Pennsylvania 'Unprecedented' level of chronic wasting disease found on Reynoldsville farm
'Unprecedented' level of chronic wasting disease found on Reynoldsville
farm
By Bob Frye Monday, Aug. 25, 2014, 6:51 p.m. Updated less than a minute
ago
Researchers from around the country are getting to study chronic wasting
disease because of an “unprecedented” find.
Officials with the Pennsylvania Department of Agriculture announced in
April that a 5-year-old captive deer on a farm in Reynoldsville, Jefferson
County, tested positive for the disease. Subsequent testing of the deer on the
farm found six more with CWD.
That doubled the number of cases in the state, which now stands at 14.
“This is an unprecedented level of infection in a captive deer herd,”
agriculture secretary George Greig said.
snip...
Sunday, August 24, 2014
USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program
Goals TSE PRION October 17 – 23, 2013
Thursday, July 31, 2014
Pennsylvania Helps State and National Researchers Combat Chronic Wasting
Disease
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CHRONIC WASTING DISEASE CWD
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM
Sunday, July 13, 2014
Louisiana deer mystery unleashes litigation 6 does still missing from CWD
index herd in Pennsylvania Great Escape
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO
LOUISIANA and INDIANA
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd
Pennsylvania Update May 28, 2013
*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana,
quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
Saturday, June 29, 2013
*** PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE
IN INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN
LOUISIANA
Tuesday, June 11, 2013
*** CWD GONE WILD, More cervid escapees from more shooting pens on the
loose in Pennsylvania
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
”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.
Saturday, February 04, 2012
*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of fawns
sampled were between the ages of 5 to 9 months, though some were as young as 1
month.
*** Two of the six fawns with CWD detected were 5 to 6 months old.
All six of the positive fawns were taken from the core area of the CWD
eradication zone where the highest numbers of positive deer have been
identified.
Saturday, February 04, 2012
*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
Infectious agent of sheep scrapie may persist in the environment for at
least 16 years
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Sunday, September 01, 2013
hunting over gut piles and CWD TSE prion disease
Sunday, April 13, 2014
Mineral licks: motivational factors for visitation and accompanying disease
risk at communal use sites of elk and deer
Environmental Geochemistry and Health
Monday, June 18, 2012
natural cases of CWD in eight Sika deer (Cervus nippon) and five Sika/red
deer crossbreeds captive Korea and Experimental oral transmission to red deer
(Cervus elaphus elaphus)
spreading cwd around...tss
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...tss
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea 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.
: Corresponding author: Dr. Hyun-Joo Sohn (+82-31-467-1867, E-mail:
shonhj@korea.kr) 2011 Pre-congress Workshop: TSEs in animals and their
environment 5
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
snip...see more here ;
Wednesday, July 23, 2014
After the storm? UK blood safety and the risk of variant Creutzfeldt-Jakob
Disease
never say never when it comes to TSE prion disease.
85%+ of all human TSE prion disease i.e. sporadic CJD’s, have never been
proven scientifically to be of any spontaneous nature. not one single case.
sporadic CJDs simply mean unknown to date.
all iatrogenic CJD is, is sporadic cjd, until route and source of said
iatrogenic event took place, documented, and put in the academic/public domain,
and that vary rarely happens. any human TSE from any other species might just
look like any of the sub-types of the sporadic CJD’s. there has already been
documentation of other animals TSE prion disease related very closely to some
sub-types of CJD, i.e. atypical BSE, Scrapie, and atypical Nor-98 Scrapie.
please remember what was said long ago by one of the top prion Gods ;
> In the Archives of Neurology you quoted (the abstract of which was
attached to your email), we did not say CWD in humans will present like variant
CJD.
That assumption would be wrong.
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article
and call me if you have questions or need more clarification (phone:
404-639-3091). Also, we do not claim that "no-one has ever been infected with
prion disease from eating venison." Our conclusion stating that we found no
strong evidence of CWD transmission to humans in the article you quoted or in
any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
MY point, if there was a horizontal lateral transmission possibility from
animal to man, with the surveillance for both human and animal TSE prion disease
in the USA, in my honest opinion, they would never know it, and the only few
cases that have been documented, could be a direct result of horizonatl lateral
transmission, or not, just a happenstance of bad luck, a chance happening. so,
in my opinion, we cannot rule anything out.
the USA does not even test cats or dogs for TSE prion disease, and they
have been used in pet food, along with other animal carcasses. in fact, it is
still legal to take a deer from a cwd endemic area, and use it in animal feed.
only thing you cannot use, is a CWD positive deer. don’t believe me, see ;
> 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.
but, when felines get a TSE prion disease, it’s Feline Spongiform
Encephalopathy i.e. FSE, there is one documented case of sporadic CJD in a man
and his cat. ...just saying.
SEE CJD IN MAN AND HIS CAT ;
Research letters Volume 352, Number 9134 3 October 1998
Simultaneous occurrence of spongiform encephalopathy in a man and his cat
in Italy
We report the simultaneous occurrence of sporadic CJD in a man and a new
variety of FSE in his cat.
snip...
This study shows a spatio-temporal association between human and feline
prion diseases. The clinical features of the cat were different from previously
reported cases of FSE which were characterised by gradual onset of behavioural
changes preceding locomotor dysfunction and ataxia.5 Neuropathological changes
were also at variance with the diffuse spongiosis and vacuolation of brainstem
neurons, seen in FSE.5 The synaptic pattern of PrP deposition, similar in the
cat and in the patient, was atypical for a BSE-related condition. Evidence of a
new type of FSE was further provided by the detection of a type-1 PrPres, other
than the BSE-associated type 4.2 Taken together, our data suggest that the same
agent strain of sporadic CJD was involved in the patient and in his cat.
It is unknown whether these TSE occurred as the result of horizontal
transmission in either direction, infection from an unknown common source, or
the chance occurrence of two sporadic forms.
Terry S. Singeltary Sr. wrote:
Greetings list members,
ODD that some FELINE in Italy seem to have this same or maybe very similar
phenotype of TSE;
In October 1998 the simultaneous occurrence of spongiform encephalopathy in
a man and his pet cat was reported. The report from Italy noted that the cat did
not display the same clinical features as FSE cases previously seen. Indeed, the
presence of a new type of FSE was suggested. The man was diagnosed as having
sporadic CJD, and neither case (man nor cat) appeared to be affected by a
BSE-related condition.
Case‐to‐case transmission in humans: case reports and series in which
spread through everyday human contact is suggested
There are six reports in which this possible mode of transmission is
considered. The most recent is that of a couple from the USA who had been
married for 30 years.47 The husband died at age 53. He had no relevant family
history, but had had a rotator cuff repair one year before disease onset. His
wife developed symptoms four and half years after her husband's death. She was
morbidly obese and had had a previous hysterectomy, hernia repair and
cholecystectomy. Both occasionally ate brains in the form of ‘kizka’, a type of
sausage.
Immunocytochemistry confirmed pathogenic prion protein deposition in brain
tissue from both husband and wife. Full sequencing of the open reading frame of
the PRNP failed to demonstrate any pathogenic mutations.
Another suspected conjugal case has recently been shown not to be CJD. The
histopathological specimens did not stain for prion protein despite the
microscopic appearance of spongiform change.48
Sporadic CJD has been described in two co‐workers who shared a school wing
for 9 months.49 The first was a 48‐year‐old Californian‐born man of Hispanic
American descent who had had a traumatic leg amputation at age 23, but was
otherwise well. The second was a 48‐year‐old Chilean‐born male who had a blood
transfusion 6 months before onset of symptoms, and was known to eat lambs'
brains. The first patient developed symptoms 5 months after the last contact
with his colleague and was confirmed to have spCJD 2 months after this. The
second patient developed symptoms months later and died 9 months after the last
contact with his colleague.
An English woman, who died of CJD, histologically confirmed at post mortem,
was known to have contact with several affected members of a family with
familial CJD and was related to them by marriage.39 She had known one of the
family, who later died of CJD and had afternoon tea with her at family
gatherings, twice a year, for 20 years, as well as visiting in her final
illness. The woman herself died 12 years later.
There is another similar case of probable CJD, reported in a Chilean woman
who died 13 years after contact with a family with familial CJD. No details of
contact are given.
A third case of death from CJD in someone related in marriage to a family
with familial CJD has been reported in France, in a Tunisian family. No details
are given with regards to family history or contact.21
What is notable about these last three incidents of supposed infection by
social contact is that all have occurred in association with familial CJD.
Although these patients were not known to have been genetically related to their
spouses, the possibility that they came from the same gene pool cannot be
dismissed.
Simultaneous Onset of Alzheimer's Disease in a Husband and Wife in Their
Mid Fifties: What do We Really Know?
NEUROLOGY 1998;50:684-688 © 1998 American Academy of Neurology
Creutzfeldt-Jakob disease in a husband and wife
A 53-year-old man died of sporadic Creutzfeldt-Jakob disease (CJD) after a
1.5-year clinical course. Four and a half years later, his then 55-year-old
widow died from CJD after a 1-month illness. Both patients had typical clinical
and neuropathologic features of the disease, and pathognomonic
proteinase-resistant amyloid protein ("prion" protein, or PrP) was present in
both brains. Neither patient had a family history of neurologic disease, and
molecular genetic analysis of their PrP genes was normal. No medical, surgical,
or dietary antecedent of CJD was identified; therefore, we are left with the
unanswerable alternatives of human-to-human transmission or the chance
occurrence of sporadic CJD in a husband and wife.
Received May 5, 1997. Accepted in final form September 10, 1997.
for anyone interested, please see ;
*** Two of these cats have developed rear limb ataxia. Although the limited
data from this ongoing study must be considered preliminary, they raise the
potential for cervid-to-feline transmission in nature.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets? ***
Sunday, November 10, 2013
LARGE CJD TSE PRION POTENTIAL CASE STUDY AMONG HUMANS WHO TAKE DEER ANTLER
VELVET WILL BE ONGOING FOR YEARS IF NOT DECADES, but who's cares $
kind regards, terry
posted by Terry S. Singeltary Sr. at
11:14 AM
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