Monday, December 21, 2020

BSE TSE Prion in zoo animals, exotic ruminants, domestic cats, and CPD Camel Prion Disease, a review 2020

BSE TSE Prion in zoo animals, exotic ruminants, domestic cats, and CPD Camel Prion Disease, a review 2020

The BSE Inquiry / Statement No 324

Dr James Kirkwood

(not scheduled to give oral evidence)

Statement to the BSE Inquiry

James K Kirkwood BVSc PhD FIBiol MRCVS

[This witness has not been asked to give oral evidence in Phase 1 of the Inquiry] 1. I became involved in the field of TSEs through my work as Head of the Veterinary Science Group at the Zoological Society of London’s Institute of Zoology. I held this post from November 1984 until June 1996, when I took up my present post at UFAW. During this time, concurrent with the BSE epidemic, cases of scrapie-like spongiform encephalopathies occurred in animals at the Zoological Society of London’s collections at Regent’s Park and Whipsnade and in other zoos. It was appropriate to investigate the epidemiology of these cases in order to try to determine the possible impact on zoo animals and breeding programmes, and to consider how the disease in zoo animals might be controlled.

2. Throughout the period from 1985 to March 1996, I worked at the Institute of Zoology (IoZ). I was Head of the Veterinary Science Group of the IoZ and Senior Veterinary Officer of the Zoological Society of London (ZSL). I was responsible for the provision of the veterinary service for the ZSL collections.

3. During the period from 1985 to March 1996, scrapie-like spongiform encephalopathies were diagnosed in the following animals which died, or were euthanased, at London Zoo and Whipsnade:

Animal Sex Date of Death Age (mos)

Arabian Oryx Oryx leucoryx F 24.3.89 38

Greater kudu Tragelaphus strepsiceros (Linda) F 18.8.89 30

Greater kudu (Karla) F 13.11.90 19

Greater kudu (Kaz) M 6.6.91 37

Greater kudu (Bambi) M 24.10.91 36

Greater kudu (346/90) M 26.2.92 18

Greater kudu (324/90) F 22.11.92 38

Cheetah Acinonyx jubatus (Michelle) F 22.12.93 91

All these cases were described in papers published in the scientific literature (as cited below).

4. All the animals listed above were bred in captivity. The greater kudu were from a highlyinbred group whose founders were Koo (imported from West Africa in 1967), Doo (imported from a Danish Zoo in 1969) and Chester (transferred to London from Chester Zoo in 1982). The family tree of the group is shown in: Kirkwood, J.K., Cunningham, A.A., Wells, G.A.H., Wilesmith, J.W. & Barnett, J.E.F. (1993) Spongiform encephalopathy in a herd of Greater kudu Tragelaphus strepsiceros: epidemiological observations. Veterinary Record 133, 360-364: (J/VR/133/360)

5. The first case diagnosed among the ZSL’s animals was in the greater kudu ‘Linda’, which died in August 1989. Retrospective examination of the brain of the Arabian oryx that had died 5 months earlier, revealed that this animal also had brain lesions characteristic of a scrapielike spongiform encephalopathy. Diagnostic histopathology of these (and of all the other cases that occurred at London and Whipsnade) was undertaken by the Central Veterinary Laboratory. The clinical features, diagnosis and possible aetiology of these first two ZSL cases was discussed in a paper published in 1990 (Kirkwood, J.K., Wells, G.A.H., Wilesmith, J.W., Cunningham, A.A. & Jackson, S.I. (1990) Spongiform encephalopathy in an Arabian oryx Oryx leucoryx and a greater kudu Tragelaphus strepsiceros. Veterinary Record 127, 418-420).(J/VR/127/418). We noted, in this paper, that it seemed probable that these cases had a common aetiology with BSE.

6. A greater kudu ‘Frances’ which had died some 18 months earlier (17.11.87) had shown clinical signs which, in retrospect, could have been due to SE but CNS tissue had not been saved for examination so this could not be checked (Kirkwood, J.K., Cunningham, A.A., Wells, G.A.H., Wilesmith, J.W. & Barnett, J.E.F. (1993) Spongiform encephalopathy in a herd of Greater kudu Tragelaphus strepsiceros: epidemiological observations. Veterinary Record 133, 360-364)(J/VR/133/360).

7. During the following 3 years, SE was diagnosed in 5 further greater kudu in the ZSL collections (see list in point 3 above). The second confirmed case in a greater kudu occurred in the 19-month old calf (Karla) born to the first confirmed case (Linda). This case gave us concern since the calf was born after the July 1988 ban on inclusion of ruminant derived protein in ruminant feeds and it was considered to be extremely unlikely that this animal could have been exposed to contaminated feeds (the kudu diet prior to February 1987 had included a cattle pellet but pelleted diets fed from then on were thought not to contain RDP). We speculated that maternal transmission may have occurred (Kirkwood, J.K., Wells, G.A.H., Cunningham, A.A., Jackson, S.I., Scott, A.C., Dawson, M. & Wilesmith, J.W. (1992). Scrapie-like encephalopathy in greater kudu (Tragelaphus strepsiceros) which had not been fed on ruminant-derived protein. Veterinary Record 130, 365-367:J/VR/130/365).

8. Since the next three animals in which the disease was confirmed (Kaz, Bambi and 346/90) were not thought to have been exposed to contaminated feeds, and were not born to dams who had been clinical cases (Cunningham, A.A., Wells, G.A.H., Scott, A.C., Kirkwood, J.K. & Barnett, J.E.F. (1993) Transmissible spongiform encephalopathy in greater kudu (Tragelaphus strepsiceros). Veterinary Record 132, 68), we considered the possibility that horizontal transmission may have occurred (Kirkwood, J.K., Cunningham, A.A., Wells, G.A.H., Wilesmith, J.W. & Barnett, J.E.F. (1993) Spongiform encephalopathy in a herd of Greater kudu Tragelaphus strepsiceros: epidemiological observations. Veterinary Record 133, 360-364: J/VR/132/68). The occurrence of SE in a greater kudu (324/90), that had been born in another zoo and was not thought to have been exposed to feeds contaminated with RDP, 27 months after being introduced to the group at Regent’s Park, was further cause for concern that transmission may have occurred between animals (Kirkwood, J.K., Cunningham, A.A., Austin, A.R.,Wells, G.A.H & Sainsbury, A.W. (1994) Spongiform encephalopathy in a Greater kudu Tragelaphus strepsiceros introduced into an affected group. Veterinary Record 134, 167-168: J/VR/134/167).

9. At that time, around 1993, the most likely explanation of the pattern of events seemed to be that the disease in kudu was the same as that in cattle: that it had originally entered the group in contaminated feed but that thereafter transmission may have occurred between individuals (Cunningham, A.A., Wells, G.A.H., Scott, A.C., Kirkwood, J.K. & Barnett, J.E.F. (1993) Transmissible spongiform encephalopathy in greater kudu (Tragelaphus strepsiceros).Veterinary Record 132, 68). In view of this and the likelihood that individuals of a wide range of species of zoo animals had been exposed we recommended (Kirkwood, J.K., Cunningham, A.A., Wells, G.A.H., Wilesmith, J.W. & Barnett, J.E.F. (1993) Spongiform encephalopathy in a herd of Greater kudu Tragelaphus strepsiceros: epidemiological observations. Veterinary Record 133, 360-364 ) that all zoo animals that may have been exposed to contaminated feeds should be observed closely and that because of the potentially serious implications for captive breeding programmes, well-described by my colleague Mr Andrew Cunningham (Cunningham, A.A. (1991) Bovine spongiform encephalopathy and British Zoos. Journal of Zoo and Wildlife Medicine 11, 605-634: J/ZWM/11/605), there was a need for caution about exporting such animals. In addition the kudu were kept isolated from other zoo animals. A very cautious approach was taken and the keeper staff used separate tools for cleaning out the kudu dens and paddocks, changed overalls and boots, used latex gloves, and, for a period until it seemed (for reasons mentioned below) less likely that the situation in kudu differed from that in cattle, collected wastes for incineration. Management practices were reviewed again in March 1996 when it was announced that cases of new variant CJD had occurred which might be related to the BSE agent. In order to pre-empt any public concern that might follow this announcement, the walkways past the kudu paddock were closed to the public. No cases have occurred in the kudu group since 1992.

10. The case of SE in a cheetah that occurred during the period, involved a 7 year-old female which had been born and lived all her life at Whipsnade (except for the final stages when she was moved to the Animal Hospital at Regent’s Park for diagnosis and treatment). This animal, which died in December 1993, had been fed on cuts of meat and bone from carcases of cattle unfit for human consumption and it was thought likely that she had been exposed to spinal cord (Kirkwood, J.K., Cunningham, A.A., Flach, E.J., Thornton, S.M. & Wells, G.A.H. (1995) Spongiform encephalopathy in another captive cheetah (Acinonyx jubatus): evidence for variation in susceptibility or incubation periods between species. Journal of Zoo and Wildlife Medicine 26, 577-582: J/ZWM/26/577).

11. During the period we also collated information on cases of SE that occurred in wild animals at or from other zoos in the British Isles. The total number of cases of which I was aware in June 1996, when I presented a review on occurrence of spongiform encephalopathies in zoo animals (at the Royal College of Pathologists’ Symposium on Transmitting prions: BSE, CJD, and other TSEs, The Royal Society, London, 4th July 1996), was 25, involving 10 species. The animals involved were all from the families Bovidae and Felidae, and comprised: 1 Nyala Tragelaphus angasi, 5 Eland Taurotragus oryx, 6 greater kudu Tragelaphus strepsiceros, 1 Gemsbok Oryx gazella, 1 Arabian oryx Oryx leucoryx, 1 Scimitar-horned oryx Oryx dammah, 4 Cheetah Acinonyx jubatus, 3 Puma Felis concolor 2 Ocelot Felis pardalis, and 1 Tiger Panthera tigris. (A spongiform encephalopathy, which was thought probably to have a different aetiology, had also been reported in 3 ostriches Struthio camelus in Germany). This list did not include cases of BSE in domesticated species in zoos (ie BSE in Ankole or other cattle, or SEs, assumed to be scrapie, in mouflon sheep Ovis musimon).

12. Since the time the above statistics were published, a few further cases have occurred in animals at or from zoos in the British Isles. The total number of cases in cheetah that have now been documented has, as far as I am aware, risen to seven (Vitaud, C., Flach, E.J., Thornton, S.M. & Capello, R. (1998) Clinical observations on four cases of feline spongiform encephalopathy in cheetahs (Acinonyx jubatus). Proceedings of the European Association of Zoo and Wildlife Veterinarians, Chester, UK, 21st-24th May 1998. Pp 133-138). There has also been a case in a bison.

13. Epidemiological aspects of the majority of these cases (those diagnosed up to the end of 1993) were considered in paper published in 1994 (Kirkwood, J.K. & Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record 135, 296-303:J/VR/135/296.) This paper was based on a paper presented at the Consultation on BSE with the Scientific Veterinary Committee of the Commission of the European Communities held in Brussels, 14-15th September 1993 (Kirkwood, J.K. & Cunningham, A.A. (1993) Spongiform encephalopathy in captive wild animals in Britain: epidemiological observations. In R. Bradley & B Marchant (Eds) Transmissible spongiform encephalopathies. Proceedings of a Consultation on BSE with the Scientific Veterinary Committee of the Commission of the European Communities, 14-15 September 1993, Brussels. European Commission. Pp 29-47:M9 tab 46). 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.

14. Among the affected bovids were others (including scimitar horned oryx and eland) which, like some of the kudu, were born some considerable time after the July 1988 ban on inclusion of RDP in ruminant feeds (Kirkwood, J.K. & Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record 135, 296-303:J/VR/135/296). The source of infection to these animals was puzzling. However, as it emerged that many cases of BSE were continuing to occur in domestic cattle born after the July 1988 ban on inclusion of RDP in ruminant feeds, it was clear that the ban had not been immediately effective, and it was therefore possible (or, at least, impossible to rule out) that the late cases in zoo ungulates were also due to exposure to contaminated feeds.

15. We drew attention to the fact that, from a taxonomic perspective, the incidence of cases was strikingly patchy (Kirkwood, J.K. & Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record 135, 296-303. Also Kirkwood, J.K., Cunningham, A.A., Flach, E.J., Thornton, S.M. & Wells, G.A.H. (1995) Spongiform encephalopathy in another captive cheetah (Acinonyx jubatus): evidence for variation in susceptibility or incubation periods between species? Journal of Zoo and Wildlife Medicine 26, 577-582) Compared with many other species of exotic ruminants, few kudu were present in the UK but there had been 6 cases of SE among them. The picture seemed similar in the felids. Compared with other species of exotic felids (eg lions in which no cases had occurred), there were relatively small numbers of puma and cheetah in the UK but (at that time) there had been 3 and 4 cases among these respectively. Almost certainly a wider range of species were exposed to contaminated feeds than those in which cases have occurred or been detected. However, we were cautious about drawing firm conclusions about variation in susceptibility between species because (i) incubation periods vary between species and we thought other cases may emerge and (ii) because the variation might be related to differences in intensity of exposure.


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.


SPONGIFORM ENCEPHALOPATHY IN A CAPTIVE PUMA

an article in yesterday's Times (attached) which suggested that the puma concerned had never ''eaten any part of a cow or sheep which, in the opinion of Government Scientists, could transmit the species to a different species''.

3. You explained to me that this was INCORRECT. The position was as set out in the briefing for Prime Minister's questions attached to Mr Taylor's note. The puma had probably been fed low quality beef meat in the form of split carcasses. ...


Spongiform Encephalopathy in Captive Wild Animals in Britain


Sun, Dec 20, 2020 4:54 pm

Subject: TSE in exotic ruminants

TSE in exotic ruminants


NUMBER OF CONFIRMED CASES OF FSE IN DOMESTIC CATS BY YEAR Year Reported No. of cases Year of Onset No. of cases

1988 0 1988 0

1989 0 1989 1

1990 12 1990 16

1991 12 1991 11

1992 10 1992 14

1993 11 1993 10

1994 16 1994 14

1995 8 1995 4

1996 6 1996 7

1997 6 1997 8

1998 4 1998 1

1999 2 1999 1

2000 1 2000 1

2001 1 2001 1

2002 0 2002 0

2003 0 2003 0

2004 0 2004 0

2005 0 2005 0

2006 0 2006 0

2007 0 2007 0

2008 0 2008 0

2009 0 2009 0

2010 0 2010 0

2011 0 2011 0

2012 0 2012 0

2013 0 2013 0

2014 0 2014 0

2015 0 2015 0

2016 0 2016 0

2017 0 2017 0

2018 0 2018 0

2019 0 2019 0

2020 0 2020 0

Total 89 Total 89 Data valid to 30 November 2020 Includes one case from Guernsey 

Published 11 February 2015 Last updated 21 December 2020 - hide all updates







SE DIAGNOSES IN EXOTIC SPECIES

KUDU 6

GEMSBOK 1

NYALA 1

ORYX 2

ELAND 6

CHEETAH 4*

PUMA 3

TIGER 1

OCELOT 2

BISON (bison bison) 1

ANKOLE COW 2

* Excludes one cheetah in Australia and one in ROI - litter mates born in GB, and another in France also born in G.B. [figures to 1 January 1998]

FELINE SPONGIFORM ENCEPHALOPATHY

TOTAL TO DATE 81 (Plus 1 in N Ireland, 1 in Norway, 1 in Lichtenstein )

YEAR Cases 

1990 12

1991 12

1992 10

1993 11

1994 16

1995 8

1996 6

1997 6


Exotic species
Species Number of cases Dates affected
Ankole Cow 2 1991, 95
Bison 1 1996
Asian Leopard Cat (1) 1 2005
Cheetah 5 1992, 98
Eland 6 1989, 95
Gemsbok 1 1987
Kudu 6 1989, 92
Lion 4 1998, 2001
Nyala 1 1986
Ocelot 3 1994, 99
Oryx 2 1989, 92
Puma 3 1992, 95
Tiger 3 1995, 99
As at 12 January 2006.
A total of 38 cases of spongiform encephalopathy have been confirmed in exotic species, the last one in 2005.
(1) Felis (Prionailurus) bengalensis.
BSE TSE PRION STATISTICS
ZOO ANIMALS AND TSE PRION DISEASE
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
Vet Rec 1997 Sep 13;141(11):270-1 Baron-T, Belli-P Madec-J-Y Moutou-F Vitaud-C Savey-M Spongiform encephalopathy in an imported cheetah in France. CNEVA-Lyon, Laboratoire de Pathologie Bovine, France.

Proc Soc Exp Biol Med 1996 Apr;211(4):306-22 Narang H Origin and implications of bovine spongiform encephalopathy. [tiger]

Vet Rec. 1994 Nov 12;135(20):488. Benbow G. Spongiform encephalopathies in zoo animals. comment

Vet Rec 1994 Oct 29;135(18):440 Swainston J. comment

Vet Rec 1994 Sep 24;135(13):296-303 Kirkwood JK, Cunningham AA Epidemiological observations on spongiform encephalopathies

Vet Rec 1994 Feb 12;134(7):167-8 Kirkwood JK, Cunningham AA, Austin AR, Wells GA, Sainsbury AW Spongiform encephalopathy in a greater kudu

Vet Rec. 1993 Oct 9;133(15):360-4. Kirkwood JK, et al. Spongiform encephalopathy in a herd of greater kudu

Vet Rec. 1993 Jan 16;132(3):68. Cunningham AA, et al. Transmissible spongiform encephalopathy in greater kudu

Vet Rec. 1992 Nov 7;131(19):431-4. Willoughby K, et al. Spongiform encephalopathy in a captive puma

Aust Vet J 1992 Jul;69(7):171 Peet RL, Curran JM Spongiform encephalopathy in an imported cheetah

Vet Rec 1992 Apr 25;130(17):365-7 Kirkwood JK, Wells GA, Cunningham AA, Jackson SI, Scott AC, Dawson M, Wilesmith JW Scrapie-like encephalopathy in a greater kudu

Acta Neuropathol (Berl) 1992;84(5):559-69 Jeffrey M, Scott JR, Williams A, Fraser H Ultrastructural features of spongiform encephalopathy

Vet Rec. 1991 Oct 5;129(14):320 Synge BA, et al. Spongiform encephalopathy in a Scottish cat.

Vet Rec 1991 Sep 14;129(11):233-6 Wyatt JM, Pearson GR, Naturally occurring scrapie-like s

Vet Rec. 1991 Jun 1;128(22):532. Pearson GR, et al. Feline spongiform encephalopathy.

Vet Rec. 1991 Mar 30;128(13):311. Kock R. Spongiform encephalopathies in ungulates.

Vet Rec. 1991 Feb 2;128(5):115. Gibson PH. Spongiform encephalopathies in ungulates. comment

Vet Rec 1990 Dec 15;127(24):586-8 Leggett MM, Dukes J, Pirie HM A spongiform encephalopathy in a cat.

Done JT. Vet Rec. 1990 Nov 10;127(19):484. Spongiform encephalopathy in pigs.

Vet Rec. 1990 Oct 27;127(17):418-20. Kirkwood JK, et al. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu.

Vet Rec. 1990 Sep 29;127(13):338. Dawson M, et al. Primary parenteral transmission of bovine spongiform encephalopathy to the pig.

Vet Rec. 1990 May 19;126(20):513 no authors listed Spongiform encephalopathy in a cat.

Vet Rec 1990 May 12;126(19):489-90 Gibson PH Spongiform encephalopathy in an eland.

Nature. 1990 Mar 15;344(6263):183 Aldhous P. Antelopes die of "mad cow" disease.

Vet Rec 1990 Apr 21;126(16):408-9 Fleetwood AJ, Furley CW Spongiform encephalopathy in an eland.

Vet Pathol. 1988 Sep;25(5):398-9 Jeffrey M, Wells GA Spongiform encephalopathy in a nyala (Tragelaphus angasi) Lasswade Veterinary Laboratory, Midlothian



2020

Monday, November 30, 2020 

Tunisia has become the second country after Algeria to detect a case of CPD Camel Prion Disease within a year 

REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019

Scientific Commission/September 2019

Tunisia has become the second country after Algeria to detect a case of CPD within a year

10.2. Prion disease in dromedary camels 


SUNDAY, DECEMBER 20, 2020 

Second passage of chronic wasting disease of mule deer in sheep compared to classical scrapie after intracranial inoculation


MONDAY, NOVEMBER 30, 2020 

***> REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019 BSE, TSE, PRION

see updated concerns with atypical BSE from feed and zoonosis...terry


TUESDAY, SEPTEMBER 29, 2020 

ISO's Updated 22442 Animal Tissue Standards — What Changed? TSE Prion!


WEDNESDAY, MAY 29, 2019 

Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!


WEDNESDAY, OCTOBER 28, 2020 

EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary Submission


2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains

PLEASE NOTE;

2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains

Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).

In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.


SUNDAY, OCTOBER 11, 2020 

Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ 


THURSDAY, SEPTEMBER 24, 2020 

The emergence of classical BSE from atypical/ Nor98 scrapie


MONDAY, DECEMBER 14, 2020 

Experimental oral transmission of chronic wasting disease to sika deer (Cervus nippon)


cwd scrapie pigs oral routes 

***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** 

>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** 

***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). 

***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. 




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..... 


***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are; 

BSE TESTING (failed terribly and proven to be a sham) 

BSE SURVEILLANCE (failed terribly and proven to be a sham) 

BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham) 

these are facts folks. trump et al just admitted it with the feed ban. 

see; 

FDA Reports on VFD Compliance 

John Maday 

August 30, 2019 09:46 AM VFD-Form 007 (640x427) 

Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.


SUNDAY, SEPTEMBER 1, 2019 

***> FDA Reports on VFD Compliance 


THURSDAY, AUGUST 20, 2020 

***> Why is USDA "only" BSE TSE Prion testing 25,000 samples a year? <***


THURSDAY, DECEMBER 17, 2020 

THE MAD COW BSE TSE PRION THAT STOLE CHRISTMAS DECEMBER 2003, WHAT REALLY HAPPENED, A REVIEW 2020 


***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.

https://www.nature.com/articles/srep11573 

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 long 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*** 

=============== 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. 

============== 

https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf 

***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 

http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20 

PRION 2016 TOKYO

Saturday, April 23, 2016

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

Taylor & Francis

Prion 2016 Animal Prion Disease Workshop Abstracts

WS-01: Prion diseases in animals and zoonotic potential

Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 

http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

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

*** 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. 

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160

1: J Infect Dis 1980 Aug;142(2):205-8

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

snip...

The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

PMID: 6997404


Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"

Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.

snip...

76/10.12/4.6


Nature. 1972 Mar 10;236(5341):73-4.

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

Gibbs CJ Jr, Gajdusek DC.

Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

C. J. GIBBS jun. & D. C. GAJDUSEK

National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).



Wednesday, February 16, 2011

IN CONFIDENCE

SCRAPIE TRANSMISSION TO CHIMPANZEES

IN CONFIDENCE


> However, to date, no CWD infections have been reported in people.
key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** 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).***
Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Prion 2017 Conference
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. 
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. 
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
Prion Conference 2018
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip…
see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry
Prion 2018 Conference
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
International Conference on Emerging Diseases, Outbreaks & Case Studies & 16th Annual Meeting on Influenza March 28-29, 2018 | Orlando, USA
Qingzhong Kong
Case Western Reserve University School of Medicine, USA
Zoonotic potential of chronic wasting disease prions from cervids
Chronic wasting disease (CWD) is the prion disease in cervids (mule deer, white-tailed deer, American elk, moose, and reindeer). It has become an epidemic in North America, and it has been detected in the Europe (Norway) since 2016. The widespread CWD and popular hunting and consumption of cervid meat and other products raise serious public health concerns, but questions remain on human susceptibility to CWD prions, especially on the potential difference in zoonotic potential among the various CWD prion strains. We have been working to address this critical question for well over a decade. We used CWD samples from various cervid species to inoculate transgenic mice expressing human or elk prion protein (PrP). We found infectious prions in the spleen or brain in a small fraction of CWD-inoculated transgenic mice expressing human PrP, indicating that humans are not completely resistant to CWD prions; this finding has significant ramifications on the public health impact of CWD prions. The influence of cervid PrP polymorphisms, the prion strain dependence of CWD-to-human transmission barrier, and the characterization of experimental human CWD prions will be discussed.
Speaker Biography Qingzhong Kong has completed his PhD from the University of Massachusetts at Amherst and Post-doctoral studies at Yale University. He is currently an Associate Professor of Pathology, Neurology and Regenerative Medicine. He has published over 50 original research papers in reputable journals (including Science Translational Medicine, JCI, PNAS and Cell Reports) and has been serving as an Editorial Board Member on seven scientific journals. He has multiple research interests, including public health risks of animal prions (CWD of cervids and atypical BSE of cattle), animal modeling of human prion diseases, mechanisms of prion replication and pathogenesis, etiology of sporadic Creutzfeldt-Jacob disease (CJD) in humans, normal cellular PrP in the biology and pathology of multiple brain and peripheral diseases, proteins responsible for the α-cleavage of cellular PrP, as well as gene therapy and DNA vaccination.
SATURDAY, FEBRUARY 23, 2019 

Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019


TUESDAY, NOVEMBER 04, 2014 

Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011

Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "


Transmission Studies

Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS

resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.

snip.... 


Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ 

Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations

In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species. 


Prions in Skeletal Muscles of Deer with Chronic Wasting Disease 

Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure. 


*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.

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 

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


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 ; 


*** 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 ***


*** 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. 


> However, to date, no CWD infections have been reported in people. 

sporadic, spontaneous CJD, 85%+ of all human TSE, just not just happen. never in scientific literature has this been proven.

if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;



key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry 

*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***

*** 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).*** 



FRIDAY, JULY 26, 2019 

Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species


TUESDAY, JANUARY 21, 2020 

***> 2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020


CWD TSE PRION AND ZOONOTIC, ZOONOSIS, POTENTIAL

Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY 

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

From: Steve Dealler 

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

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

Dear Terry,

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

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

Steve Dealler =============== 


Stephen Dealler is a consultant medical microbiologist  deal@airtime.co.uk 

BSE Inquiry Steve Dealler

Management In Confidence

BSE: Private Submission of Bovine Brain Dealler

snip...see full text;

MONDAY, FEBRUARY 25, 2019

***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019


***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***

***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<*** 

***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***

***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<*** 

***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***


Transmissible Spongiform Encephalopathy TSE Prion End of Year Report

CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020

zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum


4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein. 


***> PIGS, WILD BOAR, CWD <***

***> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE  A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASE

HYPOTHOSIS AND SPECIFIC AIMS

HYPOTHOSIS 

BSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALS


Final Report – CJD Foundation Grant Program A. 

Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.


Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018

Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.



Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research

Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease 

Author item MOORE, SARAH - Orise Fellow item Kunkle, Robert item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item SMITH, JODI - Iowa State University item KANTHASAMY, ANUMANTHA - Iowa State University item WEST GREENLEE, M - Iowa State University item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:

Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent. 

Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC. 

Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). 

Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.



Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research

Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP 

Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.

Interpretive Summary:

Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.


cwd scrapie pigs oral routes 

***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** 

>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** 

***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). 

***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. 




WHAT IF???

TUESDAY, DECEMBER 01, 2020 

Sporadic Creutzfeldt Jakob Disease sCJD and Human TSE Prion Annual Report December 14, 2020 


Wednesday, December 16, 2020 

Expanding spectrum of prion diseases Prusiner et al


THURSDAY, DECEMBER 17, 2020 

Exposure Risk of Chronic Wasting Disease in Humans 


Terry S. Singeltary Sr., Bacliff, Texas USA, 77518, Galveston Bay...on the bottom! <flounder9@verizon.net>
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