Thursday, December 19, 2019

TSE surveillance statistics exotic species and domestic cats Update December 2019

TSE surveillance statistics: exotic species and domestic cats

September 2019

Contents

Number of confirmed cases of FSE in domestic cats by year..............................................1

Number of confirmed cases of FSE in domestic cats by year of birth..................................1

Number of TSEs in exotic species by year reported ............................................................2

Transmissible Spongiform Encephalopathies in exotic species...........................................3

1

Number of confirmed cases of FSE in domestic cats by year

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

2019 0

Total 89

Data valid to 30 September 2019

Includes one case from Guernsey

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

2019 0

Total 89

1

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

Year of Birth No. of cases

1976 1

1977 1

1980 1

1981 2

1982 7

1983 8

1984 7

1985 7

1986 11

1987 11

1988 12

1989 8

1990 5

1991 2

1992 1

1993 2

1995 2

1996 1

Total 89

Data valid to 30 September 2019

Includes one case from Guernsey

2

Number of TSEs in exotic species by year reported

Year Number

1988 2

1989 3

1990 1

1991 5

1992 6

1993 2

1994 1

1995 6

1996 2

1997 1

1998 3

1999 3

2000 1

2001 1

2002 0

2003 0

2004 0

2005 1

2006 0

2007 1

2008 0

2009 0

2010 0

2011 0

2012 0

2013 0

2014 0

2015 0

2016 0

2017 0

2018 0

2019 0

Total 39

Data valid to 30 September 2019

Includes a small number of cases not presented as BSE suspects but identified at post mortem examination.

3

Transmissible Spongiform Encephalopathies in exotic species

In exotic species, the last one was in 2007.

SPECIES No. DATES AFFECTED

Ankole cow 2 1991, 95

Bison 1 1996

Cheetah 5 1992 – 98

Eland 6 1989 – 95

Gemsbok 1 1987

Kudu 6 1989 – 92

Asian Leopard Cat1 1 2005

Lion 5 1998 - 2007

Nyala 1 1986

Ocelot 3 1994 – 99

Oryx 2 1989, 92

Puma 3 1992 – 95

Tiger 3 1995 – 99

Data valid to 30 September 2019

1Felis (Prionailurus) bengalensis. 


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






CHRONIC WASTING DISEASE CWD TSE PRION TRANSMITS TO PIGS BY ORAL ROUTES!!!

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 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" 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. 




***> Subject: Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban? <***

Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies 2017 Annual Report

1a. Objectives (from AD-416): 

Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.

1b. Approach (from AD-416): 

The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.

3. Progress Report: 

All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.

4. Accomplishments 

1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. 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.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, 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.
3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.

Review Publications 
Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.
Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78.
Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114.
Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155.
Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005.



FRIDAY, APRIL 20, 2018 

*** Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban? 

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


CDC

New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES

Mad Camel Disease

Volume 24, Number 6—June 2018 Research 

Prion Disease in Dromedary Camels, Algeria Abstract

Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.

SNIP...

The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.

Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (27) should be investigated to trace the possible origin of CPD from other countries. Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (28). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (28).

On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (29). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (30).

Such genetic homogeneity also might be reflected in PRNP. Studies on PRNP variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep. In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (13). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.

The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock. https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article ;

***> IMPORTS AND EXPORTS <***

***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***


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.....


THE USA FDA MAD COW FEED BAN OF 1997 WAS NOTHING MORE THAN INK ON PAPER, NEVER ENFORCED...terry

SUNDAY, SEPTEMBER 1, 2019 

FDA Reports on VFD Compliance

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.


WEDNESDAY, JULY 31, 2019 

The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L


TUESDAY, JULY 30, 2019 

Guidelines for reporting surveillance data on Transmissible Spongiform Encephalopathies (TSE) in the EU within the framework of Regulation (EC) No 999/2001 APPROVED: 9 July 2019


In summary, our results establish aerosols as a surprisingly efficient modality of prion transmission. This novel pathway of prion transmission is not only conceptually relevant for the field of prion research, but also highlights a hitherto unappreciated risk factor for laboratory personnel and personnel of the meat processing industry. In the light of these findings, it may be appropriate to revise current prion-related biosafety guidelines and health standards in diagnostic and scientific laboratories being potentially confronted with prion infected materials. While we did not investigate whether production of prion aerosols in nature suffices to cause horizontal prion transmission, the finding of prions in biological fluids such as saliva, urine and blood suggests that it may be worth testing this possibility in future studies.



Adriano Aguzzi ''We even showed that a prion AEROSOL will infect 100% of mice within 10 seconds of exposure''

WOW!...tss

THURSDAY, AUGUST 08, 2019 

Raccoons accumulate PrPSc after intracranial inoculation with the agents of chronic wasting disease (CWD) or transmissible mink encephalopathy (TME) but not atypical scrapie


Bovine spongiform encephalopathy Update

Ray Bradley

Veterinary Laboratories Agency, New Haw, Addlestone, KT15 3NB, United Kingdom, Email: raybradley@btinternet.com

Received 8 July 2002, accepted 24 July 2002

snip...

TSE IN CAPTIVE WILD ANIMALS

TSE almost certainly related to BSE (but as yet not proven by experimental challenge) has been reported in five species of captive wild Felidae in Great Britain (GB) (Bradley 1997). These are: cheetah 5 cases (with five further cases in cheetah exported from the UK to Ireland (1), Australia (1) and France (2+1unknown)), lions 3, ocelots 3, pumas 3 and tigers 3. All of these are assumed to have been exposed following consumption of uncooked cattle carcasses containing infected central nervous tissue. This might have been present in heads, necks or other parts of the vertebral column. Protection was secured by the 1990 SBO ban and there have been very few cases that were born thereafter. TSE has also been reported in captive wild Bovidae in GB (Bradley 1997), but not elsewhere or in any natural environment inhabited by these animals. Eight species have been affected. In two, a nyala and a greater kudu, brain tissue has been inoculated into in-bred strains of mice. This shows the disease is experimentally transmissible and that the agent responsible is biologically indistinguishable from the BSE agent, i.e. it is of the same strain type (Bruce et al. 1994). The number of confirmed TSE by species is: Arabian oryx, bison, gemsbok, nyala and scimitar-horned oryx, one each; ankole, two; eland and greater kudu, six. All these species have presumably been exposed to infected MBM in concentrate diets that had similar formulations to those used in cattle feed before 1988. The reason for the cases occurring after 1988 (BAB cases) is, as in cattle, presumably cross contamination of diets with MBM intended for use in non-ruminant species. So far as records permit, no cases have been reported in animals born after January 1993.


BSE is considered to occur in 16 species: cattle, domestic cats, nyala and greater kudu (types of antelopes), gemsbok, eland, Arabian oryx, scimitar-horned oryx, ankole, bison, cheetah, lion, tiger, puma, ocelot and humans (brains from Variant Creutzfeldt-Jakob Disease (vCJD) patients). Other than feline spongiform encephalopathy (FSE) in domestic cats, all these are rare diseases in captive wild animals in the UK. Cases of FSE have also been found in cheetah in Ireland, France and Australia, but only in captive animals exported from the UK. There have not been any reports of naturally occurring cases of TSE in pigs or poultry. The spread of BSE is associated with concentrate feeding and the vehicle of infectivity was meat and bonemeal (MBM). There is continuing controversy on the origin of BSE. There were changes in rendering practices and evidence suggest this may have changed the evolution of the epidemic. 



 It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.
 
snip...

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). 

 
NEW URL ;
 



41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.
 
Histopathological support to various other published MAFF experiments
 
42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).
 


 It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.
 
snip...


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).


Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY Date: Thu, 17 Oct 2002 17:04:51 -0700 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: BSE-L

Greetings BSE-L,

is there any other CWD surveys/testing in the UK on their deer? what sort of testing has been done to date on UK/EU deer? any input would be helpful... thank you

DEER SPONGIFORM ENCEPHALOPATHY SURVEY

3. This will be a low key study with no publicity to avoid unnecessary media interest. It will be carried out in two stages ;

(I) A small scale examination of around 30 deer brains to establish the normal histology of the healthy brain; and

(II) A larger scale random examination of 300 or more adult deer brains drawn from both deer farms and parks to establish whether there is any evidence of a cervine spongiform encephalopathy. ...


Ministry of Agriculture Fisheries and Food Veterinary Investigation Centre West House. Station Road. Thirsk Y07 IPZ Telephone: 0845·522065 Fax: 0845·525224

Your reference

Our reference RJH/ASB

Date 4 November 1992

DEER SPONGIFORM ENCEPHALOPATHY SURVEY

Dear Paul

I have now found time to review the 10 deer- brains collected from Mr Walker farm··via Winchester Via Winchester VIC. In answer to your specific question was there sufficient difference in preservation of brain tissue to warrant the extra effort involved in rapid brain removal on the farm, the answer is definitely "Yes." The original five brains (Winchester ref M487/11) showed varying degrees of autolytic vacuolation affecting both white and grey matter throughout the brain. vacuolation and separation of Purkinje cells and marked perivascular spaces. These artifacts made interpretation of subtle, specific pathological vacuolation more difficult. By contrast the second submission (Winchester reference N736/2) showed excellent preservation of white and grey matter. Any vacuolar Change present could be confidently interpreted as pathological albeit of unknown pathogenesis.

I can only reiterate the comments made by Gerald Wells and myself at the preliminary discussion at Weybridge in Autumn 1991. If the survey's purpose is an accurate histopathological interpretation of brain tissue. the material must be collected in a pristine state. This is particularly valid when looking for ar unrecognised and undefined spongiform encephalopathy in a new species. Deer brains are very large structures which take a lot of fixation and therefore must be handled sympathetically from the start. We have already seen the problems encountered in comparatively smaller hound brains where delayed fixation was a major limitation on interpretation of true pathological change.

The bottom line must be that if a pathologist's expertise is to be used, it is critical to collect artefact free brain material. If the politics or economics do not allow this, then I would suggest that an electron microscopy survey in­volving detection of scrapie associated fibrils would be much more appropriate.

Best wishes Yours sincerely

R J HIGGINS VIO 92/11.4/2.1


HOUND SURVEY

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

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

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

J W WILESMITH Epidemiology Unit 18 October 1991

Mr. R Bradley

cc: Mr. G A H Wells


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


HOUND SURVEY PATHOLOGICAL REPORT (see positive results) and MAD DOGS AND ENGLISHMAN...

ya'll thought i was making this stuff up didn't ya...i don't make this stuff up!


It is clear that the designing scientists must also have shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.


second supplementary


snip...see history and full text here;

MONDAY, FEBRUARY 25, 2019

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


THURSDAY, DECEMBER 19, 2019 

The emergence of classical BSE from atypical/Nor98 scrapie


CWD WEBINAR CWD YESTERDAY! December 11, 2019

Dr. Mckenzie and CIDRAP on CWD TSE Prion



Texas CWD Symposium: Transmission by Saliva, Feces, Urine & Blood

the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.

https://www.youtube.com/watch?v=bItnEElzuKo&index=6&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj

''On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis. ''

Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS

See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...


WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO


cwd update on Wisconsin from Tammy Ryan...


Wyoming CWD Dr. Mary Wood

''first step is admitting you have a problem''

''Wyoming was behind the curve''

wyoming has a problem...


SATURDAY, JANUARY 19, 2019 

Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS


TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?

OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?

apparently, no ID though. tell me it ain't so please...

23:00 minute mark

''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''


Wyoming CWD Dr. Mary Wood

''first step is admitting you have a problem''

''Wyoming was behind the curve''

wyoming has a problem...


the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.


Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark... 


SATURDAY, JANUARY 19, 2019 

Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS 


for those that believe in all things stupid, like ted nugent, and say that cwd is not adversely affecting, look no further than Colorado, here's your sign...

Colorado Chronic Wasting Disease Response Plan December 2018

I. Executive Summary Mule deer, white-tailed deer, elk and moose are highly valued species in North America. Some of Colorado’s herds of these species are increasingly becoming infected with chronic wasting disease (CWD). As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds.

snip...

(the map on page 71, cwd marked in red, is shocking...tss)


ORIGIN OF CHRONIC WASTING DISEASE TSE PRION?

COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?

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

IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989


ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;

''it pains me to no end to even contemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end

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


Here is the latest on the cwd tse prion...terry

FRIDAY, NOVEMBER 08, 2019 

***> EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III


WEDNESDAY, NOVEMBER 20, 2019 

Sheep Are Susceptible to the Bovine Adapted Transmissible Mink Encephalopathy agent by Intracranial Inoculation and Have Evidence of Infectivity in Lymphoid Tissues

***> ''indicating that sheep inoculated with the bovine TME agent harbor infectivity in their lymph nodes despite a lack of detection with conventional immunoassays.''


WEDNESDAY, NOVEMBER 20, 2019 

Review: Update on Classical and Atypical Scrapie in Sheep and Goats


FRIDAY, NOVEMBER 15, 2019 

Southwest Wisconsin CWD, Deer and Predator Study


THURSDAY, OCTOBER 17, 2019 

Europe's uneven laws threaten scavengers and Spread Transmissible Spongiform Encephalopathy TSE Prion


TUESDAY, OCTOBER 29, 2019 

America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion


THURSDAY, DECEMBER 19, 2019 

TEXAS Val Verde County White-tailed Deer Tests Positive for Chronic Wasting Disease CWD TSE Prion State Positive NOW at 147 Confirmed


TUESDAY, DECEMBER 17, 2019 

Mississippi CWD TSE Prion Two confirmed cases with 10 more suspected this season to date


FRIDAY, DECEMBER 13, 2019 

Wisconsin New CWD Detection in a Wild Deer Harvested in Sheboygan County During the 2019 Archery Deer Season


FRIDAY, DECEMBER 13, 2019 

Tennessee CWD TSE Prion 2019 to 2020 Sample 148 Positive So Far


THURSDAY, DECEMBER 12, 2019 

Michigan Total CWD TSE Prion Positive Suspect-Positive Deer Jump To 162 confirmed to date


WEDNESDAY, DECEMBER 11, 2019 

South Dakota CWD TSE Prion Detected in Harding, Meade and Tripp Counties with 5 confirmed


TUESDAY, DECEMBER 10, 2019 

Minnesota MBAH confirms an 8-year-old white-tailed doe tested positive for CWD from hobbyist herd in Douglas County


SATURDAY, DECEMBER 07, 2019 

Montana Chronic wasting disease CWD TSE Prion explodes to 91 Cases This Year, with 25 of those confirmed last week


WEDNESDAY, NOVEMBER 27, 2019 

Montana records first suspected case of CWD in wild elk 


SATURDAY, DECEMBER 07, 2019 

Arkansas CWD-positive deer found in Independence County


MONDAY, DECEMBER 16, 2019 

Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update

***> ''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) <***

What if?


THURSDAY, DECEMBER 12, 2019 

Heidenhain Variant Creutzfeldt Jakob Disease hvCJD, sporadic spontaneous CJD and the TSE Prion December 14, 2019

22 years, rip mom dod 12/14/97 confirmed hvcjd, just made a promise to mom, and you don't break those promises, never forget, and never let them forget, before we all do...this pearl's for you! love terry


Terry S. Singeltary Sr.


at

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