P-147 Infection and detection of PrPCWD in soil from CWD infected farm in
Korea
Hyun Joo Sohn, Kyung Je Park, In Soon Roh, Hyo Jin Kim, Hoo Chang Park,
Byounghan Kim
Animal and Plant Quarantine Agency (QIA), Korea
Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative
disorder, which is so-called as prion diseases due to the causative agents
(PrPSc). TSEs are believed to be due to the template-directed accumulation of
disease-associated prion protein, generally designated PrPSc. Chronic wasting
disease (CWD) is the prion disease that is known spread horizontally. CWD has
confirmed last in Republic of Korea in 2010 since first outbreak of CWD in 2001.
The environmental reservoirs mediate the transmission of this disease. The
significant levels of infectivity have been detected in the saliva, urine, and
feces of TSE-infected animals. Using serial protein misfolding cyclic
amplification (sPMCA), we developed a detection method for CWD PrPSc in soil
from CWD affected farm in 2010. We found to detect PrPSc in soil from CWD
infected farm, but not detect PrPSc in soil of wild cervid habitats and normal
cervid farm in Korea. We also tried the bioassay on transgenic mice
overexpressing elk prion protein (TgElk mice) to confirm infectivity of
CWD-infected farm soil and washing solution of it. As the results, there was the
presence of infectious prions in them. The attack rates were each 12.5% (1/8,
soil) and 100% (6/6, soil washing solution). Our method appears to be a very
useful technique for monitoring PrPSc levels in environmental conditions.
P-153
Experimental oral transmission of chronic wasting disease to sika deer
(Cervus nippon)
Gordon Mitchell1, Hyun-Joo Sohn2, Yoon-Hee Lee2, Antanas Staskevicius1,
Nishandan Yogasingam1, Ines Walther1, In-Soo Cho2, Aru Balachandran1
1National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food
Inspection Agency, Ottawa, Ontario, Canada; 2Animal, Plant and Fisheries
Quarantine and Inspection Agency, Ministry for Food, Agriculture, Forestry and
Fisheries, Anyang, Republic of Korea
Chronic wasting disease (CWD) persists in North American cervids, and
epidemiological evidence indicates CWD was introduced into the Republic of Korea
approximately twenty years ago through the importation of an infected elk
(Cervus elaphus) from Canada. Additional cases of CWD have since been detected
in Korean elk, and recently for the first time in their farmed sika deer (Cervus
nippon). Sika deer are also found in regions of North America and Europe,
although natural transmission to these populations has not been detected.
Understanding the pathogenesis of CWD in this species is therefore essential to
developing diagnostic and disease control strategies.
Six sika deer were orally inoculated with a brain homogenate prepared from
a farmed Canadian elk with clinical CWD. Four deer developed clinical signs
consistent with CWD and were euthanized between 21 and 24 months
post-inoculation (mpi). Two deer were removed from the study due to intercurrent
disease, at 4 and 11 mpi. At necropsy, an array of tissues and bodily fluids
were sampled and preliminary testing of brainstem and lymphoid tissue by ELISA,
immunohistochemistry and western blot confirmed CWD transmission. Aggregates of
pathological prion protein (PrPCWD) were detected in the retropharyngeal lymph
nodes, but not brainstem of the deer sampled at 4 mpi. All other deer, including
the deer tested at 11 mpi, displayed marked PrPCWD accumulation in brainstem and
lymphoid tissues. Further immunohistochemical analysis of tissues from sika deer
with clinical disease revealed widespread PrPCWD deposition in Iymphoreticular
tissues, central and peripheral nervous systems, the gastrointestinal tract and
neuroendocrine tissues. Western blot molecular profiles in sika deer brainstem
samples were similar to the original elk inoculum. Ante-mortem biopsy of
recto-anal mucosal associated lymphoid tissue, tested using
immunohistochemistry, detected infected sika deer prior to the onset of clinical
disease. These findings corroborate studies in other cervids, identifying early
and widespread PrPCWD accumulation in tissues following oral inoculation.
Efficient transmission of CWD to sika deer dictates a precautionary approach
when exposing this species to environments or other cervids potentially infected
with CWD.
- 280-
spreading cwd around...
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of
farmed elk in Saskatchewan in a single epidemic. All of these herds were
depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease
eradication program. Animals, primarily over 12 mo of age, were tested for the
presence CWD prions following euthanasia. Twenty-one of the herds were linked
through movements of live animals with latent CWD from a single infected source
herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily
infected herds.
***The source herd is believed to have become infected via importation of
animals from a game farm in South Dakota where CWD was subsequently diagnosed
(7,4). A wide range in herd prevalence of CWD at the time of herd depopulation
of these herds was observed. Within-herd transmission was observed on some
farms, while the disease remained confined to the introduced animals on other
farms.
spreading cwd around...
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim,
Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research
Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion
disease in native North America deer and Rocky mountain elks. The disease is a
unique member of the transmissible spongiform encephalopathies (TSEs), which
naturally affects only a few species. CWD had been limited to USA and Canada
until 2000.
On 28 December 2000, information from the Canadian government showed that a
total of 95 elk had been exported from farms with CWD to Korea. These consisted
of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72
elk in 1997, which had been held in pre export quarantine at the “source
farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD
surveillance program was initiated by the Ministry of Agriculture and Forestry
(MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994
were impossible to identify. CWD control measures included stamping out of all
animals in the affected farm, and thorough cleaning and disinfection of the
premises. In addition, nationwide clinical surveillance of Korean native
cervids, and improved measures to ensure reporting of CWD suspect cases were
implemented.
Total of 9 elks were found to be affected. CWD was designated as a
notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and
2005.
Since February of 2005, when slaughtered elks were found to be positive,
all slaughtered cervid for human consumption at abattoirs were designated as
target of the CWD surveillance program. Currently, CWD laboratory testing is
only conducted by National Reference Laboratory on CWD, which is the Foreign
Animal Disease Division (FADD) of National Veterinary Research and Quarantine
Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the
human consumption was confirmed as positive. Consequently, all cervid – 54 elks,
41 Sika deer and 5 Albino deer – were culled and one elk was found to be
positive. Epidemiological investigations were conducted by Veterinary
Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary
services.
Epidemiologically related farms were found as 3 farms and all cervid at
these farms were culled and subjected to CWD diagnosis. Three elks and 5
crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and
confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were
linked to the importation of elks from Canada in 1994 based on circumstantial
evidences.
In December 2010, one elk was confirmed as positive at Farm 5.
Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer –
were culled and one Manchurian Sika deer and seven Sika deer were found to be
positive. This is the first report of CWD in these sub-species of deer.
Epidemiological investigations found that the owner of the Farm 2 in CWD
outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced
from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed
(species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as
negative.
SCWDS BRIEFS, January 2012, Vol. 27, No. 4
Several significant research developments have been reported recently. The
hypothesis that CWD may have originated from scrapie gained support from results
of a study conducted at the USDA
- 4 - Continued…
National Animal Disease Center. White-tailed deer were inoculated
intracerebrally (IC) or a natural route (orally and intranasally) with a scrapie
isolate from the U.S. All deer inoculated IC had PrPSc accumulation and three
deer necropsied after 20 months post-inoculation (MPI) had clinical signs, brain
lesions, and widespread distribution of PrPSc in neural and lymphoid tissues.
Similarities to CWD in the deer inoculated IC included an incubation period of
21-23 months, consistent clinical signs and distribution of PrPSc in tissues,
and western blots of obex tissue that showed a molecular profile consistent with
CWD and different from the inoculum. However, there were some differences in
microscopic findings commonly seen with CWD and those in the ICinoculated deer.
All deer inoculated by the natural route were susceptible to scrapie, developed
clinical signs, were necropsied 28-33 MPI, and had PrPSc in the brain and
several lymphoid tissues. Two molecular patterns were found in the brains of
deer inoculated by the natural route, but the pattern similar to the scrapie
inoculum predominated, unlike in the deer inoculated IC. This work presents
preliminary support for a link between scrapie and CWD, which may not only
explain CWD’s origin, but could possibly have implications for its management.
Additional information on the IC inoculation study can be found in Veterinary
Research 42: 107.
snip...
In addition, it was reported in May 2011 that natural cases of CWD were
found in eight Sika deer (Cervus nippon) and five Sika/red deer crossbreeds
during epidemiological investigations of CWD cases in captive elk in
Korea.
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer ***
Wednesday, May 25, 2016
USDA APHIS National Scrapie TSE Prion Eradication Program April 2016
Monthly Report Prion 2016 Tokyo Update
Thursday, May 26, 2016 TPWD Action CWD Response Rules Recommended Adoption
of Proposed Rules May 26, 2016 But Instead Caves To Breeders and Postponed
Implementation http://chronic-wasting-disease.blogspot.com/2016/05/action-cwd-response-rules-recommended.html
Sunday, May 22, 2016
TEXAS CWD DEER BREEDERS PLEA TO GOVERNOR ABBOTT TO CIRCUMVENT TPWD SOUND
SCIENCE TO LET DISEASE SPREAD
Wednesday, May 11, 2016
CERVID TO HUMAN PRION TRANSMISSION PRION 2016 TOKYO UPDATE
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
IL-13 Transmission of prions to non human-primates: Implications for human
populations
Jean-Philippe Deslys, Emmanuel E. Comoy
CEW, Institute of Emerging Diseases and Innovative Therapies (iMETI),
Division of Prions and Related Diseases (SEPIA), Fontenay-aux-Roses, France
Prion diseases 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 prion
disease might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, prion diseases, like the other
proteinopathies, are reputed to occur spontaneously (atypical animal prion
strains, sporadic CJD summing 80 % of human prion cases).
Non-human primate models provided the first evidences supporting the
transmissibility of human prion strains and the zoonotic potential of BSE. Among
them, cynomolgus macaques brought major information for BSE risk assessment for
human health1, according to their phylogenetic proximity to humans and extended
lifetime. We used this model to assess the risk of primary (oral) and secondary
(transfusional) risk of BSE, and also the zoonotic potential of other animal
prion diseases 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' . longer incubation than BSE2. Scrapie, as recently evoked in
humanized mice3, is the third potentially zoonotic prion disease (with BSE and
L-type BSE4), thus questioning the origin of human sporadic cases. We also
observed hidden prions transmitted by blood transfusion in primate which escape
to the classical diagnostic methods and extend the field of healthy carriers. We
will present an updated panorama of our different long-term transmission studies
and discuss the implications on risk assessment of animal prion diseases for
human health and of the status of healthy carrier5.
1. Chen, C. C. & Wang, Y. H. Estimation of the Exposure of the UK
Population to the Bovine Spongiform Encephalopathy Agent through Dietary Intake
During the Period 1980 to 1996. PLoS One 9, e94020 (2014).
2. Comoy, E. E. et al. Transmission of scrapie prions to primate after an
extended silent incubation period. Sci Rep 5, 11573 (2015).
3. Cassard, H. et al. Evidence for zoonotic potential of ovine scrapie
prions. Nat Commun 5, 5821-5830 (2014).
4. Comoy, E. E. et al. Atypical BSE (BASE) transmitted from asymptomatic
aging cattle to a primate. PLoS One 3, e3017 (2008).
5. Gill O. N. et al. Prevalent abnormal prion protein in human appendixes
after bovine spongiform encephalopathy epizootic: large scale survey. BMJ. 347,
f5675 (2013).
Curriculum Vitae
Dr. Deslys co-authored more than one hundred publications in international
scientific journals on main aspects of applied prion research (diagnostic,
decontamination techniques, risk assessment, and therapeutic approaches in
different experimental models) and on underlying pathological mechanisms. He
studied the genetic of the first cases of iatrogenic CJD in France. His work has
led to several patents including the BSE (Bovine Spongiform Encephalopathy)
diagnostic test most widely used worldwide. He also wrote a book on mad cow
disease which can be downloaded here for free (http://www.neuroprion.org/pdf_docs/documentation/madcow_deslys.pdf).
His research group is Associate Laboratory to National Reference Laboratory for
CJD in France and has high security level microbiological installations
(NeuroPrion research platform) with different experimental models (mouse,
hamster, macaque). The primate model of BSE developed by his group with
cynomolgus macaques turned out to mimick remarkably well the human situation and
allows to assess the primary (oral) and secondary (transfusional) risks linked
to animal and human prions even after very long silent incubation periods. For
several years, his interest has extended to the connections between PrP and
Alzheimer and the prion mechanisms underlying neurodegenerative diseases. He is
coordinating the NeuroPrion international association (initially european
network of excellence now open to all prion researchers).
- 59-
P-088 Transmission of experimental CH1641-like scrapie to bovine PrP
overexpression mice
Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1,
Takashi Yokoyama2
1Influenza and Prion Disease Research Center, National Institute of Animal
Health, NARO, Japan; 2Department of Planning and General Administration,
National Institute of Animal Health, NARO
Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke
scrapie is characterized by a lower molecular mass of the unglycosylated form of
abnormal prion protein (PrpSc) compared to that of classical scrapie. It is
worthy of attention because of the biochemical similarities of the Prpsc from
CH1641-like and BSE affected sheep. We have reported that experimental
CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice
(Yokoyama et al. 2010). We report here the further details of this transmission
study and compare the biological and biochemical properties to those of
classical scrapie affected TgBoPrP mice.
Methods: The details of sheep brain homogenates used in this study are
described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were
intracerebrally inoculated with a 10% brain homogenate of each scrapie strain.
The brains of mice were subjected to histopathological and biochemical analyses.
Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice
was similar to that of classical scrapie affected mice. Mean survival period of
CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it
was significantly shorter than that of classical scrapie affected mice (439
days). Lesion profiles and Prpsc distributions in the brains also differed
between CH1641-like and classical scrapie affected mice.
Conclusion: We succeeded in stable transmission of CH1641-like scrapie to
TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is
likely to be more virulent than classical scrapie in cattle.
WS-02
Scrapie in swine: A diagnostic challenge
Justin J Greenlee1, Robert A Kunkle1, Jodi D Smith1, Heather W. Greenlee2
1National Animal Disease Center, US Dept. of Agriculture, Agricultural
Research Service, United States; 2Iowa State University College of Veterinary
Medicine
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.
Since swine can be fed rations containing ruminant derived components in
the United States and many other countries, we conducted this experiment to test
the susceptibility of swine to U.S. scrapie isolates by intracranial and oral
inoculation. Scrapie inoculum was a pooled 10% (w/v) homogenate derived from the
brains of clinically ill sheep from the 4th passage of a serial passage study of
the U.S scrapie agent (No. 13-7) through susceptible sheep that were homozygous
ARQ at prion protein residues 136, 154, and 171, respectively. Pigs were
inoculated intracranially (n=19) with a single 0.75 ml dose or orally (n=24)
with 15 ml repeated on 4 consecutive days. Necropsies were done on a subset of
animals at approximately six months post inoculation (PI), at the time the pigs
were expected to reach market weight. Remaining pigs were maintained and
monitored for clinical signs of TSE until study termination at 80 months PI or
when removed due to intercurrent disease (primarily lameness). Brain samples
were examined by immunohistochemistry (IHC), western blot (WB), and
enzyme-linked immunosorbent assay (ELISA). Brain tissue from a subset of pigs in
each inoculation group was used for bioassay in mice expressing porcine PRNP.
At six-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 methods: IHC (n=4), WB (n=3), or ELISA (n=5).
Interestingly, positive bioassay results were obtained from all inoculated
groups (oral and intracranial; market weight and end of study).
Swine inoculated with the agent of scrapie by the intracranial and oral
routes do not accumulate abnormal prion protein (PrPSc) to a level detectable by
IHC or WB by the time they reach typical market age and weight. However, strong
support for the fact that swine are potential hosts for the agent of scrapie
comes from positive bioassay from both intracranially and orally inoculated pigs
and multiple diagnostic methods demonstrating abnormal prion protein in
intracranially inoculated pigs with long incubation times.
Curriculum Vitae
Dr. Greenlee is Research Veterinary Medical Officer in the Virus and Prion
Research Unit at the National Animal Disease Center, US Department of
Agriculture, Agricultural Research Service. He applies his specialty in
veterinary anatomic pathology to focused research on the intra- and interspecies
transmission of prion diseases in livestock and the development of antemortem
diagnostic assays for prion diseases. In addition, knockout and transgenic mouse
models are used to complement ongoing experiments in livestock species. Dr.
Greenlee has publications in a number of topic areas including prion agent
decontamination, effects of PRNP genotype on susceptibility to the agent of
sheep scrapie, characterization of US scrapie strains, transmission of chronic
wasting disease to cervids and cattle, features of H-BSE associated with the
E211 K polymorphism, and the development of retinal assessment for antemortem
screening for prion diseases in sheep and cattle. Dr. Greenlee obtained his DVM
degree and completed the PhD/residency program in Veterinary Pathology at Iowa
State University. He is a Diplomate of the American College of Veterinary
Pathologists.
Wednesday, May 25, 2016
USDA APHIS National Scrapie TSE Prion Eradication Program April 2016
Monthly Report Prion 2016 Tokyo Update
see more here from PRION2015 Ft. Collins and more on zoonotic CWD ;
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
with CWD TSE Prions, I am not sure there is any absolute yet, other than
what we know with transmission studies, and we know tse prion kill, and tse
prion are bad. science shows to date, that indeed soil, dirt, some better than
others, can act as a carrier. same with objects, farm furniture. take it with
how ever many grains of salt you wish, or not. if load factor plays a role in
the end formula, then everything should be on the table, in my opinion. see
;
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
see ;
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil
Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable
neurological diseases likely caused by a misfolded form of the prion protein.
TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’
disease) in cattle, chronic wasting disease in deer and elk, and
Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are
unique among TSEs because they can be transmitted between animals, and the
disease agents appear to persist in environments previously inhabited by
infected animals. Soil has been hypothesized to act as a reservoir of
infectivity and to bind the infectious agent. In the current study, we orally
dosed experimental animals with a common clay mineral, montmorillonite, or whole
soils laden with infectious prions, and compared the transmissibility to unbound
agent. We found that prions bound to montmorillonite and whole soils remained
orally infectious, and, in most cases, increased the oral transmission of
disease compared to the unbound agent. The results presented in this study
suggest that soil may contribute to environmental spread of TSEs by increasing
the transmissibility of small amounts of infectious agent in the
environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
>>>Particle-associated PrPTSE molecules may migrate from locations
of deposition via transport processes affecting soil particles, including
entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several
years. Significant interest remains in developing methods that could be applied
to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests
that serine proteases and the microbial consortia in stimulated soils and
compost may partially degrade PrPTSE. Transition metal oxides in soil (viz.
manganese oxide) may also mediate prion inactivation. Overall, the effect of
prion attachment to soil particles on its persistence in the environment is not
well understood, and additional study is needed to determine its implications on
the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding,
inferring a durable environmental reservoir, and an efficient mechanism for
indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
>>>Another alternative would be an absolute prohibition on the
movement of deer within the state for any purpose. While this alternative would
significantly reduce the potential spread of CWD, it would also have the
simultaneous effect of preventing landowners and land managers from implementing
popular management strategies involving the movement of deer, and would deprive
deer breeders of the ability to engage in the business of buying and selling
breeder deer. Therefore, this alternative was rejected because the department
determined that it placed an avoidable burden on the regulated
community.<<<
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben
C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and
animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk
are contagious prion diseases where environmental reservoirs have a direct link
to the transmission of disease. Using protein misfolding cyclic amplification we
demonstrate that scrapie PrPSc can be detected within circulating dusts that are
present on a farm that is naturally contaminated with sheep scrapie. The
presence of infectious scrapie within airborne dusts may represent a possible
route of infection and illustrates the difficulties that may be associated with
the effective decontamination of such scrapie affected premises.
snip...
Discussion
We present biochemical data illustrating the airborne movement of scrapie
containing material within a contaminated farm environment. We were able to
detect scrapie PrPSc within extracts from dusts collected over a 70 day period,
in the absence of any sheep activity. We were also able to detect scrapie PrPSc
within dusts collected within pasture at 30 m but not at 60 m distance away from
the scrapie contaminated buildings, suggesting that the chance of contamination
of pasture by scrapie contaminated dusts decreases with distance from
contaminated farm buildings. PrPSc amplification by sPMCA has been shown to
correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to
assume that faecal, urine, skin, parturient material and saliva-derived prions
may contribute to this mobile environmental reservoir of infectivity. This work
highlights a possible transmission route for scrapie within the farm
environment, and this is likely to be paralleled in CWD which shows strong
similarities with scrapie in terms of prion dissemination and disease
transmission. The data indicate that the presence of scrapie prions in dust is
likely to make the control of these diseases a considerable challenge.
Saturday, October 03, 2015
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO
2015
Thursday, September 24, 2015
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE
Prion Testing
*** I cannot stress enough to all of you, for the sake of your family and
mine, before putting anything in the freezer, have those deer tested for CWD.
...terry
***raw and uncut
Sunday, August 23, 2015
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig
and take her to the dance in Texas
Friday, August 07, 2015
*** Texas CWD Captive, and then there were 4 ?
Thursday, August 06, 2015
*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Thursday, July 09, 2015
TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed
Herd with Testing of Exposed Animals
Wednesday, July 01, 2015
TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Wednesday, March 18, 2015
Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18,
2015
Wednesday, March 25, 2015
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Thursday, May 02, 2013
*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY
TEXTING
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West
Texas
2011 – 2012
Friday, October 28, 2011
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
Greetings TAHC et al,
A kind greetings from Bacliff, Texas.
In reply to ;
Texas Animal Health Commission (TAHC) Announcement October 27, 2011
I kindly submit the following ;
***for anyone interested, here is some history of CWD along the Texas, New
Mexico border, and my attempt to keep up with it...terry
snip...
see history CWD Texas, New Mexico Border ;
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
Sunday, October 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009 2009 Summary of Chronic
Wasting Disease in New Mexico New Mexico Department of Game and Fish
These results suggest that cattle experimentally inoculated with CWD may
have some limited amount of prion infectivity outside of the brain and spinal
cord that may represent a previously unrecognized risk for transmission. This
information could have an impact on regulatory officials developing plans to
reduce or eliminate TSEs and farmers with concerns about ranging cattle on areas
where CWD may be present.
Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease - (Abstract Only) -
(12-Aug-15) Transmission of chronic wasting disease to sentinel reindeer
(Rangifer tarandus tarandus) - (Abstract Only) - (12-Aug-15) Transmission of
scrapie prions to primate after an extended silent incubation period - (Peer
Reviewed Journal) Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573. Transmission of the agent of
sheep scrapie to deer results in PrPSc with two distinct molecular profiles -
(Abstract Only) Greenlee, J., Moore, S.J., Smith, J.., West Greenlee, M.H.,
Kunkle, R. 2015. Scrapie transmits to white-tailed deer by the oral route and
has a molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum. Prion 2015. p. S62.
Monday, April 04, 2016
Limited amplification of chronic wasting disease prions in the peripheral
tissues of intracerebrally inoculated cattle
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
J Vet Diagn Invest 20:698–703 (2008)
Chronic wasting disease in a Wisconsin white-tailed deer farm
Delwyn P. Keane,1 Daniel J. Barr, Philip N. Bochsler, S. Mark Hall, Thomas
Gidlewski, Katherine I. O’Rourke, Terry R. Spraker, Michael D. Samuel
Abstract.
In September 2002, chronic wasting disease (CWD), a prion disorder of
captive and wild cervids, was diagnosed in a white-tailed deer (Odocoileus
virginianus) from a captive farm in Wisconsin. The facility was subsequently
quarantined, and in January 2006 the remaining 76 deer were depopulated. Sixty
animals (79%) were found to be positive by immunohistochemical staining for the
abnormal prion protein (PrPCWD) in at least one tissue; the prevalence of
positive staining was high even in young deer. Although none of the deer
displayed clinical signs suggestive of CWD at depopulation, 49 deer had
considerable accumulation of the abnormal prion in the medulla at the level of
the obex. Extraneural accumulation of the abnormal protein was observed in 59
deer, with accumulation in the retropharyngeal lymph node in 58 of 59 (98%), in
the tonsil in 56 of 59 (95%), and in the rectal mucosal lymphoid tissue in 48 of
58 (83%). The retina was positive in 4 deer, all with marked accumulation of
prion in the obex. One deer was considered positive for PrPCWD in the brain but
not in the extraneural tissue, a novel observation in white-tailed deer. The
infection rate in captive deer was 20- fold higher than in wild deer. Although
weakly related to infection rates in extraneural tissues, prion genotype was
strongly linked to progression of prion accumulation in the obex. Antemortem
testing by biopsy of recto– anal mucosal-associated lymphoid tissue (or other
peripheral lymphoid tissue) may be a useful adjunct to tonsil biopsy for
surveillance in captive herds at risk for CWD infection.
Key words: Cervids; chronic wasting disease; prion; transmissible
spongiform encephalopathy.
State pays farmer $298,000 for infected deer herd
Jan. 16, 2016 8:05 p.m.
The State of Wisconsin paid nearly $300,000 to the Eau Claire County farmer
whose deer herd was depopulated after it was found to be infected with chronic
wasting disease.
Rick Vojtik, owner of Fairchild Whitetails in Fairchild, received an
indemnity payment of $298,770 for 228 white-tailed deer killed on his farm,
according to officials with the Department of Agriculture, Trade and Consumer
Protection.
The money was taken from the agency's general program revenue funded by
Wisconsin taxpayers.
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after gaining approval
from surrounding landowners, and confirmed that the fenced had been cut or
removed in at least four separate locations; that the fence had degraded and was
failing to maintain the enclosure around the Quarantined Premises in at least
one area; that at least three gates had been opened;and that deer tracks were
visible in and around one of the open areas in the sand on both sides of the
fence, evidencing movement of deer into the Quarantined Premises.
The overall incidence of clinical CWD in white-tailed deer was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
HOW IS CWD AND WHAT ABOUT THOSE GAME FARMS IN WISCONSIN, HOW IS THAT
WORKING OUT ?
Monday, May 16, 2016
Governor Walker Announces Several Initiatives to Combat Chronic Wasting
Disease in Wisconsin
Sunday, May 08, 2016
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE
ABYSS UPDATE
Wednesday, February 10, 2016
*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD
***
Sunday, January 17, 2016
*** Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of
$298,770 for 228 white-tailed deer killed on farm ***
http://chronic-wasting-disease.blogspot.com/2016/01/wisconsin-captive-cwd-lotto-pays-out.html
Sunday, May 08, 2016
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE
ABYSS UPDATE
http://chronic-wasting-disease.blogspot.com/2016/05/wisconsin-chronic-wasting-disease-cwd.html
Tuesday, May 03, 2016
Arkansas Chronic Wasting Disease CWD TSE Prion and Elk Restoration Project
and Hunkering Down in the BSE Situation Room USDA 1998
Monday, April 25, 2016
Arkansas AGFC Phase 2 sampling reveals CWD positive deer in Madison and
Pope counties
Tuesday, April 19, 2016
Arkansas First Phase of CWD sampling reveals 23 percent prevalence rate in
focal area With 82 Confirmed to Date
http://chronic-wasting-disease.blogspot.com/2016/04/arkansas-first-phase-of-cwd-sampling.html
Wednesday, May 11, 2016
PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL
CONTROL MEASURES
Friday, April 22, 2016
Missouri MDC finds seven new cases of ChronicWasting Disease CWD during
past‐season testing
Friday, April 22, 2016
COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM IS MINIMAL AND LIMITED
KANSAS CWD CASES ALARMING
Wednesday, March 02, 2016 Kansas Chronic Wasting Disease CWD TSE Prion 52
cases 2015 updated report 'ALARMING'
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
Sunday, May 22, 2016
Arkansas Commission approves hunting regulations, hears new proposals for
CWD management
I could go on, for more see ;
Thursday, March 31, 2016
*** Chronic Wasting Disease CWD TSE Prion Roundup USA April 1, 2016
***
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
*** Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from
Deer and Elk in Animal Feed Singeltary Submission ***
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards
Singeltary Comment Submission
Sunday, March 20, 2016
*** UPDATED MARCH 2016 URGENT Docket No. FDA-2003-D-0432 (formerly
03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
Monday, April 11, 2016
*** DECLARATION OF EXTRAORDINARY EMERGENCY DUE TO A FOREIGN ANIMAL DISEASE
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION CHRONIC WASTING DISEASE CWD IN
THE UNITED STATES AND NORTH AMERICA ?
From: Terry S. Singeltary Sr.
Sent: Saturday, February 06, 2016 12:11 PM
To: SACAH.Management@aphis.usda.gov
Subject: Secretary's Advisory Committee on Animal Health; Meeting [Docket
No. APHIS-2016-0007] Singeltary Submission
Hello Mrs. R.J. Cabrera and USDA et al,
I would kindly like to submit and comment on the Secretary's Advisory
Committee on Animal Health; Meeting [Docket No. APHIS-2016-0007] ;
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
snip...see full text ;
*** SEE CWD HIGH INFECTION RATE MAPS FOR COLORADO ! ***
Friday, May 27, 2016
Canine Prions: A New Form of Prion Disease EP-021 PRION 2016 TOKYO
Monday, May 09, 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
Tuesday, May 10, 2016
2015 PDA Virus & TSE Safety Forum Meeting Report
>>>Recently transmission of prions from blood of patients with
sporadic CJD to humanized mice could be demonstrated.<<<
>>>Further-on, urine samples of a control population (normal and
neurological population) showed no signal in the study; *** however, in samples
from patients with sporadic CJD and vCJD, a signal was detected in both patient
populations.<<<
Meeting Report: 2015 PDA Virus & TSE Safety Forum
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild ***
Wednesday, January 20, 2016
Exportation of Live Animals, Hatching Eggs, and Animal Germplasm From the
United States [Docket No. APHIS-2012-0049] RIN 0579-AE00 2016-00962
Transmissible Spongiform Encephalopthy TSE Prion Disease
*** Kuru Video
Kuru: The Science and The Sorcery
*** Scrapie Video
*** Human Mad Cow Video
*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video
2014
***Moreover, L-BSE has been transmitted more easily to transgenic mice
overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
***It has been suggested that some sporadic CJD subtypes in humans may
result from an exposure to the L-BSE agent.
*** Lending support to this hypothesis, pathological and biochemical
similarities have been observed between L-BSE and an sCJD subtype (MV genotype
at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and
another sCJD subtype (MM genotype) [15].
snip...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far
*** but the possibility that a small proportion of human cases so far
classified as "sporadic" CJD are of zoonotic origin could not be excluded.
*** Moreover, transmission experiments to non-human primates suggest that
some TSE agents in addition to Classical BSE prions in cattle (namely L-type
Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME)
and chronic wasting disease (CWD) agents) might have zoonotic potential.
snip...
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
*** Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
*** These atypical BSE cases constitute an unforeseen first threat that
could sharply modify the European approach to prion diseases.
Second threat
snip...
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
in June 2014 confirmed as USA case NOT European ***
Monday, November 3, 2014
USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014
National Prion Disease Pathology Surveillance Center Cases Examined1
(October 7, 2014)
***6 Includes 11 cases in which the diagnosis is pending, and 19
inconclusive cases;
***7 Includes 12 (11 from 2014) cases with type determination pending in
which the diagnosis of vCJD has been excluded.
***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob
disease (sCJD),
***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)
***and 21 cases of sporadic Fatal Insomnia (sFI).
Subject: *** Becky Lockhart 46, Utah’s first female House speaker, dies
diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type
disease
what is CJD ? just ask USDA inc., and the OIE, they are still feeding the
public and the media industry fed junk science that is 30 years old.
why doesn’t some of you try reading the facts, instead of rubber stamping
everything the USDA inc says.
sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and
there is much concern now for CWD and risk factor for humans.
My sincere condolences to the family and friends of the House Speaker Becky
Lockhart. I am deeply saddened hear this.
with that said, with great respect, I must ask each and every one of you
Politicians that are so deeply saddened to hear of this needless death of the
Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am
seriously going to ask you all this...I have been diplomatic for about 17 years
and it has got no where. people are still dying. so, are you all stupid or
what??? how many more need to die ??? how much is global trade of beef and other
meat products that are not tested for the TSE prion disease, how much and how
many bodies is this market worth?
Saturday, January 17, 2015
*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed
with the extremely rare Creutzfeldt-Jakob disease
*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report ***
Thursday, January 15, 2015
41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE
Prion: Case Report
Thursday, April 14, 2016
*** Arizona 22 year old diagnosed with Creutzfeldt Jakob Disease CJD
Aired on 27 Jun 2011
Interview with Terry Singeltaryv Sr., founder of CJD Watch, a USA-based
non-profit organization which tracks occurrences of and raises awareness about
Creutzfeldt-Jakob Disease (CJD), a neurological condition which has no known
cure and is always fatal. We learn that meat consumption heightens the risk of
contracting prion-related diseases.
*** Creutzfeldt-Jakob Disease Public Health Crisis VIDEO
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
snip...
I asked someone recently, what sort of hunting legacy do you want to leave
your children, did you want to have where all you have are blind, slobbering,
drooling, stumbling, or maybe even healthy looking subclinical cwd infected
cervid, to go on and expose who knows what (cause cwd is spreading, it has
mutated, and nobody can stop it so far), but is this what we want to leave our
children? the only answer I ever seem to get from anyone in the industry, is
just let cwd take care of itself. well hell, how is that working for us so
far?
this cwd tse prion must be stopped. the vertical and lateral transmission
of this cwd tse prion agent amongst cervids, if cwd jumps species (if it has not
already), and transmits the same ways vertical and lateral in other species, and
the other species are as susceptible from so many different routes and sources,
simply put, we’re screwed. just saying. I am not trying to scare anyone, I am
simply presenting the facts, you must make your own decision or not. we have
ignored these tse prion disease way too long.
these blogs are for educational use. I do not advertise or make money from
them.
MOM DOD 12/14/97 confirmed hvCJD, just made a promise to mom, never forget,
and never let them forget...
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
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