort Collins, CO USA; 2University of Kentucky; Lexington, KY USAPresenting author; Email: [email protected]

Background. Chronic wasting disease (CWD) of cervids is characterized by its efficient transmission among animals. Although bioassay and in vitro amplification studies have confirmed the infectious nature of saliva, urine, blood and feces, uncertainties remain regarding the mechanisms of this facile horizontal transmission. Notable among these is a specific understanding of the means by which prion infectivity is transferred to a body fluid or excretion.

Objectives. The chief objective of this work was to provide tissue-level insights into the process of prion shedding via the salivary glands by means of enhanced immunohistochemistry (IHC).

Methods. Formalin fixed, paraffin-embedded tissues from CWD-infected white-tailed deer (WTD) were evaluated for the presence of PrPCWD using sensitive amplified immunohistochemistry (IHC) methods employing, citrate buffer-based heat-induced epitope retrieval, tyramide signal amplification (TSA), and a polyclonal anti-prion protein antisera.

Results. Here we show that enhanced IHC techniques are capable of detecting pathogenic prion protein (PrPCWD) in the salivary glands of infected WTD. Utilizing optimized TSA we have detected granular to clumped, intra-cytoplasmic PrPCWD deposits in parotid and mandibular salivary gland ductular epithelial cells of WTD infected with CWD for 19 to 27 months. Salivary PrPCWD was not detected in sham-inoculated or naïve WTD. PrPCWD was not identified in any other salivary gland cell types.

Discussion. We present immunohistochemical evidence for PrPCWD accumulation in the salivary gland ductules, which provides a tissue level correlate to the infectivity present in cervid saliva and may explain the manner by which prions transit to saliva, and thereby facilitate the high degree of CWD horizontal transmission. These findings complement work by Haley et al. (this symposium) demonstrating the presence of CWD prions in salivary glands through the in vitro amplification assay PMCA.

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

Oral.44: Genetic Variability and Association with Prion Disease Susceptibility of the Prion Gene in the Mammalian Order Carnivora

Paula Stewart,1 Karen Griffin,8 Jon E. Swenson,2 Jens Persson,11 Olof Liberg,11 Jon M. Arnemo,3, 4 Thierry Baron,5 Martin Groschup,6 Danielle Gunn-Moore,9 Simon Girling,10 Michael W. Miller,8 Michael Tranulis7 and Wilfred Goldmann,1,

1The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh; Easter Bush, Midlothian, UK; 2Department of Ecology and Natural Resources Management, Norwegian University of Life Sciences; As, Norway; 3Department of Forestry and Wildlife Management, Hedmark University College; Campus Evenstad, Norway; 4Department of Wildlife, Fish and Environmental Studies, Faculty of Forest Sciences, Swedish University of Agricultural Sciences; Umea, Sweden; 5Agence Française de Sécurité Sanitaire des Aliments; Lyon, France; 6Friedrich Loeffler Institut; Riems, Germany; 7Department of Basic Sciences & Aquatic Medicine, Norwegian School of Veterinary Science; Oslo, Norway; 8Wildlife Research Center, Colorado Division of Wildlife; Fort Collins, CO USA; 9Small Animal Hospital, Royal (Dick) School of Veterinary Studies, University of Edinburgh; Edinburgh, UK; 10The Royal Zoological Society of Scotland, Edinburgh Zoo; Edinburgh, UK; 11Grimsö Wildlife Research Station, Department of Ecology, Swedish University of Agricultural Sciences ; Riddarhyttan, SwedenPresenting author; Email: [email protected]

Carnivores are exposed to significant levels of CWD in some regions of the US and Canada. Indeed it has been proposed recently that mountain lions prey selectively on prioninfected mule deer. It is likely that predators have also at least occasionally been exposed to other prion diseases, such as sheep scrapie in other countries. How susceptible are predators and scavengers to prion diseases? It is well known that the prion protein sequence is important as a major modulator of susceptibility and pathogenesis of prion disease. For example, prion disease susceptibility in sheep, goats and deer is modulated by at least 15 different polymorphisms of the PrP protein. PrP sequencing of carnivore species has not been done in great numbers and the degree of genetic variation of their PrP in wild and domesticated populations has not been addressed in any detail. However, to estimate the genetic risk of populations to diseases such as CWD one needs to understand the genetic variation of the target species.

We have analyzed the prion protein sequence of over 450 samples from over 20 species/subspecies of the suborders feliformia (cat-like) and caniformia (dog-like) representing ~320 samples from wild populations (US, Europe), ~110 samples from companion animals and ~25 samples from zoo collections. Within these samples were nine FSE cat cases, including the index case from the UK and six FSE cheetahs.

We established the PrP protein variants in our sample set and conclude that the number of PrP variants is small, with slightly more variability in caniformia than feliformia. All feline prion sequences have a characteristic alanine change in their repeat region that is not seen in any other species; all canine PrP encode aspartic acid in position 163, which is not present in any other species with the exception of wolverines. We hypothesis that these differences may explain some of the difference observed in prion disease susceptibility. The analysis of the FSE cases revealed no additional mutations therefore excluding the possibility of particularly susceptible PrP genotypes.

Although the general susceptibility of predators to CWD has not been established, we predict that it is unlikely that species such as mountain lion and black bear will be protected by resistant alleles, whereas wolf and wolverine may have a slightly higher susceptibility threshold.

W.G. and P.S. supported by Institute Strategic Grant funding from the BBSRC, UK.

http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf


Monday, February 14, 2011

THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER


NO, NO, NOT NO, BUT HELL NO !


Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html


Monday, August 8, 2011

Susceptibility of Domestic Cats to CWD Infection

http://felinespongiformencephalopat...8/susceptibility-of-domestic-cats-to-cwd.html


UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


Sunday, November 01, 2009

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

http://chronic-wasting-disease.blogspot.com/2009/11/american-crows-corvus-brachyrhynchos.html


Monday, July 13, 2009

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2009/07/deer-carcass-decomposition-and.html


(please note, there has never been a documneted case of CSE i.e. mad dog disease, BUT, if you read the history, and the data sent to me by maff/defra, and the transmission studies did show something, but another cases of screwed up testing, and then a determination of simply not doing anymore studies because of money and the fact that so many other species came down with it, there was really no need to try and prove a case of canine spongiform encephalopathy due to media and hype. that was my take on it, read up the history and correspondense ;


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

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

TSE & HOUNDS

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.

http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf


76 pages on hound study;

http://web.archive.org/web/20030327022236/http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf


The signs of canine cognitive dysfunction syndrome or "old dog syndrome" commonly seen in dogs are:

snip...see full text ;

http://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html


Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

Date: Fri, 16 May 2003 11:47:37 -0500

From: "Terry S. Singeltary Sr." To: [email protected]

http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html


http://www.mad-cow.org/zoo_cites_annotated.html#ccc


http://www.mad-cow.org/zoo_cites_annotated.html#ddd


http://www.mad-cow.org/zoo_cites_annotated.html#tig


http://www.mad-cow.org/zoo_cites_annotated.html#bbb


Ravensden, Marwell, Chester, Port Lympne, London, Whipsnade, Woburn, and Edinburgh are 8 known BSE affected British zoos.

Woburn Safari Park apparently killed the lion by feeding it split cattle spinal cords and skulls.

http://www.mad-cow.org/zoo_cites_annotated.html#aaab


TSS


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## Michihunter (Jan 8, 2003)

Could you be a bit more specific Terry? In the reports you listed I'm finding that the belief is that the spread may actually be reduced by ungulate eating cats such as Mountain Lions. Furthermore, the statement that sticks out to me the most is the following:

_*Whether non-cervid species (including humans) may be susceptible to CWD infection and/or act as reservoirs for infection in nature remains unknown. In vitro and in vivo studies of the CWD species barrier indicate the potential for a host range extending beyond cervid species, although no evidence for this has thus far been detected in nature.*_


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## terry (Sep 13, 2002)

Michihunter said:


> Could you be a bit more specific Terry? In the reports you listed I'm finding that the belief is that the spread may actually be reduced by ungulate eating cats such as Mountain Lions. Furthermore, the statement that sticks out to me the most is the following:
> 
> _*Whether non-cervid species (including humans) may be susceptible to CWD infection and/or act as reservoirs for infection in nature remains unknown. In vitro and in vivo studies of the CWD species barrier indicate the potential for a host range extending beyond cervid species, although no evidence for this has thus far been detected in nature.*_




Greetings again Michihunter ;


i guess we interpret the findings of the study differently. 

i simply disagree that big cats, or wolves, either would be a tool to help eradicate CWD. of the contrary, i was very specific as to WHY this should not happen. 


'Whether non-cervid species (including humans) may be susceptible to CWD infection and/or act as reservoirs for infection in nature remains unknown. In vitro and in vivo studies of the CWD species barrier indicate the potential for a host range extending beyond cervid species, although no evidence for this has thus far been detected in nature.'


i read the above statement as that they have not documented any CWD in any other species in the wild......yet, bbbut, the potential is there. therefore, any eradication efforts to use big cats or the wolf, would be .............in my opinion.......ignorant, stupid, idiotic, crazy, just a few words to offer up my view on the matter.

my view is the same for big cats in the wild in the USA, as it would be for the wolves. these animals are carnivores, and if you start using them to try and eradicate CWD, or any other TSE, you will simply spread the TSE agent. if you read about the 'Hound Study', those hounds had some sort of TSE, and they knew it, and even said as much, and WHY they stopped all testing on scrapie to chimps, they feared the reality of what they knew would happen, they knew/know that all these TSE are capable of transmitting to other species. i suppose the biggest piece of evidence that i have goes back to the typical scrapie and potential transmission to humans. they feared this so bad, the officials had the evidence decades ago, but chose to ignore, cover up, and went as far to scramble the brains again (BSE to sheep studies and the brain blunder there from, thousands of brains, archived to study for transmission studies, and at the end, they had cow brains $$$) do you realize how many times in the UK, in the USA, they come up with this excuse? cow brains here on two different cows that the USA officials intentionally tried to cover up. and a third one they succeeding in covering up, the infamous stumbling and staggering highly suspect mad cow in Texas, Austin officials over road a call to test, and sent that mad cow straight to be rendered...........this is all fact.......but i am straying from the topic........my point ;



please read line 5 ;


Wednesday, February 16, 2011

IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES

IN CONFIDENCE

Wednesday, February 16, 2011 IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES

IN CONFIDENCE

reference...

RB3.20

TRANSMISSION TO CHIMPANZEES

1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.

2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, ilp and i/v) :

3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.

4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.

5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.

R. Bradley

23 September 1990

CVO (+Mr Wells' comments)

Dr T W A Little

Dr B J Shreeve

90/9.23/1.1.

http://collections.europarchive.org...einquiry.gov.uk/files/yb/1990/09/23001001.pdf




also, all the evidence from big cats zoo TSE in the past from being fed SRM, and death from TSE there from, or the evidence of the feline TSE i.e. feline spongiform encephalopathy (FSE) in the UK in domestic cats from BSE SRM. 



Monday, February 14, 2011

THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER

NO, NO, NOT NO, BUT HELL NO !

Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html



Monday, August 8, 2011

Susceptibility of Domestic Cats to CWD Infection

http://felinespongiformencephalopat...8/susceptibility-of-domestic-cats-to-cwd.html



UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010



http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


Monday, July 13, 2009

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2009/07/deer-carcass-decomposition-and.html



http://www.mad-cow.org/zoo_cites_annotated.html#ccc


http://www.mad-cow.org/zoo_cites_annotated.html#ddd


http://www.mad-cow.org/zoo_cites_annotated.html#tig


http://www.mad-cow.org/zoo_cites_annotated.html#bbb


Ravensden, Marwell, Chester, Port Lympne, London, Whipsnade, Woburn, and Edinburgh are 8 known BSE affected British zoos.

Woburn Safari Park apparently killed the lion by feeding it split cattle spinal cords and skulls.


http://www.mad-cow.org/zoo_cites_annotated.html#aaab



Feline spongiform encephalopathy (FSE) 

FSE was first identified in the United Kingdom in 1990. 

Most cases have been reported in the United Kingdom, where the epidemic has been consistent with that of the BSE epidemic. Some other countries (e.g. Norway, Liechtenstein and France) have also reported cases. 

Most cases have been reported in domestic cats but there have also been cases in captive exotic cats (e.g. Cheetah, Lion, Asian, leopard cat, Ocelot, Puma and Tiger). 

The disease is characterised by progressive nervous signs, including ataxia, hyper-reactivity and behavioural changes and is fatal. 

The chemical and biological properties of the infectious agent are identical to those of the BSE and variantCreutzfeldt-Jakob agents. These findings support the hypothesis that the FSE epidemic resulted from the consumption of food contaminated with the BSE agent. 

The FSE epidemic has declined as a result of tight controls on the disposal of specified risk material and other animal by-products.


http://vla.defra.gov.uk/science/sci_tse_stats_exotic.htm



>>> The FSE epidemic has declined as a result of tight controls on the disposal of specified risk material and other animal by-products.



USA, as late as 2007, 10 years (one decade) POST USA partial and voluntary mad cow feed ban, that was nothing but ink on paper....let's see shall we ;




10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

___________________________________

PRODUCT

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.

REASON

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI

___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm



please see other mad cow feed in commerce here ;




Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation

http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html



Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)

PRION DISEASE UPDATE 2010 (11)

http://www.promedmail.org/pls/apex/..._BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129



can someone please tell me how many TSE prion test that are done on any domestic cat or dog in the USA ???


then ask yourself how many tons of this (including deer and or elk) are rendered and fed back to food producing animals for humans and animals, that go untested, every year. then ask yourself, just how long mad cow disease (all species i.e. TSE), how long have these TSE been in the USA ???


PLEASE NOTE * 

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...


http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf



Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque


"BSE-L IN NORTH AMERICA MAY HAVE EXISTED FOR DECADES"


http://transmissiblespongiformencep.../06/transmissibility-of-bse-l-and-cattle.html




again, the use of big cats or wolves to try and eradicate CWD or any other TSE in the wild, in my opinion, would be insane...

so Michihunter, at the end, you interpret the science much different than i do, and that's o.k., but i stand fast on my interpretation of the science...


kind regards,
terry


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## Michihunter (Jan 8, 2003)

Thank you for your thoughts. And for what its worth, I don't necessarily disagree with your assessment. I was merely stating what I felt was the message being relayed in those findings. Keep up the great work.


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## terry (Sep 13, 2002)

Michihunter said:


> Thank you for your thoughts. And for what its worth, I don't necessarily disagree with your assessment. I was merely stating what I felt was the message being relayed in those findings. Keep up the great work.




my bad. i have been a bit uneasy lately with the political turmoil (not here). 

sometimes in those studies, it's hard to figure out what they are saying. a lot of times, they would not say shinola, even if they had a mouth full.:SHOCKED:

i must not stray from my goals, and stay focused...:help:


thanks....terry


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