Saturday, December 05, 2015

CWD Prions Remain Infectious after Passage Through the Digestive System of Coyotes (Canis latrans)

CWD Prions Remain Infectious after Passage Through the Digestive System of Coyotes (Canis latrans)

 

DOI:10.1080/19336896.2015.1086061 Tracy A. Nicholsa*, Justin W. Fischera, Terry R. Sprakerbc, Qingzhong Kongd & Kurt C. VerCauterena

 

Publishing models and article dates explained

 

Received: 7 Jul 2015 Accepted: 18 Aug 2015 Accepted author version posted online: 04 Dec 2015

 

Abstract

 

Chronic wasting disease (CWD) is a geographically expanding prion disease of wild and captive cervids in North America. Disease can be transmitted directly, animal to animal, or indirectly via the environment. CWD contamination can occur residually in the environment via soil, water, and forage following deposition of bodily fluids such as urine, saliva, and feces, or by the decomposition of carcasses. Recent work has indicated that plants may even take up prions into the stems and leaves. When a carcass or gut pile is present in the environment, a large number of avian and mammalian species visit and consume the carrion. Additionally, predators like coyotes, likely select for disease-compromised cervids. Natural cross-species CWD transmission has not been documented, however, passage of infectious prion material has been observed in the feces of crows. In this study we evaluated the ability of CWD-infected brain material to pass through the gastrointestinal tract of coyotes (Canis latrans) following oral ingestion, and be infectious in a cervidized transgenic mouse model. Results from this study indicate that coyotes can pass infectious prions via their feces for at least three days post ingestion, demonstrating that mammalian scavengers could contribute to the translocation and contamination of CWD in the environment.

 


 

Greetings,

 

disturbing to say the least. even if this species Coyotes (Canis latrans) is or is not susceptible to CWD TSE Prion, the cwd prion remains infectious after passage through the digestive system.

 

I remember the late Dr. Joe Gibbs telling me this and being very concerned with the chicken and the survival of the TSE prion to the digestive system with the chicken, and the concerns of further spreading in chicken liter and such from feces.

 

so what does that tell us.

 

besides risk of spreading the cwd tse prion through salvia, feces, urine, environmental contamination, if these animals were rendered for feed they could spread the cwd tse prion agent that way as well.

 

there is science showing the canine is susceptible to the TSE Prion.

 

By the lay public only having access to Prion Journal from these short abstracts now, it is difficult to discuss, debate, and decipher the full threat of these TSE Prion disease, therefore making it very difficult for the lay public to comment on such important policy making. therefore, only the Government, corporate interest, and lobbyist there from, have all the data when ask to comment on such issues, but the lay public does not have such access. rather a stacked deck if you ask me. sure would be nice for open access for the lay public. just my opinion, from a lay person.

 

so I will have to be brief.

 

I have been worried about the canine species with regards to the TSE BSE mad cow type disease and the spreading there from by the canine species, with feed being a concern, amongst other things.

 

cwd is spreading, and states are now falling to cwd faster than I can keep up with them. this is getting nasty to say the least, and in my opinion, North America is oblivious to the true incident of the BSE TSE in the bovine, the CWD in Cervid, and or Scrapie in sheep and goat, and I am not even sure if they test mink for TME anymore, and then you have the atypicals there from. the TSE prion surveillance in the USA and all of North America, feed ban, testing, srm removals, all tragic failures or monumental blunders in my opinion, if you look at the history of the facts.

 

IT is paramount that we include all animal species in animal feed with regards to the feed ban. this voluntary ban with regards to cwd for cervid is absolutely insane, is and has been an accident waiting to happen, and needs to be addressed asap.

 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all feed containing animal parts be banned to all livestock food producing animals for human and animal consumption, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.

 

***However, this recommendation is guidance and not a requirement by law.

 

======

 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

31 Jan 2015 at 20:14 GMT

 


 

Saturday, January 31, 2015

 

European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route

 


 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

Singeltary et al

 

31 Jan 2015 at 20:14 GMT

 


 

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

 

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

 

Date: Fri, 16 May 2003 11:47:37 –0500

 

From: "Terry S. Singeltary Sr." To: fdadockets@oc.fda.gov

 

Greetings FDA,

 

i would kindly like to comment on;

 

Docket 03D-0186

 

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

 


 

*** see what DEFRA replied to me with in regards to the HOUND STUDY long ago ;

 

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

 


 

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, identify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.

 


 

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

 


 

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...

 


 

76 pages on hound study;

 

snip...

 


 

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).

 


 

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...

 


 

NEW URL ;

 


 

Friday, March 8, 2013

 

Dogs may have been used to make Petfood and animal feed

 


 

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.

 


 

Monday, March 26, 2012

 

CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE

 


 

2013

 

Strain characteristics of the in vitro-adapted rabbit and dog BSE agent remained invariable with respect to the original cattle BSE prion, suggesting that the naturally low susceptibility of rabbits and dogs to prion infections should not alter their zoonotic potential if these animals became infected with BSE.

 

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

 

Neurobiology of Disease

 

Bovine Spongiform Encephalopathy Induces Misfolding of Alleged Prion-Resistant Species Cellular Prion Protein without Altering Its Pathobiological Features

 

Enric Vidal3, Natalia Fernández-Borges1, Belén Pintado4, Montserrat Ordóñez3, Mercedes Márquez6, Dolors Fondevila5,6, Juan María Torres7, Martí Pumarola5,6, and Joaquín Castilla1,2 + Author Affiliations

 

1CIC bioGUNE, 48160 Derio, Bizkaia, Spain,

 

2IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Bizkaia, Spain,

 

3Centre de Recerca en Sanitat Animal, Campus de la Universitat Autònoma de Barcelona (UAB)-IRTA, 08193 Bellaterra, Barcelona, Spain,

 

4Centro Nacional de Biotecnología, Campus de Cantoblanco, 28049 Cantoblanco, Madrid, Spain,

 

5Department of Animal Medicine and Surgery, Veterinary Faculty, UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain,

 

6Murine Pathology Unit, Centre de Biotecnologia Animal i Teràpia Gènica, UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain, and

 

7Centro de Investigación en Sanidad Animal-Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, 28130 Valdeolmos, Madrid, Spain

 

Author contributions: E.V., N.F.-B., and J.C. designed research; E.V., N.F.-B., B.P., M.O., M.M., D.F., and J.C. performed research; E.V., N.F.-B., B.P., and J.C. contributed unpublished reagents/analytic tools; E.V., N.F.-B., B.P., M.O., M.M., D.F., J.M.T., M.P., and J.C. analyzed data; E.V. and J.C. wrote the paper.

 

Abstract

 

Bovine spongiform encephalopathy (BSE) prions were responsible for an unforeseen epizootic in cattle which had a vast social, economic, and public health impact. This was primarily because BSE prions were found to be transmissible to humans. Other species were also susceptible to BSE either by natural infection (e.g., felids, caprids) or in experimental settings (e.g., sheep, mice). However, certain species closely related to humans, such as canids and leporids, were apparently resistant to BSE. In vitro prion amplification techniques (saPMCA) were used to successfully misfold the cellular prion protein (PrPc) of these allegedly resistant species into a BSE-type prion protein. The biochemical and biological properties of the new prions generated in vitro after seeding rabbit and dog brain homogenates with classical BSE were studied. Pathobiological features of the resultant prion strains were determined after their inoculation into transgenic mice expressing bovine and human PrPC. Strain characteristics of the in vitro-adapted rabbit and dog BSE agent remained invariable with respect to the original cattle BSE prion, suggesting that the naturally low susceptibility of rabbits and dogs to prion infections should not alter their zoonotic potential if these animals became infected with BSE. This study provides a sound basis for risk assessment regarding prion diseases in purportedly resistant species.

 

Received January 18, 2013. Revision received March 7, 2013. Accepted March 23, 2013. Copyright © 2013 the authors 0270-6474/13/337778-09$15.00/0

 


 

Monday, March 8, 2010

 

Canine Spongiform Encephalopathy aka MAD DOG DISEASE

 


 

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.

 


 

 

Friday, April 17, 2015

 

Assessing Transmissible Spongiform Encephalopathy Species Barriers with an In Vitro Prion Protein Conversion Assay

 

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

 


 

 

Veterinary Pathology Onlinevet.sagepub.com Published online before print February 27, 2014, doi: 10.1177/0300985814524798 Veterinary Pathology February 27, 2014 0300985814524798

 

Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats

 

D. M. Seelig1⇑ A. V. Nalls1 M. Flasik2 V. Frank1 S. Eaton2 C. K. Mathiason1 E. A. Hoover1 1Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA 2Department of Biomedical Sciences, Colorado State University, Fort Collins, CO, USA D. M. Seelig, University of Minnesota, Department of Veterinary Clinical Sciences, Room 339 VetMedCtrS, 6192A (Campus Delivery Code), 1352 Boyd Ave, St Paul, MN 55108, USA. Email address: dseelig@umn.edu

 

Abstract

 

Chronic wasting disease (CWD) is an efficiently transmitted, fatal, and progressive prion disease of cervids with an as yet to be fully clarified host range. While outbred domestic cats (Felis catus) have recently been shown to be susceptible to experimental CWD infection, the neuropathologic features of the infection are lacking. Such information is vital to provide diagnostic power in the event of natural interspecies transmission and insights into host and strain interactions in interspecies prion infection. Using light microscopy and immunohistochemistry, we detail the topographic pattern of neural spongiosis (the “lesion profile”) and the distribution of misfolded prion protein in the primary and secondary passage of feline CWD (FelCWD). We also evaluated cellular and subcellular associations between misfolded prion protein (PrPD) and central nervous system neurons and glial cell populations. From these studies, we (1) describe the novel neuropathologic profile of FelCWD, which is distinct from either cervid CWD or feline spongiform encephalopathy (FSE), and (2) provide evidence of serial passage-associated interspecies prion adaptation. In addition, we demonstrate through confocal analysis the successful co-localization of PrPD with neurons, astrocytes, microglia, lysosomes, and synaptophysin, which, in part, implicates each of these in the neuropathology of FelCWD. In conclusion, this work illustrates the simultaneous role of both host and strain in the development of a unique FelCWD neuropathologic profile and that such a profile can be used to discriminate between FelCWD and FSE.

 

prion chronic wasting disease immunohistochemistry interspecies cat feline spongiform encephalopathy transmissible spongiform encephalopathy adaptation species barrier

 


 

Monday, August 8, 2011 Susceptibility of Domestic Cats to CWD Infection

 

Oral.29: Susceptibility of Domestic Cats to CWD Infection

 

Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†

 

Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu

 

Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness.

 

*** Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.

 


 


 

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.

 


 

www.landesbioscience.com

 

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

 


 


 

FELINE SPONGIFORM ENCEPHALOPATHY FSE

 


 


 

A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY

 


 

4.21 Three cases of SE’s with an unknown infectious agent have been reported in ostriches (Struthio Camellus) in two zoos in north west Germany (Schoon @ Brunckhorst, 1999, Verh ber Erkeg Zootiere 33:309-314). These birds showed protracted central nervous symptoms with ataxia, disturbances of balance and uncoordinated feeding behaviour. The diet of these birds had included poultry meat meal, some of which came from cattle emergency slaughter cases.

 


 

SE1806

 

TRANSMISSION STUDIES OF BSE TO DOMESTIC FOWL BY ORAL EXPOSURE TO BRAIN HOMOGENATE

 

1 challenged cock bird was necropsied (41 months p.i.) following a period of ataxia, tremor, limb abduction and other neurological signs. Histopathological examination failed to reveal any significant lesions of the central or peripheral nervous systems...

 

1 other challenged cock bird is also showing ataxia (43 months p.i.).

 

snip...

 

94/01.19/7.1

 


 

A notification of Spongiform Encephalopathy was introduced in October 1996 in respect of ungulates, poultry and any other animal.

 

4.23 MAFF have carried out their own transmission experiments with hens. In these experiments, some of the chickens exposed to the BSE agent showed neurological symptoms. However MAFF have not so far published details of the symptoms seen in chickens. Examination of brains from these chickens did not show the typical pathology seen in other SE’s. 4.24 A farmer in Kent in November 1996 noticed that one of his 20 free range hens, the oldest, aged about 30 months was having difficulty entering its den and appeared frightened and tended to lose its balance when excited. Having previously experienced BSE cattle on his farm, he took particular notice of the bird and continued to observe it over the following weeks. It lost weight, its balance deteriorated and characteristic tremors developed which were closely associated with the muscles required for standing. In its attempts to maintain its balance it would claw the ground more than usual and the ataxia progressively developed in the wings and legs, later taking a typical form of paralysis with a clumsy involuntary jerky motion. Violent tremors of the entire body, particularly the legs, became common, sparked off by the slightest provocation. This is similar to that seen in many BSE cases where any excitement may result in posterior ataxia, often with dropping of the pelvis, kicking and a general nervousness. Three other farmers and a bird breeder from the UK are known to have reported having hens with similar symptoms. The bird breeder who has been exhibiting his birds for show purposes for 20 years noticed birds having difficulty getting on to their perch and holding there for any length of time without falling. Even though the bird was eating normally, he noticed a weight loss of more than a pound in a bird the original weight of which was 5 pounds. 4.25 Histological examination of the brain revealed degenerative pathological changes in hens with a minimal vacuolation. The presence of PrP immunostaining of the brain sections revealed PrP-sc positive plaques and this must be regarded as very strong evidence to demonstrate that the hens had been incubating Spongiform Encephalopathy.

 


 

OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER 2002

 

OPINION

 

1. Necrophagous birds as possible transmitters of BSE. The SSC considers that the evaluation of necrophagous birds as possible transmitters of BSE, should theoretically be approached from a broader perspective of mammals and birds which prey on, or are carrion eaters (scavengers) of mammalian species. Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons, eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could be considered possible vectors of transmission and/or spread of TSE infectivity in the environment. In view also of the occurrence of Chronic Wasting Disease (CWD) in various deer species it should not be accepted that domestic cattle and sheep are necessarily the only source of TSE agent exposure for carnivorous species. While some information is available on the susceptibility of wild/exotic/zoo animals to natural or experimental infection with certain TSE agents, nothing is known of the possibility of occurrence of TSE in wild animal populations, other than among the species of deer affected by CWD in the USA.

 

1 The carrion birds are animals whose diet regularly or occasionally includes the consumption of carcasses, including possibly TSE infected ruminant carcasses.

 

C:\WINNT\Profiles\bredagi.000\Desktop\Necrophagous_OPINION_0209_FINAL.doc

 


 

snip...

 

skroll down to the bottom ;

 


 

Sunday, July 07, 2013

 

Could avian scavengers translocate infectious prions to disease-free areas initiating new foci of chronic wasting disease?

 

Prion. 2013 Jul 3;7(4). [Epub ahead of print]

 


 

Below, the entire scientific literature of 46 papers on zoo TSE, many obscure and expensive to obtain, are summarized from full text. The overall picture that emerges is appalling -- the British zoo cover-up has not only affected animals in their own zoos but also other zoos worldwide through the sale of contaminated speciality chows and through export and exchange of rare and endangered species involved in conservation programs. All the zoos involved are named by name here (unlike in the journal articles). Why protect a zoo that feeds cheetahs split spinal cords from cattle throughout the BSE epidemic? (Better to have tossed them the zoo veterinarian.) Names are important for zoos which would not want to export their healthy animals to these facilities or import possibly preclinical animals for their own endangered species breeding programs or release into wild populations. Medical scientists doing unrelated research want to know if animals in their programs are already incubating prion disease.

 

Ravensden, Marwell, Chester, Port Lympne, London, Whipsnade, Woburn, and Edinburgh are 8 known BSE affected British zoos. Woburn Safari Park apparently killed the lion by feeding it split cattle spinal cords and skulls.

 


 

The table below summarizes results in the 1999 PNAS paper. Penetrance of the disease is very high and many animals did not yet display symptoms . This paper was the first (and only one) to look at non-symptomatic zoo animals for prion infection (shown below in red). In the TSE column of the table, '+' signs indicate confirmed, 'p' indicates suspicious/probable, '-' means CNS study negative for TSE.(shown as brown), 'pc' means positive diagnosis in preclinical animal. PNAS 96:4046-4051 199 30 Mar 1999 full text see comment PNAS 96[9] 4738-4739, April 27, 1999 by Will and Ironside C R Acad Sci III 1997 Dec;320(12):971-9 N Bons et al. C R Acad Sci III 1996 Aug;319(8):733-6 Lancet Volume 348, Number 9019 6 July 1996

 

The 82 zoo animals with BSE:

 

Id TSE Genus Species Subsp Birth Origin Death Place of Death 654 x Microcebus murinus - 1997 U.Montpellier 1998 U.Montpellier 656 x Microcebus murinus - 1997 U.Montpellier 1998 U.Montpellier 481 + Eulemur fulvus mayottensis 1974 Madagascar 1992 Montpellier zoo 474 + Eulemur fulvus mayottensis 1974 Madagascar 1990 Montpellier zoo 584 - Eulemur fulvus mayottensis 1984 Montpellier 1991 Montpellier zoo 455 + Eulemur fulvus mayottensis 1983 Montpellier 1989 Montpellier zoo - + Eulemur fulvus mayottensis 1988 Montpellier 1992 Montpellier zoo - + Eulemur fulvus mayottensis 1995 Montpellier 1996 Montpellier zoo - + Eulemur fulvus albifrons 1988 Paris 1992 Montpellier zoo - + Eulemur fulvus albifrons 1988 Paris 1990 Montpellier zoo - + Eulemur fulvus albifrons 1988 Paris 1992 Montpellier zoo 456 + Eulemur fulvus albifrons 1988 Paris 1990 Montpellier zoo 586 + Eulemur mongoz - 1979 Madagascar 1998 Montpellier zoo - p Eulemur mongoz - 1989 Mulhouse 1991 Montpellier zoo - p Eulemur mongoz - 1989 Mulhouse 1990 Montpellier zoo - p Eulemur macaco - 1986 Montpellier 1996 Montpellier zoo - p Lemur catta - 1976 Montpellier 1994 Montpellier zoo - p Varecia variegata variegata 1985 Mulhouse 1990 Montpellier zoo - p Varecia variegata variegata 1993 xxx 1994 Montpellier zoo 455 + Macaca mulatta - 1986 Ravensden UK 1992 Montpellier zoo - p Macaca mulatta - 1986 Ravensden UK 1993 Montpellier zoo - p Macaca mulatta - 1988 Ravensden UK 1991 Montpellier zoo - p Saimiri sciureus - 1987 Frejus France 1990 Frejus zoo 700 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo 701 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo 702 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo 703 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo 704 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo 705 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo 706 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 707 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 708 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 709 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 710 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 711 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 712 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 713 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 714 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 715 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 716 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo 717 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo x p genus species - - Lille zoo 1996 Lille zoo y p genus species - - Lille zoo 1996 Lille zoo z p genus species - - Lille zoo 1996 Lille zoo

 

1 + Actinonyx jubatus cheetah 1986 Marwell zoo 1991 Pearle Coast AU Duke + Actinonyx jubatus cheetah 1984 Marwell zoo 1992 Colchester zoo? UK Saki + Actinonyx jubatus cheetah 1986 Marwell zoo 1993 unknown UK Mich + Actinonyx jubatus cheetah 1986 Whipsnade 1993 Whipsnade UK Fr1 + Actinonyx jubatus cheetah 1987 Whipsnade 1997 Safari de Peaugres FR Fr2 + Actinonyx jubatus cheetah 1991 Marwell zoo 1997 Safari de Peaugres Fr xx + Actinonyx jubatus cheetah 19xx xxx zoo 199x Fota zoo IR yy + Actinonyx jubatus cheetah 19xx yyy zoo 1996+ yyyy zoo UK zz + Actinonyx jubatus cheetah 19xx zzz zoo 1996+ yyyy zoo UK

 

aaa + Felis concolor puma 1986 Chester zoo 1991 Chester zoo UK yy + Felis concolor puma 1980 yyy zoo 1995 yyyy zoo UK zz + Felis concolor puma 1978 zzz zoo 1995 zzzz zoo UK

 

xxx + Felis pardalis ocelot 1987 xxx 1994 Chester zoo UK zzz + Felis pardalis ocelot 1980 zzz 1995 zzzz zoo UK

 

85 + Felis catus cat 1990+ various 1999+ various UK LI NO 19 + Canis familia. dog 1992+ various 1999+ various UK

 

Fota + Panthera tigris tiger 1981 xxx zoo 1995 xxxx zoo UK yy + Panthera tigris tiger 1983 yyy zoo 1998 yyyy zoo UK

 

Lump + Panthera leo lion 1986 Woburn SP 1998 Edinburgh zoo UK [since 1994]

 

1 + Taurotragus oryx eland 1987 Port Lympne 1989 Port Lympne zoo UK Moll + Taurotragus oryx eland 1989 xx UK 1991 not Port Lympne UK Nedd + Taurotragus oryx eland 1989 xx UK 1991 not Port Lympne UK Elec + Taurotragus oryx eland 1990 xx UK 1992 not Port Lympne Uk Daph p Taurotragus oryx eland 1988 xx UK 1990 not Port Lympne UK zzz + Taurotragus oryx eland 1991 zz UK 1994 zzz UK yyy + Taurotragus oryx eland 1993 yy UK 1995 yyy UK

 

Fran p Tragelaphus strepsi. kudu 1985 London zoo 1987 London zoo UK Lind + Tragelaphus strepsi. kudu 1987 London zoo 1989 London zoo UK Karl + Tragelaphus strepsi. kudu 1988 London zoo 1990 London zoo UK Kaz + Tragelaphus strepsi. kudu 1988 London zoo 1991 London zoo UK Bamb pc Tragelaphus strepsi. kudu 1988 London zoo 1991 London zoo UK Step - Tragelaphus strepsi. kudu 1984 London zoo 1991 London zoo UK 346 pc Tragelaphus strepsi. kudu 1990 London zoo 1992 London zoo UK 324 + Tragelaphus strepsi. kudu 1989 Marwell zoo 1992 London zoo UK

 

xxx + Tragelaphus angasi nyala 1983 Marwell zoo 1986 Marwell zoo UK

 

yy + Oryx gazella gemsbok 1983 Marwell zoo 1986 Marwell zoo UK zz + Oryx gazella gemsbok 1994+ zzz zoo 1996+ zzzz zoo UK

 

xx + Oryx dammah scim oryx 1990 xxxx zoo 1993 Chester zoo UK

 

yy + Oryx leucoryx arab oryx 1986 Zurich zoo 1991 London zoo UK

 

yy + Bos taurus ankole cow 1987 yyy zoo 1995 yyyy zoo UK zz + Bos taurus ankole cow 1986 zzz zoo 1991 zzzz zoo UK

 

xx + Bison bison Eu bison 1989 xxx zoo 1996 xxxx zoo UK

 


 

TSE - UK: EXOTIC ANIMALS Sat, 7 Jun 1997 a HREF="dpreslar@fas.org">Dorothy Preslar Briefing to the TSE conference hosted by the New Zealand MAFF

 

In a written reply to the House of Commons, Agriculture Minister of State Jeff Rooker has provided details of Transmissible Spongiform Encephalopathy in animals other than livestock. His report includes confirmed cases of TSE in 2 ankole cows, 1 bison, 3 cheetah, 6 eland, 1 gemsbok, 6 kudu, 1 nyala, 2 ocelot, 1 Arabian oryx, 1 scimitar horned oryx, 3 pumas and 1 tiger, 77 domestic cats.

 

SE Diagnoses In Exotic Species UK MAFF site as it appeared in August 1997

 

kudu 6 gemsbok 1 nyala 1 oryx 2 eland 6 cat (domestic) 78 cheetah 4 + 1 Australia + 1 France + 1 Ireland puma 3 tiger 1 ocelot 2 bison (bison bison) 1 ankole 2 BSE in Great Britain: A Progress Report published twice yearly dated May 1996.

 

kudu 6 gemsbok 1 nyala 1 oryx 2 eland 6 cat 70 cheetah 2 UK + 1 AU + 1 ROI puma 3 tiger 1 ocelot 2 ankole cow 2 http://www.mad-cow.org/may99_zoo_news.html

 

TSEs in Exotic Ruminants TSEs have been detected in exotic ruminants in UK zoos since 1986. These include antelopes (Eland, Gemsbok, Arabian and Scimitar oryx, Nyala and Kudu), Ankole cattle and Bison. With hindsight the 1986 case in a Nyala was diagnosed before the first case of BSE was identified. The TSE cases in exotic ruminants had a younger onset age and a shorter clinical duration compared to that in cattle with BSE. All the cases appear to be linked to the BSE epidemic via the consumption of feed contaminated with the BSE agent. The epidemic has declined as a result of tight controls on feeding mammalian meat and bone meal to susceptible animals, particularly from August 1996.

 

References: Jeffrey, M. and Wells, G.A.H, (1988) Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet.Path. 25. 398-399

 

Kirkwood, J.K. et al (1990) Spongiform encephalopathy in an Arabian oryx (Oryx leucoryx) and a Greater kudu (Tragelaphus strepsiceros) Veterinary Record 127. 418-429.

 

Kirkwood, J.K. (1993) Spongiform encephalopathy in a herd of Greater kudu (Tragelaphus strepsiceros): epidemiological observations. Veterinary Record 133. 360-364

 

Kirkwood, J. K. and Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record. 135. 296-303.

 

Food and Agriculture Organisation (1998) Manual on Bovine Spongiform Encephalopathy.

 


 

Volume 3, Number 8 01 August 2003

 

Previous

 

Next

 

Newsdesk

 

Tracking spongiform encephalopathies in North America

 

Xavier Bosch

 

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.

 

49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.

 

Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.

 

Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.

 

To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.

 

Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.

 

Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.

 

Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.

 

Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.

 

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.

 

CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.

 


 

THE LANCET Infectious Diseases Vol 3 August 2003

 

Tracking spongiform encephalopathies in North America

 


 

Friday, December 14, 2012

 

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

 

snip...

 

In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

 

Animals considered at high risk for CWD include:

 

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

 

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

 

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

 

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

 

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

 

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

 

snip...

 

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).

 

The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).

 

Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

 

snip...

 

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

 

snip...

 

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

 

snip...

 

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

 

snip...

 

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

 

snip...

 


 

Saturday, January 31, 2015

 

European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route

 


 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.

 

***However, this recommendation is guidance and not a requirement by law.

 

======

 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

31 Jan 2015 at 20:14 GMT

 


 

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

 

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

 

Date: Fri, 16 May 2003 11:47:37 –0500

 

From: "Terry S. Singeltary Sr." To: fdadockets@oc.fda.gov

 

Greetings FDA,

 

i would kindly like to comment on;

 

Docket 03D-0186

 

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

 


 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

Singeltary et al

 

31 Jan 2015 at 20:14 GMT

 


 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

*** It also suggests a similar cause or source for atypical BSE in these countries. ***

 

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.

 

*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.

 

*** It also suggests a similar cause or source for atypical BSE in these countries. ***

 

see page 176 of 201 pages...tss

 


 

*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***

 

Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats

 

SUMMARY: We are reopening the comment period for our proposed rule that would revise completely the scrapie regulations, which concern the risk groups and categories established for individual animals and for flocks, the use of genetic testing as a means of assigning risk levels to animals, movement restrictions for animals found to be genetically less susceptible or resistant to scrapie, and recordkeeping requirements. This action will allow interested persons additional time to prepare and submit comments.DATES: The comment period for the proposed rule published on September 10, 2015 (80 FR 54660-54692) is reopened. We will consider all comments that we receive on or before December 9, 2015. ...

 


 


 


 

Comment from Terry Singeltary

 

This is a Comment on the Animal and Plant Health Inspection Service (APHIS) Proposed Rule: Scrapie in Sheep and Goats

 

For related information, Open Docket Folder Docket folder icon

 

Comment View document:Indeed, much science has changed about the Scrapie TSE prion, including more science linking Scrapie to humans. sadly, politics, industry, and trade, have not changed, and those usually trump sound science, as is the case with all Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing animals and the OIE. we can look no further at the legal trading of the Scrapie TSE prion both typical and atypical of all strains, and CWD all stains. With as much science of old, and now more new science to back this up, Scrapie of all types i.e. atypical and typical, BSE all strains, and CWD all strains, should be regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE, and all trading partners to take heed to the latest science on the TSE prion disease, all of them, and seriously reconsider the blatant disregards for human and animal health, all in the name of trade, with the continued relaxing of TSE Prion trade regulations through the 'NEGLIGIBLE BSE RISK' PROGRAM, which was set up to fail in the first place. If the world does not go back to the 'BSE RISK ASSESSMENTS', enhance, and or change that assessment process to include all TSE prion disease, i.e. 'TSE RISK ASSESSMENT', if we do not do this and if we continue this farce with OIE and the USDA et al, and the 'NEGLIGIBLE BSE RISK' PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they will continue to mutate and spread among species of human and animal origin, and they will continue to kill. ...

 

please see ;

 

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.

 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),

 

***is the third potentially zoonotic PD (with BSE and L-type BSE),

 

***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

 

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

 

***thus questioning the origin of human sporadic cases***

 

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

 


 

***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

 


 

please see file attachment for full submission and recent science and my deep concerns on the TSE Prion disease... No documents available. AttachmentsView All (1) scrapie-usa-blogspot-com View Attachment:

 


 

view full submission ;

 


 

Singeltary submission ;

 

Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose

 

*** DOCUMENT ID: APHIS-2006-0118-0411

 


 

the cwd tse prion aka mad cow type disease is not your normal pathogen.

 

The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.

 

you cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.

 

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.

 

the TSE prion agent also survives Simulated Wastewater Treatment Processes.

 

IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.

 

you can bury it and it will not go away.

 

The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.

 

it’s not your ordinary pathogen you can just cook it out and be done with.

 

that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

 

cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?

 

much science has come forth showing that indeed humans are at risk from CWD. ignore this at your own risk.

 

*** PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS ***

 

*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***

 

O18

 

Zoonotic Potential of CWD Prions

 

Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

 

***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***

 

P.105: RT-QuIC models trans-species prion transmission

 

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

 

Additionally, human rPrP was competent for conversion by CWD and fCWD.

 

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

 


 

HD.13: CWD infection in the spleen of humanized transgenic mice

 

Liuting Qing and Qingzhong Kong Case Western Reserve University; Cleveland, OH USA

 

Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrPSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrPSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrPSc-positive humanized mouse spleen already led to prion disease in most animals. These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.

 


 

From: Terry S. Singeltary Sr.

 

Sent: Saturday, November 15, 2014 9:29 PM

 

To: Terry S. Singeltary Sr.

 

Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984

 

THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE

 

R. G. WILL

 

1984

 

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

 

snip...

 


 

85%+ of all human tse prion disease is sporadic CJD.

 

see what the NIH prion Gods say themselves ;

 

‘’In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong.’’

 

‘’Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.’’

 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

 


 

*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

 


 

now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”

 

From: TSS (216-119-163-189.ipset45.wt.net)

 

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

 

Date: September 30, 2002 at 7:06 am PST

 

From: "Belay, Ermias"

 

To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

 

Sent: Monday, September 30, 2002 9:22 AM

 

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Dear Sir/Madam,

 

In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

 

Ermias Belay, M.D. Centers for Disease Control and Prevention

 

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

 

From: Sent: Sunday, September 29, 2002 10:15 AM

 

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

 

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

 

Thursday, April 03, 2008

 

A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.

 

snip...

 

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

 

snip... full text ;

 


 

CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.

 

Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.

 


 

I urge everyone to watch this video closely...terry

 

*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***

 


 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

 


 

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

 

Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.

 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),

 

***is the third potentially zoonotic PD (with BSE and L-type BSE),

 

***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

 

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

 

***thus questioning the origin of human sporadic cases...TSS

 

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

 


 

Longitudinal Detection of Prion Shedding in Saliva and Urine by CWD-Infected Deer by RT-QuIC

 

Davin M. Henderson1, Nathaniel D. Denkers1, Clare E. Hoover1, Nina Garbino1, Candace K. Mathiason1 and Edward A. Hoover1# + Author Affiliations

 

1Prion Research Center, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523

 

ABSTRACT Chronic Wasting Disease (CWD) is an emergent, rapidly spreading prion disease of cervids. Shedding of infectious prions in saliva and urine is thought to be an important factor in CWD transmission. To help elucidate this issue, we applied an in vitro amplification assay to determine the onset, duration, and magnitude of prion shedding in longitudinally collected saliva and urine samples from CWD-exposed white-tailed deer. We detected prion shedding as early as 3 months after CWD exposure and sustained shedding throughout the disease course. We estimated that a 50% lethal dose (LD50) for cervidized transgenic mice would be contained in 1 ml of infected deer saliva or 10 ml or urine. Given the average course of infection and daily production of these body fluids, an infected deer would shed thousands of prion infectious doses over the course of CWD infection. The direct and indirect environmental impact of this magnitude of prion shedding for cervid and non-cervid species is surely significant.

 

Importance: Chronic wasting disease (CWD) is an emerging and uniformly fatal prion disease affecting free ranging deer and elk and now recognized in 22 United States and 2 C anadian Provinces. It is unique among prion diseases in that it is transmitted naturally though wild populations. A major hypothesis for CWD's florid spread is that prions are shed in excreta and transmitted via direct or indirect environmental contact. Here we use a rapid in vitro assay to show that infectious doses of CWD prions are in fact shed throughout the multi-year disease course in deer. This finding is an important advance in assessing the risks posed by shed CWD prions to animals as well as humans.

 

FOOTNOTES

 

↵#To whom correspondence should be addressed: Edward A. Hoover, Prion Research Center, Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, US Email: edward.hoover@colostate.edu

 


 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

 

***Title: Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus)

 

Authors

 

item Moore, S - item Kunkle, Robert item Nicholson, Eric item Richt, Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin

 

Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A

 

Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of North American cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, but CWD has not been reported in free-ranging caribou (Rangifer tarandus caribou) or farmed reindeer. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWD-wtd), mule deer (Odocoileus hemionus; CWD-md), or elk (Cervus elaphus nelsoni; CWD-elk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWD-wtd, CWD-md, or CWD-elk. Two years after challenge of inoculated reindeer, non-inoculated control reindeer were introduced into the same pen as the CWD-wtd inoculated reindeer (n=4) or into a pen adjacent to the CWD-md inoculated reindeer (n=2). Reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrP-CWD). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (MPI). PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 div="" mpi="">
 

***We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naive reindeer both directly and indirectly.

 

Last Modified: 12/3/2015

 


 

***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 div="" mpi="">
 

***We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naive reindeer both directly and indirectly.

 

Tuesday, September 29, 2015

 

*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both directly and indirectly

 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

 


 

*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.

 


 

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

 

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

 

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

 

RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.

 

SUMMARY:

 


 

For Immediate Release Thursday, October 2, 2014

 

Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov

 

*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

 

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).

 


 

*** see history of this CWD blunder here ;

 


 

On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.

 


 

The overall incidence of clinical CWD in white-tailed deer was 82%

 

Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)

 


 

”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.

 


 

Sunday, January 06, 2013

 

USDA TO PGC ONCE CAPTIVES ESCAPE

 

*** "it‘s no longer its business.”

 


 

CWD, spreading it around...

 

for the game farm industry, and their constituents, to continue to believe that they are _NOT_, and or insinuate that they have _NEVER_ been part of the problem, will only continue to help spread cwd. the game farming industry, from the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet mills, shooting pens, to large ranches, are not the only problem, but it is painfully obvious that they have been part of the problem for decades and decades, just spreading it around, as with transportation and or exportation and or importation of cervids from game farming industry, and have been proven to spread cwd. no one need to look any further than South Korea blunder ;

 

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

 

spreading cwd around...

 

Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.

 

***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.

 


 

spreading cwd around...

 

Friday, May 13, 2011

 

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

 

Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea

 

Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.

 

On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.

 

All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.

 

Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.

 

Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.

 

Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).

 

In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.

 

Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.

 

All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.

 

Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.

 

In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.

 

In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.

 


 


 


 


 

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication

 

The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.

 


 

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production

 

Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.

 


 

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

 

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.

 


 

A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing

 

Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE

 

In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.

 


 

PL1

 

Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.

 

Claudio Soto

 

Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.

 

Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.

 

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

 

***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

 

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Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.

 


 

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98 | Veterinary Record | January 24, 2015

 

EDITORIAL

 

Scrapie: a particularly persistent pathogen

 

Cristina Acín

 

Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’

 

From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).

 

Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.

 

Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.

 

The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).

 

In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.

 

Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).

 

In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.

 

The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).

 

Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).

 

So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?

 

What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.

 

References

 

snip...

 

98 | Veterinary Record | January 24, 2015

 


 

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

 

Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C. Maddison, BSc, PhD3 + Author Affiliations

 

1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS UK, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and chronic wasting disease of deer/elk are contagious prion diseases where environmental reservoirs are directly implicated in the transmission of disease. In this study, the effectiveness of recommended scrapie farm decontamination regimens was evaluated by a sheep bioassay using buildings naturally contaminated with scrapie. Pens within a farm building were treated with either 20,000 parts per million free chorine solution for one hour or were treated with the same but were followed by painting and full re-galvanisation or replacement of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype VRQ/VRQ were reared within these pens and their scrapie status was monitored by recto-anal mucosa-associated lymphoid tissue. All animals became infected over an 18-month period, even in the pen that had been subject to the most stringent decontamination process. These data suggest that recommended current guidelines for the decontamination of farm buildings following outbreaks of scrapie do little to reduce the titre of infectious scrapie material and that environmental recontamination could also be an issue associated with these premises.

 

SNIP...

 

Discussion

 

Thorough pressure washing of a pen had no effect on the amount of bioavailable scrapie infectivity (pen B). The routine removal of prions from surfaces within a laboratory setting is treatment for a minimum of one hour with 20,000 ppm free chlorine, a method originally based on the use of brain macerates from infected rodents to evaluate the effectiveness of decontamination (Kimberlin and others 1983). Further studies have also investigated the effectiveness of hypochlorite disinfection of metal surfaces to simulate the decontamination of surgical devices within a hospital setting. Such treatments with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous treatment of the pen surfaces did not effectively remove the levels of scrapie infectivity over that of the control pens, indicating that this method of decontamination is not effective within a farm setting. This may be due to the high level of biological matrix that is present upon surfaces within the farm environment, which may reduce the amount of free chlorine available to inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had also became scrapie positive within nine months, with all animals in this pen being RAMALT positive by 18 months of age. Pen D was no further away from the control pen (pen A) than any of the other pens within this barn. Localised hot spots of infectivity may be present within scrapie-contaminated environments, but it is unlikely that pen D area had an amount of scrapie contamination that was significantly different than the other areas within this building. Similarly, there were no differences in how the biosecurity of pen D was maintained, or how this pen was ventilated compared with the other pens. This observation, perhaps, indicates the slower kinetics of disease uptake within this pen and is consistent with a more thorough prion removal and recontamination. These observations may also account for the presence of inadvertent scrapie cases within other studies, where despite stringent biosecurity, control animals have become scrapie positive during challenge studies using barns that also housed scrapie-affected animals (Ryder and others 2009). The bioassay data indicate that the exposure of the sheep to a farm environment after decontamination efforts thought to be effective in removing scrapie is sufficient for the animals to become infected with scrapie. The main exposure routes within this scenario are likely to be via the oral route, during feeding and drinking, and respiratory and conjunctival routes. It has been demonstrated that scrapie infectivity can be efficiently transmitted via the nasal route in sheep (Hamir and others 2008), as is the case for CWD in both murine models and in white-tailed deer (Denkers and others 2010, 2013). Recently, it has also been demonstrated that CWD prions presented as dust when bound to the soil mineral montmorillonite can be infectious via the nasal route (Nichols and others 2013). When considering pens C and D, the actual source of the infectious agent in the pens is not known, it is possible that biologically relevant levels of prion survive on surfaces during the decontamination regimen (pen C). With the use of galvanising and painting (pen D) covering and sealing the surface of the pen, it is possible that scrapie material recontaminated the pens by the movement of infectious prions contained within dusts originating from other parts of the barn that were not decontaminated or from other areas of the farm.

 

Given that scrapie prions are widespread on the surfaces of affected farms (Maddison and others 2010a), irrespective of the source of the infectious prions in the pens, this study clearly highlights the difficulties that are faced with the effective removal of environmentally associated scrapie infectivity. This is likely to be paralleled in CWD which shows strong similarities to scrapie in terms of both the dissemination of prions into the environment and the facile mode of disease transmission. These data further contribute to the understanding that prion diseases can be highly transmissible between susceptible individuals not just by direct contact but through highly stable environmental reservoirs that are refractory to decontamination.

 

The presence of these environmentally associated prions in farm buildings make the control of these diseases a considerable challenge, especially in animal species such as goats where there is lack of genetic resistance to scrapie and, therefore, no scope to re-stock farms with animals that are resistant to scrapie.

 

Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE) Accepted October 12, 2014. Published Online First 31 October 2014

 


 

Monday, November 3, 2014

 

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

 


 

PPo3-22:

 

Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

 

Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK

 

Key words: scrapie, evironmental persistence, sPMCA

 

Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.

 


 

Willingham, Erin McNulty, Kelly Anderson, Jeanette Hayes-Klug, Amy Nalls, and Candace Mathiason Colorado State University; Fort Collins, CO USA

 

Chronic wasting disease (CWD) is the transmissible spongiform encephalopathy (TSE), of free-ranging and captive cervids (deer, elk and moose).

 

The presence of infectious prions in the tissues, bodily fluids and environments of clinical and preclinical CWD-infected animals is thought to account for its high transmission efficiency. Recently it has been recognized that mother to offspring transmission may contribute to the facile transmission of some TSEs. Although the mechanism behind maternal transmission is not yet known, the extended asymptomatic TSE carrier phase (lasting years to decades) suggests that it may have implications in the spread of prions.

 

Placental trafficking and/or secretion in milk are 2 means by which maternal prion transmission may occur. In these studies we explore these avenues during early and late infection using a transgenic mouse model expressing cervid prion protein. Na€ıve and CWD-infected dams were bred at both timepoints, and were allowed to bear and raise their offspring. Milk was collected from the dams for prion analysis, and the offspring were observed for TSE disease progression. Terminal tissues harvested from both dams and offspring were analyzed for prions.

 

We have demonstrated that

 

(1) CWDinfected TgCerPRP females successfully breed and bear offspring, and

 

(2) the presence of PrPCWD in reproductive and mammary tissue from CWD-infected dams.

 

We are currently analyzing terminal tissue harvested from offspring born to CWD-infected dams for the detection of PrPCWD and amplification competent prions. These studies will provide insight into the potential mechanisms and biological significance associated with mother to offspring transmission of TSEs.

 

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

 

P.157: Uptake of prions into plants

 

Christopher Johnson1, Christina Carlson1, Matthew Keating1,2, Nicole Gibbs1, Haeyoon Chang1, Jamie Wiepz1, and Joel Pedersen1 1USGS National Wildlife Health Center; Madison, WI USA; 2University of Wisconsin - Madison; Madison, WI USA

 

Soil may preserve chronic wasting disease (CWD) and scrapie infectivity in the environment, making consumption or inhalation of soil particles a plausible mechanism whereby na€ıve animals can be exposed to prions. Plants are known to absorb a variety of substances from soil, including whole proteins, yet the potential for plants to take up abnormal prion protein (PrPTSE) and preserve prion infectivity is not known. In this study, we assessed PrPTSE uptake into roots using laser scanning confocal microscopy with fluorescently tagged PrPTSE and we used serial protein misfolding cyclic amplification (sPMCA) and detect and quantify PrPTSE levels in plant aerial tissues. Fluorescence was identified in the root hairs of the model plant Arabidopsis thaliana, as well as the crop plants alfalfa (Medicago sativa), barley (Hordeum vulgare) and tomato (Solanum lycopersicum) upon exposure to tagged PrPTSE but not a tagged control preparation. Using sPMCA, we found evidence of PrPTSE in aerial tissues of A. thaliana, alfalfa and maize (Zea mays) grown in hydroponic cultures in which only roots were exposed to PrPTSE. Levels of PrPTSE in plant aerial tissues ranged from approximately 4 £ 10 ¡10 to 1 £ 10 ¡9 g PrPTSE g ¡1 plant dry weight or 2 £ 105 to 7 £ 106 intracerebral ID50 units g ¡1 plant dry weight. Both stems and leaves of A. thaliana grown in culture media containing prions are infectious when intracerebrally-injected into mice. ***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.

 

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***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.***

 

SEE ;

 

Friday, May 15, 2015

 

Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions

 

Report

 


 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

 

*** Title: Transmission of scrapie prions to primate after an extended silent incubation period

 

item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -

 

Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573. Interpretive Summary: The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent.

 

***The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy.

 

***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

Technical Abstract: Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health. In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.

 

***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

 


 

Evidence for zoonotic potential of ovine scrapie prions

 

Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics

 

Abstract

 

Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 

Subject terms: Biological sciences• Medical research At a glance

 


 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

 

Title: Transmission of the agent of sheep scrapie to deer results in PrPSc with two distinct molecular profiles

 

item Greenlee, Justin item Moore, Sarah - item Smith, Jodi item West Greenlee, Mary - item Kunkle, Robert

 

Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: March 31, 2015 Publication Date: May 25, 2015 Citation: Greenlee, J., Moore, S.J., Smith, J.., West Greenlee, M.H., Kunkle, R. 2015.

 

Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum. Prion 2015. p. S62. Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes reveal PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile type readily passes to deer.

 


 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

 

Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease Authors

 

item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -

 

Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A

 

Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.

 


 

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.

 


 

White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

 

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS

 

Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.

 

see full text ;

 


 

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

 

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

 


 

White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation

 

snip...

 

It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that

 

1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and

 

2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.

 

This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.

 


 


 

2012

 

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

 

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

 

snip...

 

The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.

 

*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

 

Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.

 


 

2011

 

*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.

 


 

October 03, 2015

 

*** TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015

 


 

Thursday, November 26, 2015

 

TEXAS CWD TSE PRION REPORTING TURKEY OF THE YEAR AWARD GOES TO SHANNON TOMPKINS OF THE HOUSTON CHRONICLE

 


 

Monday, November 30, 2015

 

*** Report on the Investigation of the Nineteenth Case of Bovine Spongiform Encephalopathy (BSE) in Canada November 2015 ***

 


 

Monday, October 26, 2015

 

*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015

 


 

Wednesday, October 07, 2015

 

Deer Prion Proteins Modulate the Emergence and Adaptation of Chronic Wasting Disease Strains

 


 

Friday, August 14, 2015

 

*** Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation

 


 

Friday, August 14, 2015

 

Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015

 


 

Tuesday, September 22, 2015

 

*** Host Determinants of Prion Strain Diversity Independent of Prion Protein Genotype

 


 

Friday, August 28, 2015

 

*** Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection

 


 

Sunday, October 25, 2015

 

*** USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE LIVESTOCK CWD SCRAPIE TSE PRION ***

 


 

Thursday, July 03, 2014 How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets?

 


 

Sunday, April 13, 2014

 

Mineral licks: motivational factors for visitation and accompanying disease risk at communal use sites of elk and deer

 

Environmental Geochemistry and Health

 


 

Sunday, July 07, 2013

 

Could avian scavengers translocate infectious prions to disease-free areas initiating new foci of chronic wasting disease?

 

Prion. 2013 Jul 3;7(4). [Epub ahead of print]

 


 

Sunday, December 29, 2013

 

Impacts of wildlife baiting and supplemental feeding on infectious disease transmission risk: A synthesis of knowledge

 


 

Sunday, September 01, 2013

 

hunting over gut piles and CWD TSE prion disease

 


 

Friday, October 26, 2012

 

CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT PRODUCTS, BAITING, AND MINERAL LICKS

 


 

Friday, October 26, 2012

 

CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT PRODUCTS, BAITING, AND MINERAL LICKS

 


 

Wednesday, October 17, 2012

 

Prion Remains Infectious after Passage through Digestive System of American Crows (Corvus brachyrhynchos)

 


 

Monday, February 14, 2011

 

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

 


 

Sunday, November 01, 2009

 

AS THE CROW FLIES, SO DOES CWD

 

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

 

Greetings,

 

THIS potential vector of transmission is very disturbing. I don't know what the flight paths, and or travel of either species of birds, or if there are others, there are many birds that eat meat and or are scavengers. But the disturbing part is the amount of territory they can cover and spread their feces. PLUS, this goes back to what the late Dr. Gibbs told me, and what the late Harash Narang book showed, Dr. Gibbs stating that the TSE agent could spread through the digestinal track, and survive, and could still have the potential to spread, and Harash Narang's book 'The Link', page 135, where a farmers around Kent have chickens with BSE. MAFF was aware of this and was suppose to do some studies? BUT, regardless whether or not these birds become clinical and die, the fact that the above studies showed that the TSE agent survived the digestinal tract, and went on to further infect mice via feces, is very disturbing, and further enhances transmission studies must be done asap. PLUS, this should be the final straw for chicken litter being fed back to cattle and other food producing animals for humans and animals. AND not to forget the Red Necked Ostrich and BSE? ...TSS

 


 

Monday, July 13, 2009

 

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease

 


 


 


 


 


 


 


 


 


 


 


 


 

 

Terry S. Singeltary Sr.

 

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