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

Posted Feb 14 2011 11:22am
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

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

Margaret A. Wild1,5, N. Thompson Hobbs2, Mark S. Graham1,4 and Michael W. Miller3 1 National Park Service, Biological Resource Management Division, 1201 Oak Ridge Drive, Suite 200, Fort Collins, Colorado 80525, USA 2 Natural Resource Ecology Laboratory, Colorado State University, Fort Collins, Colorado 80523-1499, USA 3 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, Colorado 80526-2097, USA 5 Corresponding author (email: margaret_wild@nps.gov)

ABSTRACT: Effective measures for controlling chronic wasting disease (CWD), a contagious prion disease of cervids, remain elusive. We review theoretic relationships between predation and host-parasite dynamics and describe a mathematical model to evaluate the potential influence of random removal through harvest or culling and selective predation by wolves (Canis lupus) upon CWD dynamics in deer (Odocoileus spp.) populations. Imposing nonselective mortality representing a 15% annual harvest or cull 51 yr after CWD introduction lowered both deer population size and steady state CWD. Selective (4x) mortality at the same 15% predation rate caused a more modest reduction in deer population size accompanied by a relatively rapid decline in CWD prevalence and elimination of the disease from a closed population. The impacts of selective predation on epidemic dynamics were sensitive to assumptions on parameter estimates; however, within expected ranges, the results of selective predation were consistent and robust. We suggest that as CWD distribution and wolf range overlap in the future, wolf predation may suppress disease emergence or limit prevalence. Key words: Canis lupus, chronic wasting disease, deer, host-parasite, Odocoileus spp., predator-prey, selective predation, wolf.

4 Current address: National Park Service, New River Gorge National River, PO Box 246, 104 Main Street, Glen Jean, West Virginia 25846, USA

http://www.jwildlifedis.org/cgi/content/abstract/47/1/78



----- Original Message -----

From: Terry S. Singeltary Sr.

To: jwdwda@ Cc: margaret_wild@ ; wda.manager@ ; krose@ ; wda@ ; WildlifeDisease@gmail.com ; Jenny_Powers@  ; rcarleton@  

Sent: Tuesday, January 25, 2011 11:05 PM

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

Greetings JWD et al,

AS a layperson, one with no PhDs, old and medically retired, but one that has followed the Transmissible Spongiform Encephalopathy saga for 13 years, daily, I kindly would like to submit this. It probably is not the correct way to submit things, and i am not the most educated and or diplomatic person in the world, but this is very, very, important to me, one that i would not wish on my worst enemy. it you have ever seen it, you will never forget. please take the time to read over all of this. ...

Thank You,

with kindest regards, terry

I _strongly_ disagree with the following suggestion of removal of prion disease i.e. CWD in the following study that was published in your journal, and only hope that and suggestion of this will be will be denied. please see my reasons why, i.e. mainly, you will only spread the disease ;

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

Margaret A. Wild1,5, N. Thompson Hobbs2, Mark S. Graham1,4 and Michael W. Miller3 1 National Park Service, Biological Resource Management Division, 1201 Oak Ridge Drive, Suite 200, Fort Collins, Colorado 80525, USA 2 Natural Resource Ecology Laboratory, Colorado State University, Fort Collins, Colorado 80523-1499, USA 3 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, Colorado 80526-2097, USA 5 Corresponding author (email: margaret_wild@nps.gov)

ABSTRACT: Effective measures for controlling chronic wasting disease (CWD), a contagious prion disease of cervids, remain elusive. We review theoretic relationships between predation and host-parasite dynamics and describe a mathematical model to evaluate the potential influence of random removal through harvest or culling and selective predation by wolves (Canis lupus) upon CWD dynamics in deer (Odocoileus spp.) populations. Imposing nonselective mortality representing a 15% annual harvest or cull 51 yr after CWD introduction lowered both deer population size and steady state CWD. Selective (4x) mortality at the same 15% predation rate caused a more modest reduction in deer population size accompanied by a relatively rapid decline in CWD prevalence and elimination of the disease from a closed population. The impacts of selective predation on epidemic dynamics were sensitive to assumptions on parameter estimates; however, within expected ranges, the results of selective predation were consistent and robust. We suggest that as CWD distribution and wolf range overlap in the future, wolf predation may suppress disease emergence or limit prevalence.

Key words: Canis lupus, chronic wasting disease, deer, host-parasite, Odocoileus spp., predator-prey, selective predation, wolf.

4 Current address: National Park Service, New River Gorge National River, PO Box 246, 104 Main Street, Glen Jean, West Virginia 25846, USA

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

http://www.jwildlifedis.org/cgi/content/abstract/47/1/78?maxtoshow=&hits=10&RESULTFORMAT=&fulltext=prion&searchid=1&FIRSTINDEX=0&volume=47&issue=1&resourcetype=HWCIT



Greetings again JWD et al,

AS a layperson, but one that has followed the TSE saga since 1997 daily, after the loss of my Mother to the Heidenhain Variant of Creutzfeldt Jakob Disease, I would kindly like to make the following comments please.

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

"We suggest that as CWD distribution and wolf range overlap in the future, wolf predation may suppress disease emergence or limit prevalence."

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

NEGATIVE, NEGATIVE, NEGATIVE, you cannot eradicate or control cwd by spreading to other species, and or letting them consume infected carcasses to spread infection miles away by shedding via feces, urine, etc. to the environment. Plus, if you look at old transmission studies i.e. the 'hound study', you will see that there were strange pathology in transmission studies.

i kindly disagree using wolf to try and eradicate CWD for the following reasons.

Tuesday, January 25, 2011

Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions

snip...

Our findings demonstrate that cervid PrPSc, upon strain adaptation by serial passages in vitro or in cervid transgenic mice, is capable of converting human PrPC to produce PrPSc with unique biochemical properties, likely representing a new human prion strain. The newly generated CWD-huPrPSc material has been inoculated into transgenic mice expressing human PrP to study infectivity and disease phenotype and this data will be published elsewhere.

snip...

Besides the importance of our results for public health in relation to the putative transmissibility of CWD to humans, our data also illustrate a very important and novel scientific concept related to the mechanism of prion transmission across species barriers. Today the view is that species barrier is mostly controlled by the degree of similarity on the sequence of the prion protein between the host and the infectious material (4). In our study we show that the strain and moreover the stabilization of the strain plays a major role in the inter-species transmission. In our system there is no change on the protein sequence, but yet strain adaptation results in a complete change on prion transmissibility with potentially dramatic consequences. Therefore, our findings lead to a new view of the species barrier that should not be seen as a static process, but rather a dynamic biological phenomenon that can change over time when prion strains mature and evolve. It remains to be investigated if other species barriers also change upon progressive strain adaptation of other prion forms (e.g. the sheep/human barrier).

Our results have far-reaching implications for human health, since they indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc, suggesting that CWD might be infectious to humans. Interestingly our findings suggest that unstable strains from CWD affected animals might not be a problem for humans, but upon strain stabilization by successive passages in the wild, this disease might become progressively more transmissible to man.

please see full text and many thanks to the Professor Soto and the other Authors of this study AND to The Journal Of Biological Chemistry for the free full text !!!

http://www.jbc.org/content/early/2011/01/04/jbc.M110.198465.long


see full text and more here ;

http://chronic-wasting-disease.blogspot.com/2011/01/generation-of-new-form-of-human-prpsc.html


Is anybody even looking at the dogs, especially with CWD, Scrapie, BSE (?$) now so widespread?



Friday, January 21, 2011

Strain-Specific Barriers against Bovine Prions in Hamsters

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/strain-specific-barriers-against-bovine.html



NA, na, na........they know what they will find, Canine Spongiform Encephalopathy, and it was documented, but then they decided not to push the issue anymore, they had enough mad cow disease in different species to deal with. so they screwed the brains up with dogs and deer in the UK. then we took a page or two from the UKs testing protocols and USDA screwed the brains up with cattle, again, and again, and again. then played the stupid card. ya can't fix stupid. ... TSS


Monday, March 8, 2010

Canine Spongiform Encephalopathy aka MAD DOG DISEASE

Greetings,

Another Big Myth about Transmissible Spongiform Encephalopathy, is that TSE will not transmit to dogs. This is simply NOT TRUE. IT is perfectly legal to feed dogs and cats here in the USA bovine meat and bone meal. Canine dementia is real. how many dogs and cats here in the USA are tested for mad cow disease ? I just received this F.O.I.A. request, and thought I would post it here with a follow up on MAD DOG DISEASE. This is a follow up with additional data I just received on a FOIA request in 2009 ;

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



Monday, March 8, 2010

Canine Spongiform Encephalopathy aka MAD DOG DISEASE

http://caninespongiformencephalopathy.blogspot.com/


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



TSE & HOUNDS

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

HOUND STUDY

snip...

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/20060307063542/www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf



Some of the changes do, however, appear to be neurodegenerative in nature and may represent age-associated or incidental pathology, or, ineed, changes of a neurological 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



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.

http://collections.europarchive.org/tna/20080102174910/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

updated url...tss

http://collections.europarchive.org/tna/20080102204938/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



============end...TSS=============



HOUND SURVEY

I am sorry, but I really could have been a co-signatory of Gerald's minute.

I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding.

If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service.

J W WILESMITH Epidemiology Unit 18 October 1991

Mr. R Bradley

cc: Mr. G A H Wells

http://collections.europarchive.org/tna/20081106102318/http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf



3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.

http://collections.europarchive.org/tna/20080103034308/http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf



37. Putative TSE in hounds - work started 1990 -(see para 41)

Robert Higgins, a Veterinary Investigation Officer at Thirsk, had been working on a hound survey in 1990. Gerald Wells and I myself received histological sections from this survey along with the accompanying letter (YB90/11.28/1.1) dated November 1990. This letter details spongiform changes found in brains from hunt hounds failing to keep up with the rest of the pack, along with the results of SAF extractions from fresh brain material from these same animals. SAFs were not found in brains unless spongiform changes were also present. 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

1. I have had no further submission of material or communication regarding this survey since January 1991.

http://collections.europarchive.org/tna/20080103024918/http://www.bseinquiry.gov.uk/files/yb/1991/10/17001001.pdf



HOUND SURVEY PATHOLOGICAL REPORT (see positive results)

http://web.archive.org/web/20030605233318/http://www.bseinquiry.gov.uk/files/yb/1990/11/28001001.pdf



kind regards, terry



###########bse-l ############


Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY

Date: Fri, 18 Oct 2002 23:12:22 +0100

From: Steve Dealler

Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member

To: BSE-L@ References: <3daf5023.4080804@wt.net>

Dear Terry,

An excellent piece of review as this literature is desparately difficult to get back from Government sites.

What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!

Steve Dealler



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


Incubation periods for BSE are proportional to the life expectancy of the animal affected. The disease's incubation period is 18% of a cow's life expectancy and would be expected to about double when crossing to another species [---] that is, to 36% of 70 years in humans.

Steve Dealler, consultant in medical microbiology. Burnley General Hospital, Burnley BB10 2PQ deal@airtime.co.uk



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



The signs of canine cognitive dysfunction syndrome or "old dog syndrome" commonly seen in dogs are: lose of house training increased barking or whining increased anxiety or fear signs disorientation-appearing lost or confused,getting stuck behind furniture or in corners, walking in circles, becoming forgetful,walking aimlessly,staring into space, repetitious or compulsive behavior change in sleep patterns-up at night, sleep all day, lack of responsiveness other changes,may not recognize you, their name,may become more docile, more aggressive.. You can liken it to human senility. An article at the petcenter says "CDS is not "normal aging". A number of pathophysiological changes are suspected to play a role in its development. These include: * deposition of amyloid plaques in the cerebral cortex and hippocampal part of the brain * alterations in neurotransmitters, including dopamine * increased levels of monoamine oxidase B (MAOB) in the brain * increased levels of free radicals L-DEPRENYL HYDROCHLORIDE SELEGILINE HYDROCHLORIDE,BRAND NAME: ANIPRYL OR ELDEPRYL is used to help treat canine cognitive dysfunction by increasing brain concentrations of the neurotransmitter dopamine. Hopefully you can see a difference in a month or so. If you don't see a difference in the first month, your vet might tell you to try two pills a day for the next month. ANIPRYL doesn't work for all dogs. A great writeup on L-DEPRENYL can be found at

http://www.petsinfo.org/elderlydogs1.html.

"One third of canine CD patients respond extremely well to treatment with deprenyl by regaining their youthful vigor; another one third respond reasonably well; and one third do not respond at all (perhaps there is a variant of CD with different neuropathology). The bottom line is that for any dog that is slowing down to the point that problems become apparent, treatment with deprenyl is the logical route once other organic causes for reduced mental function have been ruled out. Here is a write up on selegline " Selegiline has immune-system-boosting and anti-neurodegenerative effects. ....

Taken consistently in low doses, selegiline tends to extend the life-expectancy of rats by some 20%; enhances drive, libido and endurance; and independently improves cognitive performance in Alzheimer's patients and in some healthy normals. It is used successfully to treat canine cognitive dysfunction syndrome (CDS) in dogs...Selegiline protects the brain's dopamine cells from oxidative stress. " Some also use alpha lipoic acid and r-lipoic acid. powerful antioxidants to help slow down canine cognitive dysfunction. There is a dog food that is rich in antioxidants for CDS but I am assuming if you supplement with your own antioxidants you don't have to worry if your dog likes the food or not. I know my dog Hammy has become very picky and at least if I pill him, I know he is getting his antioxidants.

http://www.thensome.com/cds.htm

Doggie Dementia

Does 14-year-old Fido get lost in his own back yard?

Does he not respond when you call his name?

Does he generally seem confused?

According to Pulse, the official magazine of the Southern California Veterinary Medical Association, just as humans in the 21st Century are living longer, so is man’s best friends—more than 7.3 million dogs in the United States are age 10 or older. And with age dogs become prone to the same age-related diseases as their human companions, including dementia.

A disease of old age affects dogs and humans alike

Kazzy, a 17-year-old Lhasa Apso, is one of the 60 percent of dogs aged 11 to 15 who suffer from one or more symptoms of canine cognitive dysfunction syndrome (CDS), also known to veterinarians as doggie dementia. "He used to be the most incredible watchdog," says his owner, Olivia Feldman-Rich. "But he’s not like that anymore. He’s quite bewildered."

Experts like Dr. Maritza Perez, a veterinarian at West Orange (NJ) Animal Hospital, say that confusion is one of the four major signs of CDS (see sidebar). Dr. Perez says dogs may "pace around in circles, get stuck behind furniture, or they don’t know where the back door is anymore."

Often the most distressing sign of CDS is that, like human patients with Alzheimer’s disease, your pet seems to forget you and your family. "A lot of people notice that when you walk in the door, and this dog that was happy to see you doesn’t get up off the couch or off the floor to greet you," says Dr. Perez. "And he doesn’t come anymore when you call him."

These symptoms, coupled with others debilitating diseases affecting older dogs, such as arthritis, all add up to a serious loss in quality of life for your canine friend. The American Veterinary Medical Association reports that some 500,000 dogs are put to sleep each year because of CDS.

Researchers say that deposits of beta-amyloid plaques in brain tissues are likely to play a role in CDS. These plaques build up and eventually inhibit transmission of the brain’s neural signals. Still, the recognized symptoms of CDS are behavioral, so a diagnosis is exclusionary, meaning it is arrived at only after all other physical and neurological causes are ruled out.

No cure yet, but relief for some dogs

Dr. Perez with a 14 year-old beagle who is on Anipryl.

While scientists search for a permanent cure for CDS, there is one treatment currently FDA-approved for CDS. Selegiline hydrochloride, whose brand name is Anipryl, may give some dogs relief from its symptoms. Researchers speculate that Anipryl works by increasing levels of dopamine, a neurotransmitter. Other treatments are currently being investigated, including diets high in anti-oxidants as well as a new drug, Adrafinil, in one Canadian study.

Dr. Perez says that Anipryl does cause an improvement in many dogs with CDS, meaning relief from at least one of the common symptoms. "We have lots of animals on it and it does work," she says. But it’s not a sure thing—Dr. Perez tried it on her own dog with no effect.

Feldman-Rich is debating putting Kazzy on Anipryl. "I’m hoping that it will give a little more balance to his life and make him a little more aware that he’s still here and we’re still here for him," she says. "I always told him that he couldn’t leave me too soon, and he’s definitely kept up his end of it, but I’d definitely like for him to feel a little more like he’s part of the family."

by Debra Utacia Krol

http://www.sciencentral.com/articles/view.php3?article_id=218391360&cat=1_6



[Image] Research letters Volume 352, Number 9134 [Image] 3 October 1998 [Previous] [Next]

[Image][Image]

Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy

[Image]

Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, Sergio Ferrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, Salvatore Monaco

Transmissible spongiform encephalopathies (TSE) encompass inherited, acquired, and sporadic mammalian neurological disorders, and are characterised by the conversion of the cellular prion protein (PrP) in an insoluble and protease-resistant isoform (PrPres). In human TSE, four types of PrPres have been identified according to size and glycoform ratios, which may represent different prion strains. Type-1 and type-2 PrPres are associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prion strain.2-4 The BSE strain has been identified in three cats with feline spongiform encephalopathy (FSE), a prion disease which appeared in 1990 in the UK.5 We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat.

A 60-year-old man, with no unusual dietary habits, was admitted in November, 1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, and myoclonus. An electroencephalogram (EEG) showed diffuse theta-delta activity. A brain magnetic resonance imaging scan was unremarkable. 10 days later, he was speechless and able to follow only simple commands. Repeat EEGs showed periodic triphasic complexes. 2 weeks after admission, he was mute, akinetic, and unable to swallow. He died in early January, 1994.

His 7-year-old, neutered, female shorthaired cat presented in November, 1993, with episodes of frenzy, twitching of its body, and hyperaesthesia. The cat was usually fed on canned food and slept on its owner's bed. No bites from the cat were recalled. In the next few days, the cat became ataxic, with hindquarter locomotor dysfunction; the ataxia got worse and there was diffuse myoclonus. The cat was killed in mid-January, 1994.

No pathogenic mutations in the patient's PrP gene were found. The patient and the cat were methionine homozygous at codon 129. Histology of the patient's brain showed neocortical and cerebellar neuronal loss, astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed a punctate pattern and paralleled spongiform changes (figure B). The cat's brain showed mild and focal spongiosis in deeper cortical layers of all four lobes (figure C), vacuolated cortical neurons (figure D), and mild astrogliosis. The cerebellar cortex and the dentate nucleus were gliosed. Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, and caudate nucleus (figure E). Western blot analysis of control and affected human and cat brain homogenates showed 3 PrP bands of 27-35 kDa. After digestion with proteinase K and deglycosylation, only samples from the affected patient and cat showed type-1 PrPres, with PrP glycoform ratios comparable to those observed in sporadic CJD1 (details available from author).

[Image]

Microscopic sections of patient and cat brains

A: Occipital cortex of the patient showing moderate spongiform degeneration and neuronal loss (haematoxylin and eosin) and B: punctate perineuronal pattern of PrP immunoreactivity; peroxidase immunohistochemistry with monoclonal antibody 3F4. C: cat parietal cortex showing mild spongiform degeneration (haematoxylin and eosin).D: vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidase immunohistochemistry with antibody 3F4 shows punctate perineuronal deposition of PrP in temporal cortex.

This study shows a spatio-temporal association between human and feline prion diseases. The clinical features of the cat were different from previously reported cases of FSE which were characterised by gradual onset of behavioural changes preceding locomotor dysfunction and ataxia.5 Neuropathological changes were also at variance with the diffuse spongiosis and vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern of PrP deposition, similar in the cat and in the patient, was atypical for a BSE-related condition. Evidence of a new type of FSE was further provided by the detection of a type-1 PrPres, other than the BSE-associated type 4.2 Taken together, our data suggest that the same agent strain of sporadic CJD was involved in the patient and in his cat.

It is unknown whether these TSE occurred as the result of horizontal transmission in either direction, infection from an unknown common source, or the chance occurrence of two sporadic forms.

1 Parchi P, Castellani R, Capellari S, et al. Molecular basis of phenotypic variablity in sporadic Creutzfeldt-Jakob disease. Ann Neurol 1996; 39: 767-78 [PubMed].

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

3 Bruce ME, Will RG, Ironside JW, et al. Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature 1997; 389: 498-501 [PubMed].

4 Hill AF, Desbruslais M, Joiner S, et al. The same prion strain causes vCJD and BSE. Nature 1997; 389: 448-50 [PubMed].

5 Pearson GR, Wyatt JM, Henderson JP, Gruffydd-Jones TJ. Feline spongiform encephalopathy: a review. Vet Annual 1993; 33: 1-10.

------------------------------------------------------------------------ Sezione di Neurologie Clinica, Dipartimento di Scienze Neurologiche e della Visione, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy (S Monaco; e mail rizzuto@Gorgorna.univr.it); and Istituto Zooprofilattico Sperimentale della Lombardia e dell' Emilia, Brescia

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

Terry S. Singeltary Sr. wrote


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


Greetings list members,

ODD that some FELINE in Italy seem to have this same or maybe very similar phenotype of TSE;

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


-------- Original Message --------

Subject: FDA BSE Update - Pet Food from Canadian Manufacturer & MAD DOG DATA

Date: Tue, 27 May 2003 08:07:58 -0500

From: "Terry S. Singeltary Sr."

To: Bovine Spongiform Encephalopathy

Statement

FOR IMMEDIATE RELEASE Statement May 26, 2003

Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

FDA BSE Update - Pet Food from Canadian Manufacturer

The Food and Drug Administration (FDA) has learned from the government of Canada that rendered material from a Canadian cow that last week tested positive for bovine spongiform encephalopathy (BSE, also known as mad cow disease ) may have been used to manufacture pet food, specifically dry dog food, some of which was reported to have been shipped to the United States. The Canadian government prevented the BSE positive cow from being processed for human food. Therefore, consumers can be assured that their food does not contain any remnants of the BSE positive cow.

It is also important to stress that there is no scientific evidence to date that dogs can contract BSE or any similar disease. In addition there is no evidence that dogs can transmit the disease to humans.

FDA notified the U.S. pet food firm, The Pet Pantry International, of Carson City, Nevada, when FDA learned that the pet food that the firm received may have included rendered material from the BSE positive cow. The manufacturer of the pet food is Champion Pet Food, Morinville, Alberta. Even though there is no known risk to dogs from eating this dog food, as a prudent measure to help assure that the U.S. stays BSE free The Pet Pantry International is asking its customers who may have purchased the suspect product to hold it for pickup by the distributor so that the dog food will not mistakenly be mixed into cattle or other feeds if any of the dog food is discarded or otherwise not used to feed dogs. The suspect dog food was produced by Champion Pet Food between February 4, 2003, and March 12, 2003.

The Pet Pantry products were packaged in 50 lb bags, distributed to franchises around the country, and sold by home delivery only. There was no retail distribution of the product. Consumers purchase Pet Pantry products by phone or email orders. The product is then delivered by the nearest franchisee directly to the consumer s home.

The product subject to this notification includes Maintenance Diet labeled with a use by date of 17FEB04 and Beef with Barley with a use by date of 05MAR04 . Consumers who have purchased dog food from The Pet Pantry since February of this year are asked to check their present supplies and see if any match the description of the product being removed. If so, consumers are asked to contact The Pet Pantry at 1-800-381-7387 for further information on how to return the product to The Pet Pantry for proper disposal. Consumers are asked not to destroy or discard the product themselves. The Pet Pantry will also use its sales records to contact consumers who purchased the affected product.

FDA is working closely with the Pet Pantry International to assure for proper disposal of the recovered product.

FDA will continue to provide updates on this case of BSE in Canada as additional information becomes available.

http://www.fda.gov/bbs/topics/NEWS/2003/NEW0910.html



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://collections.europarchive.org/tna/20080102174910/http://www.bseinquiry.gov.uk/files/ws/s324.pdf



cases have been reported in domestic cats), are characterised by long asymptomatic incubation periods followed by progressive symptoms and signs of degeneration of the brain, leading eventually to death.

http://www.bsereview.org.uk/download/draft_2.pdf

PET FOODS MAD CATS AND MAD DOGS BSE/TSEs

worse still, there is serious risk the media could get to hear of such a meeting...

snip...

Crushed heads (which inevitably involve brain and spinal cord material) are used to a limited extent but will also form one of the constituent raw materials of meat and bone meal, which is used extensively in pet food manufacturer...

http://collections.europarchive.org/tna/20080102163540/http://www.bseinquiry.gov.uk/files/yb/1989/03/17004001.pdf



2. The Parliamentary Secretary said that he was concerned about the possibility that countries in which BSE had not yet been detected could be exporting raw meat materials (in particular crushed heads) contaminated with the disease to the UK for use in petfood manufacture...

snip...

YOU explained that imported crushed heads were extensively used in the petfood industry...

http://collections.europarchive.org/tna/20080102154438/http://www.bseinquiry.gov.uk/files/yb/1989/04/14001001.pdf



In particular I do not believe one can say that the levels of the scrapie agent in pet food are so low that domestic animals are not exposed...

http://collections.europarchive.org/tna/20081105230259/http://www.bseinquiry.gov.uk/files/yb/1989/04/24003001.pdf



BSE IN PETFOOD

1. The Secretary asked on 19 April whether I was content with the advice in para 3 of the record of the meeting on 17 March with the Parliamentary Secretary (Mr Thompson). The simple answer is ''not entirely''.

2. On occasions, material obtained from slaughterhouses will be derived from sheep affected with scrapie or cattle that may be incubating BSE for use in petfood manufacture. Some of this material must be classified as high risk since it contains brain, spinal cord, spleen or lymphatic glands.

http://collections.europarchive.org/tna/20090505233052/http://www.bseinquiry.gov.uk/files/yb/1989/05/03007001.pdf



Meldrum's notes on pet foods and materials used

http://collections.europarchive.org/tna/20081105230323/http://www.bseinquiry.gov.uk/files/yb/1989/05/16001001.pdf



http://collections.europarchive.org/tna/20080102200123/http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf



IN CONFIDENCE CJD TO CATS...

It should be noted that under experimental conditions cats succumb to an encephalopathy after intracerebral inoculation of material derived from patients affected with Creutzfeldt-Jakob Disease.

http://collections.europarchive.org/tna/20080103005226/http://www.bseinquiry.gov.uk/files/yb/1989/05/18002001.pdf



Confidential BSE and __________________


3. I have thought very hard about whether the Branch should carry out a similar exercise with meat and meat products for human foods. On balance I do NOT think we should undertake it, but a final decision has not been taken and you may wish to discuss this further. ...

http://web.archive.org/web/20030509205351/http://www.bseinquiry.gov.uk/files/yb/1989/05/22012001.pdf



http://caninespongiformencephalopathy.blogspot.com/



Wednesday, January 19, 2011

EFSA BIOHAZ Scientific Opinion on the revision of the quantitative risk assessment (QRA) of the BSE risk posed by processed animal proteins (PAPs)

EFSA Journal 2011;9(1):1947

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-biohaz-scientific-opinion-on.html



Monday, January 17, 2011

MAD COW Update on Feed Enforcement Activities to Limit the Spread of BSE January 13, 2011

January 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/mad-cow-update-on-feed-enforcement.html



Friday, January 7, 2011

MEAT AND BONE MEAL AND MINERAL FEED ADDITIVES MAY INCREASE THE RISK OF ORAL PRION DISEASE TRANSMISSION

Journal of Toxicology and Environmental Health, Part A, 74:161–166, 2011 Copyright © Taylor & Francis Group, LLC ISSN: 1528-7394 print / 1087-2620 online DOI: 10.1080/15287394.2011.529066

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/meat-and-bone-meal-and-mineral-feed.html


Wednesday, December 29, 2010

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PRION END OF YEAR REPORT DECEMBER 29, 2010

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/transmissible-spongiform-encephalopathy.html


Wednesday, December 29, 2010

CWD Update 99 December 13, 2010

There are now two documented strains of CWD, and science is showing that indeed CWD could transmit to humans via transmission studies ;

PPo3-7
Prion Transmission from Cervids to Humans is Strain-dependent

Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA

Key words: CWD, strain, human transmission

Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.

Acknowledgement Supported by NINDS NS052319 and NIA AG14359.

PPo2-27
Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions

Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA

Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.

PPo2-7
Biochemical and Biophysical Characterization of Different CWD Isolates

Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany

Key words: CWD, strains, FT-IR, AFM

Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.

http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099



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



http://chronic-wasting-disease.blogspot.com/


P35

ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD

Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5

The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.

http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf



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



PRION 2010 Meeting Report International Prion Congress: From agent to disease; September 8 - 11, 2010; Salzburg, Austria Volume 4, Issue 3 July/August/September 2010

http://www.landesbioscience.com/journals/prion/article/12764/


http://chronic-wasting-disease.blogspot.com/2010/12/cwd-update-99-december-13-2010.html



Sunday, December 06, 2009

Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer

http://chronic-wasting-disease.blogspot.com/2009/12/detection-of-sub-clinical-cwd-infection.html



Thursday, December 25, 2008

Lions and Prions and Deer Demise

http://chronic-wasting-disease.blogspot.com/2008/12/lions-and-prions-and-deer-demise.html



Thursday, December 10, 2009

Chronic Wasting Disease (CWD) Susceptibility of Several North American Rodents That Are Sympatric with Cervid CWD Epidemics

http://chronic-wasting-disease.blogspot.com/2009/12/chronic-wasting-disease-cwd.html



Friday, December 11, 2009

CWD, FECES, ORAL LESIONS, Aerosol and intranasal transmission

http://chronic-wasting-disease.blogspot.com/2009/12/cwd-feces-oral-lesions-aerosol-and.html



AS THE CROW FLIES, SO DOES CWD

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



CWD, GAME FARMS, BAITING, AND POLITICS

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.html



Friday, February 20, 2009

Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2009/02/both-sides-of-fence-strategic-review-of.html



ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html



http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf


Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area Posted by Terry S. Singeltary Sr. on December 4, 2009 at 11:42am

65

Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area

Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author- tracy.a.nichols@aphis.usda.gov

Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Experimental and epidemiological data indicate that CWD can be transmitted horizontally and via blood and saliva, although the exact mode of natural transmission remains unknown. Substantial evidence suggests that prions can persist in the environment, implicating it as a potential prion reservoir and transmission vehicle. CWD- positive animals can contribute to environmental prion load via biological materials including saliva, blood, urine and feces, shedding several times their body weight in possibly infectious excreta in their lifetime, as well as through decomposing carcasses. Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions in spiked water samples at a 1:1 x106 , and protease-resistant prions in environmental and municipal-processing water samples from a CWD endemic area. Detection of CWD prions correlated with increased total organic carbon in water runoff from melting winter snowpack. These data suggest prolonged persistence and accumulation of prions in the environment that may promote CWD transmission.

snip...

The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.

snip...end...full text at ;

http://www.landesbioscience.com/


http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf


http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html


http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html



Wednesday, January 07, 2009

CWD to tighten taxidermy rules Hunters need to understand regulations

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-to-tighten-taxidermy-rules-hunters.html



CHRONIC WASTING DISEASE (CWD)

http://chronic-wasting-disease.blogspot.com/



Tuesday, January 18, 2011

Agent strain variation in human prion disease: insights from a molecular and pathological review of the National Institutes of Health series of experimentally transmitted disease

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html


Tuesday, December 14, 2010

Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010

http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html



strictly NOT private and confidential $$$

Saturday, January 22, 2011

Alzheimer's, Prion, and Neurological disease, and the misdiagnosis there of, a review 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/alzheimers-prion-and-neurological.html



14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

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

update October 2009

T. Singeltary

Bacliff, TX, USA

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

Methods
12 years independent research of available data

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

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

page 114 ;

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



To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2



Seven main threats for the future linked to prions

The NeuroPrion network has identified seven main threats for the future linked to prions.

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed. Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases....

http://www.neuroprion.org/en/np-neuroprion.html



Thursday, August 12, 2010

Seven main threats for the future linked to prions

http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html



http://prionpathy.blogspot.com/


Tuesday, November 02, 2010

BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992

http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html



Thursday, November 18, 2010

UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS

http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html



Wednesday, November 17, 2010

MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE

http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html



Tuesday, January 1, 2008

BSE OIE USDA

STATEMENT BY DR. RON DEHAVEN REGARDING OIE RISK RECOMMENDATION

March 9, 2007

http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html


2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html



Wednesday, December 22, 2010

Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease ?

http://usdameatexport.blogspot.com/2010/12/manitoba-veterinarian-has-been-fined.html



Saturday, December 18, 2010

OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html



Tuesday, December 14, 2010

(RIP MOM DOD hvCJD confirmed 12/14/97 13 year anniversary, i'm still here damn't and my promise to you is still alive.)

Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010

http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html



has everybody out there that had a loved one die from a TSE filled out a CJD Questiohnaire asking real questions pertaining to route and source of TSE agent ?



if not, why not ?


Friday, November 30, 2007



CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION


http://cjdquestionnaire.blogspot.com/



stupid is, as stupid does, and some times, you just can't fix stupid $$$


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518


----- Original Message -----

From:

To: "Terry S. Singeltary Sr."

Cc: ; ; ; ; ; ;

Sent: Friday, February 04, 2011 9:13 AM

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

Dear Mr. Singeltary,

Thank you for taking time to read our publication and provide comments. Your concern and your keen attention to the literature on prion diseases are evident and laudable. We share your passion to increase knowledge of chronic wasting disease and to work toward decreasing occurrence of the disease. Open exchange of ideas and viewpoints is what keeps science moving forward.

Best, Margaret Wild


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

Margaret A. Wild, DVM, PhD Chief Wildlife Veterinarian Biological Resource Management Division National Park Service 1201 Oak Ridge Dr., Suite 200 Fort Collins, CO 80525 Office: (970) 225-3593 Cell: (970) 214-2886 Fax: (970) 225-3585


----- Original Message -----

From: Dave Jessup

To: Terry S. Singeltary Sr.

Cc: jwdwda@; margaret_wild@ ; krose@ ; wda@ ; WildlifeDisease@ ; Jenny_Powers@ ; rcarleton@
Sent: Wednesday, January 26, 2011 9:41 AM

Subject: [Norton AntiSpam]Re: re-THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER

Dear Mr. Singeltary,

Thank you for your e-mail and extensive appended snipets from various studies and sources on prion diseases. It appears you have cc'd your e-mail to the senior author of the article in JWD you are concerned about, Dr. Margaret Wild. So, I will leave it to her to correspond with you if she feels that is appropriate.

I am not sure what you are asking the Wildlife Disease Association to do about your concerns. WDA publishes peer reviewd scientific articles in our quarterly Journal of Wildlife Diseases (articles like Dr. Wild's). We also feature a Letters category of articles. These are very distilled observations as opposed to original research, and limited to 1000 words. If you wanted to distill down you conerns about potential prion tranmsmissability to canids and people, you might have a basis for such a letter. They are not the "did too, did not" type of letters to the editor that we might find in a newspaper and instructions on how to prepare one can be found at "Instructions to Authors" on our website.

It also appears that you have cc'd your e-mail to our Editor, Dr. Jim Mills, so he should be aware of your concerns and be looking for such a Letter, if you decide to write one.

I'm sorry for your loss and the suffering of your mother with JCD.

Sincerely,

David A. Jesup WDA Executive Manager

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

Thursday, February 10, 2011

Chronic Wasting Disease Found In A White-Tailed Deer In Maryland

http://chronic-wasting-disease.blogspot.com/2011/02/chronic-wasting-disease-found-in-white.html


http://www.dnr.maryland.gov/wildlife/Hunt_Trap/deer/disease/cwdinformation.asp


CWD Maryland Emergency Response Plan 2011

http://www.dnr.maryland.gov/wildlife/pdfs/CWDResponsePlan2011.pdf


http://www.cwd-info.org/index.php/fuseaction/about.map


Thursday, February 10, 2011

CWD ILLINOIS UPDATE FEBRUARY 2011 Locations of CWD-Positive Deer - Updated 2/07/2011

http://chronic-wasting-disease.blogspot.com/2011/02/cwd-illinois-update-february-2011.html


Wednesday, February 09, 2011

CWD Minnesota deer feeding ban covering Dodge, Goodhue, Olmsted, and Wabasha counties will become effective Feb. 14, 2011

http://chronic-wasting-disease.blogspot.com/2011/02/cwd-minnesota-deer-feeding-ban-covering.html


Tuesday, January 25, 2011

Minnesota, National Veterinary Services Laboratory in Ames, Iowa, has confirmed CWD case near Pine Island

http://chronic-wasting-disease.blogspot.com/2011/01/minnesota-national-veterinary-services.html


Thursday, February 10, 2011

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31

http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html


Friday, February 04, 2011

NMLB and USDA allow scrapie prion infected mutton to enter food chain on the Navajo Reservation in New Mexico

http://scrapie-usa.blogspot.com/2011/02/nmlb-and-usda-allow-scrapie-prion.html


Friday, February 11, 2011

Creutzfeldt-Jakob disease (CJD) biannual update (2010/1) Emerging infections/CJD

http://creutzfeldt-jakob-disease.blogspot.com/2011/02/creutzfeldt-jakob-disease-cjd-biannual.html


http://chronic-wasting-disease.blogspot.com/


http://scrapie-usa.blogspot.com/


http://nor-98.blogspot.com/


http://bse-atypical.blogspot.com/


http://transmissiblespongiformencephalopathy.blogspot.com/


layperson



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