Wednesday, January 2, 2019

canine and feline spongiform encephalopathy tse prion 2019 update

EP-021 Canine Prions: A New Form of Prion Disease

Mourad Tayebi1, Monique A David2, Brian Summers3

1 University of Melbourne, Veterinary Sciences, Australia; 2Ausbiologics, Sydney, Australia; 3Royal Veterinary College, London, UK

The origin of bovine spongiform encephalopathy (BSE), which rapidly evolved into a major epidemic remains unresolved and was initially widely attributed to transmission of sheep scrapie to cattle with contaminated feed prepared from rendered sheep carcasses. Alternative transmission hypotheses also include feed contaminated with unrecognized subclinical case(s) of bovine prion disease or with prion-infected human remains. However, following the demonstration of a BSE case exhibiting the novel mutation E211 K, similar to the E200K mutation associated with most genetic CJD in humans, support for a genetic origin of prion disease in cattle is gaining momentum. In contrast to other animal species such as feline, the canine species seems to be resistant to prion disease as no canine prion cases were previously reported.

We describe here three cases of Rottweiler puppy (called RWD cases) with neurological deficits and spongiform change. We used animal bioassays and in vitro studies to show efficient interspecies transmission of this novel canidae prion isolate to other species.

Biochemical studies revealed the presence of partially proteinase K (PK)-resistant fragment and immunohistochemistry displayed staining for PrPSc in the cerebral cortex. Importantly, interspecies transmission of canine PrPSc derived from RWD3 brain homogenates following inoculation of hamsters led to signs of prion disease and replication of PrPSc in brains, spinal cords and spleens of these animals.

These findings if confirmed by further cases of prion disease in canidae and regardless of the origin of the disease would have a major impact on animal and public health.

PRION 2016 TOKYO



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.

*** DEFRA TO SINGELTARY ON HOUND STUDY AND BSE 2001 ***

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, indentify 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...

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).


Monday, February 14, 2011

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

NO, NO, NOT NO, BUT HELL NO !

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


Monday, March 8, 2010

Canine Spongiform Encephalopathy aka MAD DOG DISEASE


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

FRIDAY, DECEMBER 14, 2012


Susceptibility of domestic cats to chronic wasting disease

Candace K. Mathiason1,#, Amy V. Nalls1, Davis M. Seelig1, Susan L. Kraft2, Kevin Carnes2, Kelly R. Anderson1, Jeanette Hayes-Klug1 and Edward A. Hoover1

+ Author Affiliations

1Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523 2Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO 80523

ABSTRACT

Domestic and non-domestic 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 non-domestic 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 n=5 cats each were inoculated intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 months 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 months. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and IP/SQ (intraperitoneal/subcutaneous) routes. Upon sub-passage, feline CWD was transmitted to all IC-inoculated cats with a decreased incubation period of 23-27 months. Feline-adapted CWD (FelCWD) was demonstrated in the brains of all the affected cats by western blot and immunohistochemical analysis. Magnetic resonance imaging revealed abnormalities in clinically ill cats, which included multifocal T2 FLAIR signal hyperintensities, ventricular size increases, prominent sulci and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO secondary passage inoculated 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.

FOOTNOTES

↵# To whom correspondence should be addressed. candace.mathiason@colostate.edu, 1619 Campus Delivery, Fort Collins, CO 80523-1619, 970 491-3975

Copyright © 2012, American Society for Microbiology. All Rights Reserved.


HOWEVER, why ignore the old science and transmission studies to date ???

Species Born Onset/Died

Ocelot May 1987 Mar 1994 Ocelot Jul 1980 Oct 1995 Puma 1986 May 1991 Puma 1980 May 1995 Puma 1978 May 1995 Lion Nov 1986 Dec 1998 Tiger 1981 Dec 1995 Tiger Feb 1983 Oct 1998 Ankole 1987 May 1995 Ankole 1986 Feb 1991 Bison 1989/90 Oct 1996

Maff data on 15 May 99

kudu 6 gemsbok 1 nyala 1 oryx 2 eland 6 cheetah 9 puma 3 tiger 2 ocelot 2 bison 1 ankole 2 lion 1


Feline Spongiform Encephalopathy (FSE) FSE was first identified in the UK in 1990. Most cases have been reported in the UK, where the epidemic has been consistent with that of the BSE epidemic. Some other countries (e.g. Norway, Liechtenstein and France) have also reported cases.

Most cases have been reported in domestic cats but there have also been cases in captive exotic cats (e.g. Cheetah, Lion, Asian leopard cat, Ocelot, Puma and Tiger). The disease is characterised by progressive nervous signs, including ataxia, hyper-reactivity and behavioural changes and is fatal.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.


TSE and Surveillance Statistics Exotic species and domestic cats November 2018 

Contents Number of confirmed cases of FSE in domestic cats by year 

Number of confirmed cases of FSE in domestic cats by year of birth 

Number of TSEs in exotic species by year reported

Transmissible Spongiform Encephalopathies in exotic species

Number of confirmed cases of FSE in domestic cats by year Data valid to 30 November 2018 Includes one case from Guernsey Year Reported No. of cases 1988 0 1989 0 1990 12 1991 12 1992 10 1993 11 1994 16 1995 8 1996 6 1997 6 1998 4 1999 2 2000 1 2001 1 2002 0 2003 0 2004 0 2005 0 2006 0 2007 0 2008 0 2009 0 2010 0 2011 0 2012 0 2013 0 2014 0 2015 0 2016 0 2017 0 2018 0 Total 89 Year of Onset No. of cases 1988 0 1989 1 1990 16 1991 11 1992 14 1993 10 1994 14 1995 4 1996 7 1997 8 1998 1 1999 1 2000 1 2001 1 2002 0 2003 0 2004 0 2005 0 2006 0 2007 0 2008 0 2009 0 2010 0 2011 0 2012 0 2013 0 2014 0 2015 0 2016 0 2017 0 2018 0 Total 89


FSE: FIRST CONFIRMED CASE REPORTED IN PORTUGAL AND POTENTIAL MAD CAT ESCAPES LAB IN USA Date: August 9, 2007 at 2:27 pm PST

DIA-45 FELINE SPONGIFORM ENCEPHALOPATHY: FIRST CONFIRMED CASE REPORTED IN PORTUGAL

J.F. Silva1, J.J. Correia, 1 J. Ribeiro2, S. Carmo2 and L.Orge3

1 Faculdade de Medicina Veterinária (UTL), Lisbon, Portugal 2 Clínica Veterinária Ani+, Queluz, Portugal 3 Laboratório Nacional de Investigação Veterinária, Unidade de BSE, Lisbon, Portugal

Feline spongiform encephalopathy (FSE), affecting domestic and captive feline species, is a prion disease considered to be related to bovine spongiform encephalopathy (BSE). Here we report the first case diagnosed in Portugal, highlighting the neuroapthological findings. In 2004 a 9-year old intact female Siamese cat was referred with chronic progressive behavioural changes, polydipsia, gait abnormalities and episodes of hypersalivation. Clinical signs progressed to tetraparesis and dementia and euthanasia was performed. At necropsy, brain and spinal cord had no significative changes. Tissue samples from brain, cerebellum, brainstem and spinal cord were collected for histopathology and immunohistochemistry for detection of PrPres. Histology revealed neuropil and neuronal perikarion vacuolation in several areas of the central nervous system together with gliosis and cell rarefaction at the granular layer of the cerebellum. Immunohistochemical detection of PrPres showed a strong and widespread PrPres accumulation as granular and linear deposits as well as associated with some neurons. These findings are supportive of FSE. To the authors knowledge this is the first confirmed case of FSE reported in Portugal.




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

EMC 1 Terry S. Singeltary Sr. Vol #: 1


IN CONFIDENCE CJD TO CATS...

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


FELINE SPONGIFORM ENCEPHALOPATHY FSE




Terry S. Singeltary Sr.

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.

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



Hunting and diet




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



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



http://en.wikipedia.org/wiki/Cougar




Oral.22:



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



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



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



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



Oral.26: Minor Oral Lesions Facilitate CWD Infection



Nathaniel D. Denkers,1,† Glenn C. Telling2 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Kentuckty; Lexington, KY USA †Presenting author; Email: nddenk@colostate.edu



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



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



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



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



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



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



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



1Colorado State University; Fort Collins, CO USA; 2University of Kentucky; Lexington, KY USA†Presenting author; Email: davis.seelig@colostate.edu



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



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



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



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



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



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



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



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



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



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



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



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



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



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



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




Enzymatic Digestion of Chronic Wasting Disease Prions Bound to Soil


S A M U E L E . S A U N D E R S , † J A S O N C . B A R T Z , ‡ K U R T C . V E R C A U T E R E N , § A N D S H A N N O N L . B A R T E L T - H U N T * , †


Department of Civil Engineering, Peter Kiewit Institute, University of NebraskasLincoln, Omaha, Nebraska 68588, Department of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska 68178, and USDA Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, Fort Collins, Colorado 80521 Received November 19, 2009. Revised manuscript received April 5, 2010. Accepted April 24, 2010.



Chronic wasting disease (CWD) and sheep scrapie can be transmitted via indirect environmental routes, and it is known that soil can serve as a reservoir of prion infectivity. Given the strong interaction between the prion protein (PrP) and soil, we hypothesized that binding to soil enhances prion resistance to enzymatic digestion, thereby facilitating prion longevity in the environment and providing protection from host degradation. We characterized the performance of a commercially available subtilisin enzyme, Prionzyme, to degrade soil-bound and unbound CWD and HY TME PrP as a function of pH, temperature, and treatment time. The subtilisinenzymeeffectively degraded PrP adsorbed to a wide range of soils and soil minerals below the limits of detection. Signal loss occurred rapidly at high pH (12.5) and within 7 days under conditions representative of the natural environment (pH 7.4, 22 °C). We observednoapparent difference inenzymeeffectivenessbetween bound and unbound CWD PrP. Our results show that although adsorbed prions do retain relative resistance to enzymatic digestion compared with other brain homogenate proteins, they can be effectively degraded when bound to soil. Our results also suggest a topical application of a subtilisin enzyme solution may be an effective decontamination method to limit disease transmission via environmental “hot spots” of prion infectivity. see full text study here ;



http://www.aphis.usda.gov/wildlife_damage/nwrc/publications/10pubs/vercauteren108.pdf





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


you cannot cook the CWD 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 CWD TSE Prion agent will survive in the environment for years, if not decades.


you can bury it and it will not go away.


CWD 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.





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




Paul Brown*,dagger , Edward H. RauDagger , Bruce K. Johnson*, Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§ * Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, and Dagger Environmental Protection Branch, Division of Safety, Office of Research Services, National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France Contributed by D. Carleton Gajdusek, December 22, 1999


see full text:











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






Cathrin E. Bruederle,1* Robert M. Hnasko,1 Thomas Kraemer,2 Rafael A. Garcia,3 Michael J. Haas,3 William N. Marmer,3 and John Mark Carter1 1USDA-ARS WRRC, Foodborne Contaminants Research Unit, Albany, California, United States of America 2Forensic Toxicology, Institute of Legal Medicine, Saarland University, Homburg/Saar, Germany 3USDA-ARS ERRC, Fats, Oils and Animal Coproducts Research Unit, Wyndmoor, Pennsylvania, United States of America Neil Mabbott, EditorUniversity of Edinburgh, United Kingdom *











Wednesday, October 14, 2009


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


T.A. Nichols,1,2 Bruce Pulford,1 A. Christy Wyckoff,1,2 Crystal Meyerett,1 Brady Michel,1 Kevin Gertig,3 Edward A. Hoover,1 Jean E. Jewell,4 Glenn C. Telling5 and Mark D. Zabel1,*


1Department of Microbiology, Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; Fort Collins, CO USA; 2National Wildlife Research Center; Wildlife Services; United States Department of Agriculture; Fort Collins, CO USA; 3Fort Collins Utilities; Fort Collins; CO USA; 4Department of Veterinary Sciences; Wyoming State Veterinary Laboratory; University of Wyoming; Laramie, WY USA; 5Department of Microbiology, Immunology, Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky; Lexington, KY USA




snip...




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









OLD BSE TSE PRION HISTORY




The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences & Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s Hospital London and William Harvey Hospital Ashford April 1999




snip...




88. Natural decay: Infectivity persists for a long time in the environment. A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep, after they had grazed on land which had previously been grazed by scrapie-infected sheep, even though the land had lain fallow for three years before the healthy sheep were introduced. Brown also quoted an early experiment of his own (1991), where he had buried scrapie-infected hamster brain and found that he could still detect substantial infectivity three years later near where the material had been placed.


89. Potential environmental routes of infection: Brown discusses the various possible scenarios, including surface or subsurface deposits of TSE-contaminated material, which would lead to a build-up of long-lasting infectivity. Birds feeding on animal remains (such as gulls visiting landfill sites) could disperse infectivity. Other animals could become vectors if they later grazed on contaminated land. "A further question concerns the risk of contamination of the surrounding water table or even surface water channels, by effluents and discarded solid wastes from treatment plants. A reasonable conclusion is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge numbers of uncertainties and assumptions that attend each stage of the disposal process". These comments, from a long established authority on TSEs, closely echo my own statements which were based on a recent examination of all the evidence.


90. Susceptibility: It is likely that transmissibility of the disease to humans in vivo is probably low, because sheep that die from scrapie and cattle that die from BSE are probably a small fraction of the exposed population. However, no definitive data are available.




91. Recommendations for disposal procedures: Brown recommends that material which is actually or potentially contaminated by BSE should be: 1) exposed to caustic soda; 2) thoroughly incinerated under carefully inspected conditions; and 3) that any residue should be buried in landfill, to a depth which would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source.




snip...






(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN, AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF FILE...TSS)











PAUL BROWN SCRAPIE SOIL TEST


(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN, AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF FILE...TSS)








INCINERATION TEMPS


Requirements include:


a. after burning to the range of 800 to 1000*C to eliminate smell; well heck, this is just typical public relations fear factor control. do you actually think they would spend the extra costs for fuel, for such extreme heat, just to eliminate smell, when they spread manure all over your veg's. i think not. what they really meant were any _TSE agents_.


b. Gas scrubbing to eliminate smoke -- though steam may be omitted; c. Stacks to be fitted with grit arreaters;


snip...


1.2 Visual Imact


It is considered that the requirement for any carcase incinerator disign would be to ensure that the operations relating to the reception, storage and decepitation of diseased carcasses must not be publicly visible and that any part of a carcase could not be removed or interfered with by animals or birds.


full text;








18. The EA’s assertion at the Thruxted planning inquiry that the precautionary principle does not apply in the case of Thruxted Mill in view of the low risk entailed by its effluent discharge is entirely unfounded. The source data presented by the EA at the Thruxted Inquiry derive in part from its assumptions concerning the segregation of infectivity to the various products of rendering. The EA also stipulates a minimum particle size of 1013 molecules for human infection and assumes there is a 2500-fold reduction of infectivity by rendering, filtration and biological treatment prior to discharge. In fact, the minimum particle size may be at least 1012 times lower. The reduction in the input levels of BSE infectivity prior to discharge will also be very substantially less than implied in the EA source data, and may indeed be minimal. The EA assumes that biological treatment of the rendering effluent will reduce or eliminate BSE infectivity. This is probably the exact opposite of what is actually likely to happen.


19. In his proof of evidence at the Thruxted Inquiry, Mr Young asserted that "effective filtering of clumps of material is likely". As already mentioned, infectious prions are known to pass








[PDF]BSE INQUIRY Statement of behalf of the Environment Agency ...


File Format: PDF/Adobe Acrobat - View as HTML


... his Statement of March 1998 to the BSE Inquiry ... systems subject to regular or intermittent


contamination by rapid movement of recharge water ...


BSE INQUIRY


Statement of behalf of the Environment Agency


Concerning Thruxted Mill


By


Mr C. P. Young


Principal Hydrogeologist, Soil Waste and Groundwater Group


WRc plc; Medmenham, Bucks









Friday, February 25, 2011


Soil clay content underlies prion infection odds








Friday, February 25, 2011


Soil clay content underlies prion infection odds

 
 







Monday, February 14, 2011



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



NO, NO, NOT NO, BUT HELL NO !



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



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




Monday, August 8, 2011



Susceptibility of Domestic Cats to CWD Infection



http://felinespongiformencephalopathyfse.blogspot.com/2011/08/susceptibility-of-domestic-cats-to-cwd.html




UPDATED DATA ON 2ND CWD STRAIN



Wednesday, September 08, 2010



CWD PRION CONGRESS SEPTEMBER 8-11 2010



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




Sunday, November 01, 2009



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



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




Monday, July 13, 2009



Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease



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




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



2005



DEFRA Department for Environment, Food & Rural Affairs



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



GTN: FAX:



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



21 November 2001



Dear Mr Singeltary



TSE IN HOUNDS



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



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



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



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



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



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



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



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



I hope this is helpful



Yours sincerely 4



HUGH MCDONAGH BSE CORRESPONDENCE SECTION



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



TSE & HOUNDS



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



HOUND STUDY



AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.



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




76 pages on hound study;



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




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



snip...see full text ;



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




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



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



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



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




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





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




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





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





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



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



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





Thursday, December 25, 2008

Lions and Prions and Deer Demise

snip...

Greetings,

A disturbing study indeed, but even more disturbing, the fact that this very study shows the potential for transmission of the TSE agent into the wild of yet another species in the USA. Science has shown that the feline is most susceptible to the TSE agent. Will CWD be the demise of the mountain lions, cougars and such in the USA? How many have ever been tested in the USA? I recall there is a study taking place ;

Review A prion disease of cervids: Chronic wasting disease Christina J. Sigurdson et al ;

Mountain lion (Puma concolor) susceptibility to experimental feeding of CWD prions is currently under investigation (M. Miller and L. Wolfe, personal communication).

WHAT about multiple strains of CWD ?

snip...

see full text ;

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




Friday, August 6, 2010

Is the presence of abnormal prion protein in the renal glomeruli of feline species presenting with FSE authentic?

Correspondence

http://felinespongiformencephalopathyfse.blogspot.com/2010/08/correspondence-is-presence-of-abnormal.html




Wednesday, April 1, 2009

Immunohistochemical study of PrPSc distribution in neural and extraneural tissues of two cats with feline spongiform encephalopathy

Research article

http://felinespongiformencephalopathyfse.blogspot.com/2009/04/immunohistochemical-study-of-prpsc.html





Saturday, September 5, 2009

Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah

http://felinespongiformencephalopathyfse.blogspot.com/2009/09/possible-case-of-maternal-transmission.html



Tuesday, September 02, 2008

Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease

http://chronic-wasting-disease.blogspot.com/2008/09/fecal-transmission-of-aa-amyloidosis-in.html


http://felinespongiformencephalopathyfse.blogspot.com/



Wednesday, July 20, 2011

Canadian Researchers Receive $2.9 Million to Protect Against Prion Disease Outbreaks, Develop Novel Therapies to Treat Alzheimer's, Parkinson's and ALS



http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/canadian-researchers-receive-29-million.html




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




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




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




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




http://transmissible-mink-encephalopathy.blogspot.com/




http://creutzfeldt-jakob-disease.blogspot.com/




http://sporadicffi.blogspot.com/




http://kuru-tse.blogspot.com/




http://prionopathy.blogspot.com/




http://betaamyloidcjd.blogspot.com/




http://transmissiblespongiformencephalopathy.blogspot.com/




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




http://www.mad-cow.org/~tom/animals.html




TSS

Friday, August 6, 2010

Is the presence of abnormal prion protein in the renal glomeruli of feline species presenting with FSE authentic?

Correspondence


Is the presence of abnormal prion protein in the renal glomeruli of feline species presenting with FSE authentic?


Stephane Lezmi , Thierry GM Baron and Anna A Bencsik

BMC Veterinary Research 2010, 6:41doi:10.1186/1746-6148-6-41

Published: 4 August 2010

Abstract (provisional) In a recent paper written by Hilbe et al (BMC vet res, 2009), the nature and specificity of the prion protein deposition in the kidney of feline species affected with feline spongiform encephalopathy (FSE) were clearly considered doubtful. This article was brought to our attention because we published several years ago an immunodetection of abnormal prion protein in the kidney of a cheetah affected with FSE. At this time we were convinced of its specificity but without having all the possibilities to demonstrate it. As previously published by another group, the presence of abnormal prion protein in some renal glomeruli in domestic cats affected with FSE is indeed generally considered as doubtful mainly because of low intensity detected in this organ and because control kidneys from safe animals present also a weak prion immunolabelling. Here we revisit these studies and thought it would be helpful to relay our last data to the readers of BMC Vet res for future reference on this subject. Here we come back on our material as it is possible to study and demonstrate the specificity of prion immunodetection using the PET-Blot method (Paraffin Embedded Tissue - Blot). It is admitted that this method allows detecting the Proteinase K (PK) resistant form of the abnormal prion protein (PrPres) without any confusion with unspecific immunoreaction. We re-analysed the kidney tissue versus adrenal gland and brain samples from the same cheetah affected with TSE using this PET-Blot method. The PET-Blot analysis revealed specific PrPres detection within the brain, adrenal gland and some glomeruli of the kidney, with a complete identicalness compared to our previous detection using immunohistochemistry. In conclusion, these new data enable us to confirm with assurance the presence of specific abnormal prion protein in the adrenal gland and in the kidney of the cheetah affected with FSE. It also emphasizes the usefulness for the re-examination of any available tissue blocks with the PET-Blot method as a sensitive complementary tool in case of doubtful PrP IHC results.

http://www.biomedcentral.com/1746-6148/6/41/abstract


Discussion

These new results enable us to confirm confidently the presence of specific abnormal prion protein in the adrenal gland and in the kidney of the cheetah affected with FSE. This question is important because it becomes evidenced that urine may sustain transmission of certain forms of the transmissible spongiform encephalopathy (TSE) diseases, such as hamsters carrying infectious particles. More recently the kidney was found to accumulate abnormal PrP in other species too such as sheep [17, 18], and the urinary secretion of pathological form of PrP is seriously considered [19, 20]. Even if the origin of the production of this infectious prion particles are not yet clearly identified, the specific detection of PrPres within the glomeruli of the kidney of cheetah with FSE is in total accordance with this point.

snip...see full text ;

http://www.biomedcentral.com/content/pdf/1746-6148-6-41.pdf


Subject: CWD/POTENTIAL SOURCE/URINE/HUNTERS ? (Mrs. Doe Pee Doe in Estrus)

Date: Sun, 14 Jul 2002 08:42:51 -0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de

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

1: Hum Reprod 2002 Jul;17(7):1676-80 Bye-bye urinary gonadotrophins?: Is there a risk of prion diseaseafter the administration of urinary-derived gonadotrophins?

Balen A.

Department of Reproductive Medicine, The General Infirmary, LeedsLS2 9NS, UK. E-mail: adam.balen@leedsth.nhs.uk

Concern has been raised recently about the possibility of prionproteins appearing in the urine of animals and, possibly, humansaffected by prion disease [scrapie, bovine spongiform encephalopathy(BSE) and Creutzfeldt Jakob disease (CJD)]. A debate has started inwhich the suggestion has been made that the purification of human urinefor the provision of gonadotrophins should be discontinued. Thealternative would be to use recombinantly-derived gonadotrophinpreparations. The recombinant products, however, rely upon bovine serumduring the cell culture process and could potentially also be exposed toabnormal prion proteins. It is reassuring that the different types ofgonadotrophin preparations that are currently available are producedwith either urine or bovine serum that is sourced from countries that atthe present time appear to be free of BSE and new variant CJD. We cantherefore be reassured that the gonadotrophins that we usetherapeutically appear to be equally safe.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12093821&dopt=Abstract


what about the 100% deer urine they use to atract deer ?

just one example of many below;

CWD/POTENTIAL SOURCE/URINE/HUNTERS ?

Mrs. Doe Pee Doe in Estrus

Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urinecollected at the peak of the rut, blended with Fresh Doe Urine for anextremely effective buck enticer. Use pre-rut before the does come intoheat. Use during full rut when bucks are most active. Use duringpost-rut when bucks are still actively looking for does. 1 oz.

http://www.gamecalls.net/huntingproducts/deerlures.html


ELK SCENT/SPRAY BOTTLE * Works anytime of the year* 100 % Cow Elk-in-Heat urine (2oz.)* Economical - mix with water in spray mist bottle* Use wind to your advantage Product Code WP-ESB $9.95 http://www.elkinc.com/Scent.asp

prions in urine? [PDF] A URINE TEST FOR THE IN-VIVO DIAGNOSIS OF PRION DISEASES

http://www.sigov.si/vurs/PDF/diagnoastika-bse-urin.pdf


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Wednesday, March 18, 2009

Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay

http://chronic-wasting-disease.blogspot.com/2009/03/detection-of-cwd-prions-in-urine-and.html


Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease

Beiru Zhang*†, Yumi Une‡, Xiaoying Fu*, Jingmin Yan*, FengXia Ge*, Junjie Yao*§, Jinko Sawashita*, Masayuki Mori*, Hiroshi Tomozawa¶, Fuyuki Kametani , and Keiichi Higuchi*‡** *Department of Aging Biology, Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine, and ¶Division of Laboratory Animal Research, Research Center for Human and Environmental Science, Shinshu University, 3-1-1, Asahi, Matsumoto 390-8621, Japan; †Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, China; ‡Laboratory of Veterinary Pathology, School of Veterinary Medicine, Azabu University, 1-17-71 Fuchinobe, Sagamihara, Kanagawa 229-8501, Japan; §The Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Tokyo 183-8508, Japan; and Tokyo Institute of Psychiatry, Tokyo Metropolitan Organization for Medical Research, Tokyo 156-8585, Japan Edited by Reed B. Wickner, National Institutes of Health, Bethesda, MD, and approved April 1, 2008 (received for review January 16, 2008)

AA amyloidosis is one of the principal causes of morbidity and mortality in captive cheetahs (Acinonyx jubatus), which are in danger of extinction, but little is known about the underlying mechanisms. Given the transmissible characteristics of AA amyloidosis, transmission between captive cheetahs may be a possible mechanism involved in the high incidence of AA amyloidosis. In this study of animals with AA amyloidosis, we found that cheetah feces contained AA amyloid fibrils that were different from those of the liver with regard to molecular weight and shape and had greater transmissibility. The infectious activity of fecal AA amyloid fibrils was reduced or abolished by the protein denaturants 6 M guanidine HCl and formic acid or by AA immunodepletion. Thus, we propose that feces are a vehicle of transmission that may accelerate AA amyloidosis in captive cheetah populations. These results provide a pathogenesis for AA amyloidosis and suggest possible measures for rescuing cheetahs from extinction.

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Discussion It is currently accepted that systemic AA amyloidosis is an increasingly important cause of morbidity and mortality in captive cheetah populations (14). For conservation of this species, therefore, it is critical to elucidate the etiology of AA amyloidosis. As with sheep scrapie and cervid CWD, the routes of transmission are among the most debated and intriguing issues. InfectiousCWDprions in saliva have been identified to be involved in transmission in high-density captive situations (19, 20). Recently, available evidence indicates that an environmental reservoir of infectivity contributes to the continuation of these diseases in affected populations. These infectious agents can be transmitted by flesh flies (21) or hay mites (22) and can directly enter the environment from decomposing carcasses of infected animals (23). Environmental contamination by excreta from infected cervids has also seemed the most plausible explanation for the dissemination of CWD (24). Scrapie-infected hamsters and Creutzfeldt–Jakob disease (CJD) patients were reported to excrete urinary protease-resistant PrP isoform (25), indicating that urinary excretion from infected animals may provide a vector for horizontal transmission. However, there are studies that are not consistent with these findings (26, 27). Perhaps unrecognized nephritic conditions may underlie these discrepant observations, because it has been reported that urinary prion excretion is found only in scrapie-infected mice with lymphocytic nephritis (28). In this study, we observed several bands with high molecular weights that reacted with anti-cheetah AA antiserum in the whole urine sample, but not in the urine pellet in whichAAamyloid fibrils should be recovered. We thought that the possibility for a transmission pathway through urine might be low, but it could not be ruled out. In addition to urine, the alimentary shedding route has been considered as a possible transmission pathway (29). Abnormal prion protein is present in gut-associated lymphoid tissues of mule deer infected with CWD, consistent with an alimentary shedding route (30). In this study, we showed that the fecal fraction from a cheetah with amyloidosis had AA amyloid fibrils and possessed high transmissibility. In mouse AApoAII amyloidosis, regarded recently as another transmissible amyloidosis (5–7), we also demonstrated that the feces could serve as an agent to induce amyloidosis in recipient mice (31). These results shed new light on the etiology involved in the high incidence of AA amyloidosis in cheetahs. In this study, we unexpectedly found that the amyloid fibril fraction from feces had smaller amyloid fibrils and higher sensitivity to denaturation treatment than the liver amyloid fibril fraction. In mammalian prion, it has been demonstrated that there is a very strong correlation between seeding capability and amyloid fibril conformation (32, 33). Similarly, in yeast prion, it also has been indicated that [PSI ] with stronger infectivity typically have less stable fibrils in vivo than strains with weaker infectivity (34), and the prion strain with relatively smaller prion particles is always associated with greater frangibility and increased sensitivity to denaturants (35). The enhanced frangibility is presumably involved in the increase in seeding efficiency and prion infectivity, while the high sensitivity probably results from structural differences in inter-molecular contacts and a shorter, less stable amyloid core. The divergent ultrastructure between the fecal and the liver fibrils identified by transmission electron microscopy may be responsible for the different characteristics of transmissibility and sensitivity to denaturation treatment, analogous to prion protein. It has been reported that AA amyloidosis can be experimentally induced by i.v. or i.p. administration of AA amyloid fibrillar extracts in recipient mice (10). A few recent studies have shown that AA-containing extracts also had amyloid-inducing activity when administered orally to mice (36, 37). In AApoAII amyloidosis, we orted that an oral administration of AApoAII amyloid fibrils induced amyloidosis in recipient mice (38). Thus, it is plausible that oral ingestion of AA-containing fecal matter caused amyloid deposition in the cheetah population. At this juncture, the manner in which fecal matter is initially absorbed by the cheetahs is not clear. This may occur during mutual grooming (licking of the fur contaminated by fecal matter). Recently it was shown that a prion agent could bind to whole soil and common soil minerals and retain infectivity for a prolonged period (23, 39). Thus, soil may act as a reservoir capable of contaminating both food and fur. It is also unknown how AA fibril proteins enter the feces. Because AA amyloidosis was also in the small intestines of AA amyloidosis cheetahs, it is possible that AA proteins enter the feces through exfoliated mucosa. In conclusion, we found that cheetahs with amyloidosis pass fecal matter that had strong seeding efficiency and should be regarded as a transmission medium. To control the incidence of AA amyloidosis and reduce the likelihood of the animal’s extinction, prevention of the transmission with excretion from cheetahs with amyloidosis should be considered along with reduction of precursor SAA levels.

Materials and Methods

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http://www.pnas.org/content/105/20/7263.full.pdf+html


http://betaamyloidcjd.blogspot.com/2008/05/fecal-transmission-of-aa-amyloidosis-in.html



Tuesday, September 02, 2008

Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease

http://chronic-wasting-disease.blogspot.com/2008/09/fecal-transmission-of-aa-amyloidosis-in.html



Saturday, September 5, 2009

Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah

http://felinespongiformencephalopathyfse.blogspot.com/2009/09/possible-case-of-maternal-transmission.html



http://felinespongiformencephalopathyfse.blogspot.com/



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



http://betaamyloidcjd.blogspot.com/



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



http://www.mad-cow.org/~tom/animals.html



TSS