Thursday, January 15, 2015

41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE Prion: Case Report

http://creutzfeldt-jakob-disease.blogspot.com/2015/01/41-year-old-navy-commander-with.html

Subject: *** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type disease

what is CJD ? just ask USDA inc., and the OIE, they are still feeding the public and the media industry fed junk science that is 30 years old.

why doesn’t some of you try reading the facts, instead of rubber stamping everything the USDA inc says.

sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and there is much concern now for CWD and risk factor for humans.

My sincere condolences to the family and friends of the House Speaker Becky Lockhart. I am deeply saddened hear this.

with that said, with great respect, I must ask each and every one of you Politicians that are so deeply saddened to hear of this needless death of the Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am seriously going to ask you all this...I have been diplomatic for about 17 years and it has got no where. people are still dying. so, are you all stupid or what??? how many more need to die ??? how much is global trade of beef and other meat products that are not tested for the TSE prion disease, how much and how many bodies is this market worth?

Saturday, January 17, 2015

*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease

http://creutzfeldt-jakob-disease.blogspot.com/2015/01/becky-lockhart-46-utahs-first-female.html

*** Human Mad Cow Video

http://zoomify.uzh.ch:8080/zoomify/videos/video-009/video-009.html

*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video

http://zoomify.uzh.ch:8080/zoomify/videos/video-004/video-004.html

*** 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of

Neurological Disorders and Stroke, National Institutes of Health,

Bethesda, MD 20892.

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

PMID: 8006664 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query...p;dopt=Abstract

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

IATROGENIC TSE PRION

all iatrogenic cjd is, is sporadic CJD, until route and source of the iatrogenic event that took place, is detected, documented, placed in the academic domain as fact, and recorded, which happens very seldom due to a lot of factors, besides the incubation period, and that be mainly industry. kind of like asbestos and tobacco and the industry there from, they knew in the early 1900’s that they both were killing, and they both had long incubation, and somebody chose not to do anything about if for decades and decades. kind of like what we have here with the TSE prion disease. $$$

> In 12 of 15 hospitals with neurosurgical incidents, a decision was made to notify patients of their potential exposure.

SO, X number of patients, from 3 hospitals, where

''exposure to potentially CJD-contaminated instruments ''

took place on these patients, the final decision NOT to tell those folks about the potential exposure to the CJD TSE prion

insane, thus, the TSE prion agent continues to spread. ...please see further comments here ;

http://creutzfeldt-jakob-disease.blogspot.com/2013/11/management-of-neurosurgical-instruments.html

Tuesday, February 11, 2014

Novant Health Forsyth Medical Center Information on potential CJD exposure

http://creutzfeldt-jakob-disease.blogspot.com/2014/02/novant-health-forsyth-medical-center.html

Thursday, June 04, 2015

Catholic Medical Center v. Civil No. 14-cv-180-JL Opinion No. 2015 DNH 110 Fireman’s Fund Insurance Company Creutzfeldt Jakob Disease TSE Prion tainted medical instruments

UNITED STATES DISTRICT COURT DISTRICT OF NEW HAMPSHIRE

http://creutzfeldt-jakob-disease.blogspot.com/2015/06/catholic-medical-center-v-civil-no-14.html

Sunday, March 09, 2014

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES

http://creutzfeldt-jakob-disease.blogspot.com/2014/03/a-creutzfeldt-jakob-disease-cjd.html

Tuesday, March 11, 2014

Science and Technology Committee Oral evidence: Blood, tissue and organ screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD

Actually, it is nearer 2 per million per year of the population will develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about 1 in 30,000. So that has not really changed. When people talk about 1 per million, often they interpret that as thinking it is incredibly rare. They think they have a 1-in-a-million chance of developing this disease. You haven’t. You’ve got about a 1-in-30,000 chance of developing it.

http://creutzfeldt-jakob-disease.blogspot.com/2014/03/science-and-technology-committee-oral.html



terry

Let me translate, with sufficient forced amplification, one strain of the CWD prion can be forced to convert human prions. That conversion is most likely to occur in to individuals carrying one out of three possible gene variants. What can't be quantified is the possibility of that amplification occurring outside of a lab. There is no definitive evidence that CWD has crossed the species barrier but there are five cases were, it's unlikely to be the cause of vCJD, but it can't be completely ruled out.

Terry spare us the stories about Sporadic CJD it has a very different clinical presentation to vCJD or Mad Cow Disease. Let's confine the discussion to CWD or allied TSE diseases. On the larger scale all prion diseases are related, but the focus of this forum is hunting, lets stick with game animals and their relatives.

I, and I'm sure others, are interested in information pertaining to propabilites of human infection by CWD. If in the coming weeks we find out that deer test positive for CWD in multiple locations in Texas, then deciding whether or not to continue eating wild game meat will be on most hunters' minds. And, everyone should make informed decisions for themselves based on the current data available. I'm glad I read one of the articles Terry posted yesterday, because it has changed my perspective on things and made me ask more questions.

Describing the effects of CWD in the most infected deer population doesnt mean I'm ignoring other CWD locations. It just means I'm describing how bad it can get. I am aware that mule deer populations are declining in other areas as well, including areas where CWD is not prevalent. But, nowhere else are populations dropping as quickly as the South Converse Herd. And I don't think it is a coincidence that they have the highest rate of infection.

I'm not sure where you got 67 and 36 years. CWD was first identified there 48 years ago near the Colorado/ Wyoming border. That was when it was first identified and named.

CWD in Wisconsin is getting worse. Next month they are adding three more counties to the bait ban list due to increasing spread of CWD in those counties.

Here is an article I think I posted in the other thread yesterday. But I'll post it here too because I think it gives a good overview of the situation.
https://www.hcn.org/blogs/goat/chronic-wasting-disease-forgotten-but-not-gone

I ment to write 48, 67 was the year.

Regardless if it truly was epidemic we would already be wiped out in Wyoming and especially CO. That's hasn't happened. Drought and winter kills have been much more effective in limiting recruitment then CWD.

I didn't say anything about not linking to information about CWD or vCJD linked to meat. I was referring to Sporadic CJD that has a different clinical presentation. I'm just trying to keep things reasonably on topic not all prion diseases are transmitted through meat.

Informed decisions? This info you lab guys keep posting is suppose to give me an informed decision to make based on people splicing human genes in mice and forcing prions into them? With this type of decision making logic you shouldn't be eating any processed food or meat from the grocery store. Is that the way you guys roll?

we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease

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

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

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

TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS

http://www.mad-cow.org/00/aug00_late_news.html#ggg

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.

snip...

http://web.archive.org/web/20060307063542/http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf



terry


p.s.


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

OR-09: Canine spongiform encephalopathy—A new form of animal prion disease

Monique David, Mourad Tayebi UT Health; Houston, TX USA

It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8 Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.

Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.

In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.

If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).

References 1. Colchester AC, Colchester NT. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61; PMID:16139661; http:// dx.doi.org/10.1016/S0140-6736(05)67218-2.

2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal. ppat.1000156.

3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/ hmg/6.10.1699.

4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.

5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.

6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu (Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.

7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317- 75-11-2947.

8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.

9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30; PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.

http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf

Monday, March 26, 2012

CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE

http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html

Monday, March 8, 2010

Canine Spongiform Encephalopathy aka MAD DOG DISEASE

http://caninespongiformencephalopathy.blogspot.com/


terry

I agree. But, the folks who want to ban high fences are going to do their best to tie CWD to "pens" regardless of how big. Everyone with an agenda will use it for their personal favorite, we've already seen it tied to Alzheimer's and sage grouse etc.

All logic is tossed out when a good crisis presents itself.

By comparing the amount of PK-resistant prion protein in the two substrates, an assessment of the host’s species barrier can be made. We show that the CER assay correctly predicts known prion species barriers of laboratory mice and, as an example, show some preliminary results suggesting that bobcats (Lynx rufus) may be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting disease agent.

http://www.jove.com/video/52522/assessing-transmissible-spongiform-encephalopathy-species-barriers


>>> show some preliminary results suggesting that bobcats (Lynx rufus) may be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting disease agent.


AD.63: Susceptibility of domestic cats to chronic wasting disease

Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1

1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA

Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD. These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.

http://www.prion2013.ca/tiny_uploads/forms/Scientific-Program.pdf

www.landesbioscience.com

PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)

http://www.landesbioscience.com/journals/prion/04-Prion6-2-Pathogenesis-and-pathology.pdf

http://chronic-wasting-disease.blogspot.com/2012/05/chronic-wasting-disease-cwd-prion2012.html

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

http://felinespongiformencephalopathyfse...ats-to-cwd.html

PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)

http://www.landesbioscience.com/journals/prion/04-Prion6-2-Pathogenesis-and-pathology.pdf

http://chronic-wasting-disease.blogspot.com/2012/05/chronic-wasting-disease-cwd-prion2012.html

Thursday, May 31, 2012

CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more

http://chronic-wasting-disease.blogspot.com/2012/05/chronic-wasting-disease-cwd-prion2012.html

Monday, August 8, 2011

Susceptibility of Domestic Cats to CWD Infection

http://felinespongiformencephalopathyfse...ats-to-cwd.html

Sunday, August 25, 2013

Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission

http://chronic-wasting-disease.blogspot.com/2013/08/prion2013-chronic-wasting-disease-cwd.html

Feline Spongiform Encephalopathy (FSE) FSE was first identified in the UK in 1990. Most cases have been reported in the UK, 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 vCJD 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.

References: Leggett, M.M. et al.(1990) A spongiform encephalopathy in a cat. Veterinary Record. 127. 586-588

Synge, B.A. et al. (1991) Spongiform encephalopathy in a Scottish cat. Veterinary Record. 129. 320

Wyatt, J. M. et al. (1991) Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.

Gruffydd-Jones, T. J.et al.. (1991) Feline spongiform encephalopathy. J. Small Animal Practice. 33. 471-476.

Pearson, G. R. et al. (1992) Feline spongiform encephalopathy: fibril and PrP studies. Veterinary Record. 131. 307-310.

Willoughby, K. et al. (1992) Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record. 131. 431-434.

Fraser, H. et al. (1994) Transmission of feline spongiform encephalopathy to mice. Veterinary Record 134. 449.

Bratberg, B. et al. (1995) Feline spongiform encephalopathy in a cat in Norway. Veterinary Record 136. 444

Baron, T. et al. (1997) Spongiform encephalopathy in an imported cheetah in France. Veterinary Record 141. 270-271

Zanusso, G et al. (1998) Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy. Lancet, V352, N9134, OCT 3, Pp 1116-1117.

Ryder, S.J. et al. (2001) Inconsistent detection of PrP in extraneural tissues of cats with feline spongiform encephalopathy. Veterinary Record 146. 437-441

Kelly, D.F. et al. (2005) Neuropathological findings in cats with clinically suspect but histologically unconfirmed feline spongiform encephalopathy. Veterinary Record 156. 472-477.

http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bse/othertses/index.htm#fse

3 further cheetah cases have occured, plus 1 lion, plus all the primates, and 20 additional house cats. Nothing has been published on any of these UK cases either. One supposes the problem here with publishing is that many unpublished cases were _born_ long after the feed "ban". Caught between a rock and a hard place: leaky ban or horizontal transmission (or both).

http://www.mad-cow.org/may99_zoo_news.html

http://www.mad-cow.org/00/aug00_late_news.html#ggg

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

http://web.archive.org/web/20060303042720/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://web.archive.org/web/20040301231838/http://www.bseinquiry.gov.uk/files/yb/1989/04/24003001.pdf

http://web.archive.org/web/20060303042732/http://www.bseinquiry.gov.uk/files/yb/1989/04/25001001.pdf

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

http://web.archive.org/web/20060303042739/http://www.bseinquiry.gov.uk/files/yb/1989/05/03007001.pdf

*** Meldrum's notes on pet foods and materials used

http://web.archive.org/web/20060303042745/http://www.bseinquiry.gov.uk/files/yb/1989/05/16001001.pdf

*** BSE & Pedigree Petfoods ***

http://web.archive.org/web/20060303042725/http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf



terry

Sunday, June 14, 2015

Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion

http://madcowusda.blogspot.com/2015/06/larrys-custom-meats-inc-recalls-beef.html



terry


terry

I have a better idea. Why don't you and terry start a CJD thread and let this thread stay on topic? Evidently most of us here aren't influenced much by scare tactics, and are much more interested in the facts as they pertain to CWD.... You know, the original subject of this thread?

Go tell someone else somewhere else that the sky is falling.

Thursday, June 25, 2015

Wisconsin CWD-positive white-tailed deer found on Eau Claire County farm

http://chronic-wasting-disease.blogspot.com/2015/06/wisconsin-cwd-positive-white-tailed.html


Wednesday, March 04, 2015

*** Disease sampling results provide current snapshot of CWD in Wisconsin finding 324 positive detections statewide in 2014

http://chronic-wasting-disease.blogspot.com/2015/03/disease-sampling-results-provide.html


Tuesday, October 07, 2014

*** Wisconsin white-tailed deer tested positive for CWD on a Richland County breeding farm, and a case of CWD has been discovered on a Marathon County hunting preserve

http://chronic-wasting-disease.blogspot.com/2014/10/wisconsin-white-tailed-deer-tested.html


see;

‘’It is interesting to note that, in 2001, the State of Texas shifted its deer management strategies toward the same leanings that Kroll has suggested for Wisconsin. In Texas, the change was brought about via heavy lobbying from the high-fence deer ranching industry. This pressure helped convince the Texas Parks and Wildlife to change their regulations and allow private landowners to select the own deer biologists.’’

nothing like the wolf guarding the henhouse.

Texas just documented another case of CWD, I wonder what the Wisconsin’s Deer Czar (from TEXAS), seems Dr. Dough’s passive approach on CWD is not working out too well.

yep, while the Texas deer czar dr. dough was off to Wisconsin pushing the privately owned shooting pen industry (livestock cervid industry), Texas fell to CWD, and have now documented 7 cases of CWD to date.

IF Texas would test for CWD in the captive industry aggressively, I think we would all be shocked as to what they would find.

for your information...

According to Wisconsin’s White-Tailed Deer Trustee Dr. James Kroll, people who call for more public hunting opportunities are “pining for socialism.” He further states, “(Public) Game management is the last bastion of communism.”

“Game Management,” says James Kroll, driving to his high-fenced, two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.” Kroll, also known as Dr. Deer, is the director of the Forestry Resources Institute of Texas at Stephen F. Austin State University, and the “management” he is referring to is the sort practiced by the State of Texas. The 55-year-old Kroll is the leading light in the field of private deer management as a means to add value to the land. His belief is so absolute that some detractors refer to him as Dr. Dough, implying that his eye is on the bottom line more than on the natural world.

Kroll, who has been the foremost proponent of deer ranching in Texas for more than thirty years, doesn’t mind the controversy and certainly doesn’t fade in the heat. People who call for more public lands are “cocktail conservationists,” he says, who are really pining for socialism. He calls national parks “wildlife ghettos” and flatly accuses the government of gross mismanagement. He argues that his relatively tiny acreage, marked by eight-foot fences and posted signs warning off would-be poachers, is a better model for keeping what’s natural natural while making money off the land.

Dr. Deer Wisconsin Report: Will High-Fence Bias Skew Final Plan?

Categories: Blogs, Daniel Schmidt's Whitetail Wisdom, Deer News, Featured Tags: antler restricitons, dan schmidt, Dr. Deer, james kroll, James Kroll Wisconsin, qdm, quality deer management, texas hunting, wisconsin deer hunting March 29, 2012 According to Wisconsin’s White-Tailed Deer Trustee Dr. James Kroll, people who call for more public hunting opportunities are “pining for socialism.” He further states, “(Public) Game management is the last bastion of communism.”

OPINION BLOG

These are just two insights into the man who has been asked to provide analysis and recommended changes to Wisconsin’s deer management program. Kroll’s insights are from an article entitled “Which Side of the Fence Are You On?” by Joe Nick Patoski for a past edition of Texas Monthly. If nothing more, the article gives an unabashed look into the mind-set that will be providing the Wisconsin DNR with recommendations on how to change their deer management practices. James Kroll (also known as “Deer Dr.”) was appointed to the Wisconsin “deer czar” position last fall. He was hired by the Department of Administration and instructed to complete a review of the state’s deer management program.

Here’s a sample of the article:

“Game Management,” says James Kroll, driving to his high-fenced, two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.” Kroll, also known as Dr. Deer, is the director of the Forestry Resources Institute of Texas at Stephen F. Austin State University, and the “management” he is referring to is the sort practiced by the State of Texas. The 55-year-old Kroll is the leading light in the field of private deer management as a means to add value to the land. His belief is so absolute that some detractors refer to him as Dr. Dough, implying that his eye is on the bottom line more than on the natural world.

Kroll, who has been the foremost proponent of deer ranching in Texas for more than thirty years, doesn’t mind the controversy and certainly doesn’t fade in the heat. People who call for more public lands are “cocktail conservationists,” he says, who are really pining for socialism. He calls national parks “wildlife ghettos” and flatly accuses the government of gross mismanagement. He argues that his relatively tiny acreage, marked by eight-foot fences and posted signs warning off would-be poachers, is a better model for keeping what’s natural natural while making money off the land.

A trip to South Africa six years ago convinced Kroll that he was on the right track. There he encountered areas of primitive, lush wildlife-rich habitats called game ranches. They were privately owned, privately managed, and enclosed by high fences. He noticed how most of the land outside those fences had been grazed to the nub, used up. “Game ranches there derive their income from these animals — viewing them, hunting them, selling their meat,” he says. “There are no losers.” At his own ranch Kroll has set up a smaller version of the same thing. His land is indeed lush, verdant, with pine groves, an abundance of undergrowth, wild orchids, New Jersey tea, jack-in-the-pulpits, and other native plants. He has also set up a full-scale breeding research center and is one of twenty Texas deer breeders using artificial insemination to improve his herd. “We balance sex and age ratio,” he says. “We manage habitat. We control the population and manage for hunting. I want to leave the deer herd better than it was before we came.”

It is interesting to note that, in 2001, the State of Texas shifted its deer management strategies toward the same leanings that Kroll has suggested for Wisconsin. In Texas, the change was brought about via heavy lobbying from the high-fence deer ranching industry. This pressure helped convince the Texas Parks and Wildlife to change their regulations and allow private landowners to select the own deer biologists.

“That has given landowners more freedom,” Kroll told Texas Monthly. “(However,) You still have to let the state on your land to get a wildlife-management permit.” The key difference here is that 98 percent of Texas is comprised of private land. Wisconsin, on the other hand, consists of approximately 34.8 million acres of land, and 25.5 percent of the state’s 638,000 gun-hunters reported hunting on public land at some point during the season (2010, Duey, Rees).

According to the Wisconsin Realtors Association, more than 5.7 million acres of this land, or 16.5 percent, is publicly owned and used for parks, forests, trails, and natural resource protection. [Note: these statistics do not include the public land used for roads, government buildings, military bases, and college/school campuses.] This 5.7 million acres of public land is owned as follows:

Federal government owns approximately 1.5 million acres (4.4 percent of the state’s land area). Almost all of the federal forestland in Wisconsin is located in Chequamegon-Nicolet National Forest.

State government owns approximately 1.6 million acres (4.6 percent of the state’s land area). The land is managed by two agencies, the Board of Commissioners of Public Land (who manages lands granted by federal government) and the DNR (managing land owned by the state).

County government owns approximately 2.6 million acres (7.5 percent of the state’s land area).

Public land is located in 71 of Wisconsin’s 72 counties, with the most public land located in Bayfield County (464,673 acres). [Note: Menominee County does not have any public land, but 98 percent of the land is held in trust by the Menominee Tribe.] Twenty counties have more than 100,000 acres of public land, while only 12 counties have fewer than 10,000 acres.

What does this all mean? My initial reaction, which is one that I predicted when Kroll was named to the state’s deer trustee position, is that his team’s final recommendations — if implemented — will be heavily skewed toward the state’s larger landowners (500+ acres) and folks who own small parcels in areas comprised mostly of private land.

It is also my prediction that the final recommendations (again, if implemented) will do little, if anything, to improve deer herds and deer hunting on Wisconsin’s 5.7 million acres of public land.

Where does this leave the public-land hunter? “It will suck to be you,” said one deer manager who asked to remain anonymous out of fear for his job. “The resources and efforts will go toward improving the private land sector. This is all about turning deer hunting away from the Public Land Doctrine and more toward a European-style of management — like they have in Texas.”

I do, of course, hope these assumptions are wrong. As with all things in life, we should maintain an open mind to change. Life is all about change. However, change for the sake of change is usually a recipe for disaster. Especially when that change is driven by something more than a sincere desire to manage public resources for the greater good.

As noted yesterday (Dr. James Kroll Report: Is That All You Get For Your Money), I will provide more of my opinions and interpretation on this important issue in forthcoming installments of this blog. Read his full preliminary report here.

http://www.texasmonthly.com/story/which-side-fence-are-you

http://www.texasmonthly.com/preview/2002-02-01/feature5

http://www.deeranddeerhunting.com/deer-n...skew-final-plan

snip...see full text ;

Thursday, March 29, 2012

TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT CALLING KETTLE BLACK

http://chronic-wasting-disease.blogspot.com/2012/03/texas-deer-czar-says-wisconsin-dnr-not.html

Friday, June 01, 2012

*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS

http://chronic-wasting-disease.blogspot.com/2012/06/texas-deer-czar-to-wisconsin-ask-to.html

Tuesday, July 10, 2012

Dr. James C. Kroll Texas deer czar final report on Wisconsin

http://chronic-wasting-disease.blogspot.com/2012/07/dr-james-c-kroll-texas-deer-czar-final.html

Wednesday, March 18, 2015

Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015

http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-confirmed.html

Wednesday, March 25, 2015

Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015

http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-cases.html



UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;

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

From: David Colby To: flounder9@verizon.net

Cc: stanley@XXXXXXXX

Sent: Tuesday, March 01, 2011 8:25 AM

Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

Dear Terry Singeltary,

Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor Department of Chemical Engineering University of Delaware

===========END...TSS==============

Thursday, July 03, 2014

How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets?

http://chronic-wasting-disease.blogspot.com/2014/07/how-chronic-wasting-disease-is.html



PRION CONFERENCE 2014 HELD IN ITALY RECENTLY CWD BSE TSE UPDATE

> First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)

PRION 2014 - PRIONS: EPIGENETICS and NEURODEGENERATIVE DISEASES – Shaping up the future of prion research

Animal TSE Workshop 10.40 – 11.05 Talk Dr. L. Cervenakova First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)

http://www.prion2014.org/images/Animal_TSE_workshop.pdf

P.126: Successful transmission of chronic wasting disease (CWD) into mice over-expressing bovine prion protein (TgSB3985)

Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1 1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA

Keywords: chronic wasting disease, transmission, transgenic mouse, bovine prion protein

Background. CWD is a disease affecting wild and farmraised cervids in North America. Epidemiological studies provide no evidence of CWD transmission to humans. Multiple attempts have failed to infect transgenic mice expressing human PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal human PrPC in vitro provides additional evidence that transmission of CWD to humans cannot be easily achieved. However, a concern about the risk of CWD transmission to humans still exists. This study aimed to establish and characterize an experimental model of CWD in TgSB3985 mice with the following attempt of transmission to TgHu mice.

Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse (CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD) or elk (CWD/Elk). Animals were observed for clinical signs of neurological disease and were euthanized when moribund. Brains and spleens were removed from all mice for PrPCWD detection by Western blotting (WB). A histological analysis of brains from selected animals was performed: brains were scored for the severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain regions.

Results. Clinical presentation was consistent with TSE. More than 90% of TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres in the brain but only mice in the latter group carried PrPCWD in their spleens. We found evidence for co-existence or divergence of two CWD/ Tga20 strains based on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen by WB. However, on neuropathological examination we found presence of amyloid plaques that stained positive for PrPCWD in three CWD/WTD- and two CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and CWD/Elkinfected mice were similar but unique as compared to profiles of BSE, BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM mice tested positive for PrPCWD by WB or by immunohistochemical detection.

Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.

PRION 2014 CONFERENCE

CHRONIC WASTING DISEASE CWD

A FEW FINDINGS ;

Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.

We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.

The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.

Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.

Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.

Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.

Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.

P.28: Modeling prion species barriers and the new host effect using RT-QuIC

Kristen A Davenport, Davin M Henderson, Candace K Mathiason, and Edward A Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious.

Studies of the effects of primary or tertiary prion protein www.landesbioscience.com Prion 37 structures on trans-species prion transmission have relied upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect.

As an alternative strategy, we are using real-time quaking-induced conversion (RT-QuIC) to investigate the propensity for and the kinetics of trans-species prion conversion. RT-QuIC has the advantage of providing more defined conditions of seeded conversion to study the specific role of native PrP:PrPRES interactions as a component of the species barrier.

We are comparing chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions by seeding each prion into its native host recPrP (full-length bovine recPrP, or white tail deer recPrP) vs. into the heterologous species.

Upon establishing the characteristics of intra-species and inter-species prion seeding for CWD and BSE prions, we will evaluate the seeding kinetics and cross-species seeding efficiencies of BSE and CWD passaged into a common new host—feline—shown to be a permissive host for both CWD and BSE.

*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.

https://www.landesbioscience.com/journal...d%20Biology.pdf

Chronic Wasting Disease Susceptibility of Four North American Rodents

Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu

We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.

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


please see ;

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


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


terry

Kristen A Davenport, Davin M Henderson, Candace K Mathiason, and Edward A Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious.

Studies of the effects of primary or tertiary prion protein www.landesbioscience.com Prion 37 structures on trans-species prion transmission have relied upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect.

As an alternative strategy, we are using real-time quaking-induced conversion (RT-QuIC) to investigate the propensity for and the kinetics of trans-species prion conversion. RT-QuIC has the advantage of providing more defined conditions of seeded conversion to study the specific role of native PrP:PrPRES interactions as a component of the species barrier.

We are comparing chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions by seeding each prion into its native host recPrP (full-length bovine recPrP, or white tail deer recPrP) vs. into the heterologous species.

Upon establishing the characteristics of intra-species and inter-species prion seeding for CWD and BSE prions, we will evaluate the seeding kinetics and cross-species seeding efficiencies of BSE and CWD passaged into a common new host—feline—shown to be a permissive host for both CWD and BSE.

*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.

I assume this is an ongoing study. It's an important one because it seeks to replicate the process that produced vCJD and is the potential path for CWD to breach the species barrier. It should help quantify the real danger of CWD crossing the trans species barrier.

In one ear and out the other

Folks, just because pathogens share similar transmission vectors does not mean that the pathogen is going to somehow jump species barriers that are in place.

Canine distemper and the flu's have been around for centuries. Flu's effect people as well as canines. But we don't get distemper.

Now, can someone in a lab conjure up some gene combination that would never occur in nature to provide a means of trans specie transmission? Maybe.

But that's not what this thread was supposed to be about.

x2

Wouldn't properly cooking your venison take care of this problem? If you think about it for half a second, there's no telling what hunters have ingested over the years from wild game. I'll take my chances still.

No, it's someone like 900 degrees for 4hours... But is it actually a problem

Looks like this topic has lost its steam.

It's just the lull before the storm. TPWD is designing a strategy that (if rumors are true) will include not only killing all deer in the pen the buck came from, but all pens on the ranch. Even though they are separated by a 30' alley and have never co-mingled. After that, they do have designs on going after all ranches that have had transfers of breeder deer from that ranch (47 is the last number I've heard). Not stocker deer from what I hear, but deer that were put into pens for breeding in licensed breeding facilities.

Also, it's rumored (two different sources) that they have told the landowner that not only can he not take pictures or video the slaughter, but that he can't even be on his own ranch during the slaughter.

I hope that the last rumor above isn't true. For the state's sake. I can assure you it will cost the state more than it can imagine if they try that.

Thank God we've got all the irrelevant links out of the way. Hopefully we can focus on what the test results are from the deer, and use this thread to share relevant information about how the state proceeds.

I'd be working on a federal injunction ASAP. That's some BS. I've heard similar. Something don't smell right and it ain't on the private land owner this time.

I have heard the same about the owner. Also some other things that are very disturbing if true.

CWD in Texas now.......thanks a lot Obama