Two suspected Creutzfeldt-Jakob Disease cases reported in Vietnam
Two Vietnamese men have been hospitalized with
symptoms of the rare degenerative brain
disorder known as Creutzfeldt – Jakob Disease (CJD); however, a definitive
diagnosis could not be made, according to a Thanh Nien News report
today.
Confirmation
testing for CJD is not available in Vietnam,
according to the report.
The two men, ages 44 and 86, from Binh Phuoc Province and Ho Chi Minh City, respectively, were treated for symptoms and released. There is no treatment for CJD.
According to the Centers for Disease Control and Prevention (CDC), Prion diseases or transmissible spongiform encephalopathies (TSEs) are a family of rare progressive neurodegenerative disorders that affect both humans and animals. They are distinguished by long incubation periods, characteristic spongiform changes associated with neuronal loss, and a failure to induce inflammatory response.
The causative agents of TSEs are believed to be prions. The term “prions” refers to abnormal, pathogenic agents that are transmissible and are able to induce abnormal folding of specific normal cellular proteins called prion proteins that are found most abundantly in the brain.
Classic CJD is a human prion disease. It is a neurodegenerative disorder with characteristic clinical and diagnostic features. This disease is rapidly progressive and always fatal. Infection with this disease leads to death usually within 1 year of onset of illness.
http://outbreaknewstoday.com/two-suspected-creutzfeldt-jakob-disease-cases-reported-in-vietnam-81488/
http://outbreaknewstoday.com/two-suspected-creutzfeldt-jakob-disease-cases-reported-in-vietnam-81488/#comment-1938
Image/United States Army Center of Military History
The two men, ages 44 and 86, from Binh Phuoc Province and Ho Chi Minh City, respectively, were treated for symptoms and released. There is no treatment for CJD.
According to the Centers for Disease Control and Prevention (CDC), Prion diseases or transmissible spongiform encephalopathies (TSEs) are a family of rare progressive neurodegenerative disorders that affect both humans and animals. They are distinguished by long incubation periods, characteristic spongiform changes associated with neuronal loss, and a failure to induce inflammatory response.
The causative agents of TSEs are believed to be prions. The term “prions” refers to abnormal, pathogenic agents that are transmissible and are able to induce abnormal folding of specific normal cellular proteins called prion proteins that are found most abundantly in the brain.
Classic CJD is a human prion disease. It is a neurodegenerative disorder with characteristic clinical and diagnostic features. This disease is rapidly progressive and always fatal. Infection with this disease leads to death usually within 1 year of onset of illness.
http://outbreaknewstoday.com/two-suspected-creutzfeldt-jakob-disease-cases-reported-in-vietnam-81488/
http://outbreaknewstoday.com/two-suspected-creutzfeldt-jakob-disease-cases-reported-in-vietnam-81488/#comment-1938
Vietnam hospitals reporst two suspected CJD cases
Thanh Nien News
Ho Chi Minh City - Tuesday, September 30, 2014 09:57 Email Print
Two Vietnamese men have been hospitalized with symptoms of the rare
degenerative brain disorder known as Creutzfeldt – Jakob but doctors lack
equipment to settle on a decisive diagnosis.
The HCMC Medical University Hospital received the first patient on August
20 -- a 44-year-old from Binh Phuoc Province, Tuoi Tre newspaper reported.
The second was an 86-year-old Ho Chi Minh City local who was admitted to
the 115 People’s Hospital on September 6.
Both were discharged after being treated for their symptoms which haven't
been precisely identified.
Even if doctors could be sure they suffer from CJD, which is a rare disease
affecting about one in every million worldwide, no treatment is available.
Doctor Vo Don of the 115 hospital and his colleague Tran Ngoc Tai from the
other said the patients suffered rapidly progressive dementia and experienced
problems moving or speaking.
The 86-year-old patient, only identified as P.V.L., could only lie still
when he was admitted.
Family members said he started to forget things around two years ago and
his memory grew progressively worse.
More than a month after he was admitted, his condition rapidly
deteriorated. He had problems walking around and holding things in his
hands.
L.B.H., the other patient, initially sought treatment at a Binh Phuoc
hospital where doctors were baffled by the symptoms.
He went to two other hospitals in the city where doctors could not venture
a diagnosis.
By the time he arrived at the University hospital in Ho Chi Minh City, he
could hardly speak or raise his legs and arms.
Tests have been performed on the patients to rule out other treatable forms
of dementia such as encephalitis or meningitis.
MRI scans showed their brains' electrical patterns have become
irregular.
Doctors say the results are typical of the disease, which was once
considered a human form of mad cow disease.
But the doctors say they need to conduct tests on samples of a brain
protein called prion to decide for sure, and hospitals in Vietnam aren't
equipped for that.
Prion proteins occur in both a normal form and an infectious form, which
causes the disease.
The prions cause harm when they change into the infectious form and clump
together, leading to neuron loss and other brain damage.
Tai said the disease usually occurs at people from between 55 to 60 years
of age.
Victims of the disease forget what they've just said, then the way home and
eventually cannot recognize their own children.
Gradually, they lapse into temper tantrums, behavioral disorders and
mobility problems including seizures.
In less common cases among patients between 25 and 30, the victims suffer
mobility before mental problems.
They too end up in a vegetative state, the doctor said.
Depending on nursing conditions, patients can survive for several months or
several years and they usually die of complications such as ulceration and
bacterial infections associated with lying still for long periods of time.
Tai said the cause of the disease is not known in around 85 percent of
patients.
Another 10-15 percent inherit the disease and less than 1 percent are
infected by other patients’ tissues or tainted medical equipment.
His hospital has seen four patients whom they believe suffer the disease in
the past seven years..
Don meanwhile said his 115 hospital receives one to two suspected cases a
year.
More :
Vietnam Ho Chi Minh City CJD Creutzfeldt – Jakob brain disease
USA 4TH CASE VCJD (aka nvCJD) HUMAN MAD COW, THE SILENCE IS DEAFENING BSE,
CWD, AND SCRAPIE TSE PRION DISEASE
Greetings DSHS, Dr. Fishcer, et al,
I know that most in the USA could care less about the CJD TSE prion disease
aka mad cow type disease. but there are some of us here that will never forget.
you can cover up what ever you want. we all know. I have seen it happen too
many times here in Texas with BSE TSE prion, either the typical or the atypical
strains, or with the feed, or, with cwd, or scrapie as that goes, but we are
still here, and we will never forget...
kind regards, terry
Creutzfeld-Jacob Disease (CJD) Emerging & Acute Infectious Disease
Branch Michael Fischer
Marilyn Felkner
512-776-7676
512-776-7676
Chronic Wasting Disease Zoonosis Control Branch Eric Fonken
512-776-2155
Lab tests have confirmed a diagnosis of variant Creutzfeldt-Jakob Disease
(CJD) in a patient who recently died in Texas. Variant CJD is a rare, fatal
brain disorder, first described in 1996 in the United Kingdom and associated
with beef consumption overseas.
This is the fourth case ever reported in the United States. In each of the
three previous cases, infection likely occurred outside the United States,
including the United Kingdom and Saudi Arabia. The history of this fourth
patient includes extensive travel to Europe and the Middle East, and infection
likely occurred outside the United States. The CDC and DSHS continue to
investigate the case.
There are no Texas public health concerns or threats associated with this
case.
CDC Confirmation Information: http://www.cdc.gov/ncidod/dvrd/vcjd/other/confirmed-case-in-texas.htm
CDC Fact Sheet: http://www.cdc.gov/ncidod/dvrd/vcjd/factsheet_nvcjd.htm
Texas CJD Information: http://www.dshs.state.tx.us/idcu/disease/creutzfeldt-jakob/
Last updated June 02, 2014
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
Monday, June 02, 2014 Confirmed Variant CJD Case in Texas
SO, 4 months after the fact and still no word on this case. no information
what so ever. the silence is deafening $$$
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Transmissible Spongiform Encephalopathy TSE Prion Disease have now been
discovered in a wide verity of species across North America. typical C-BSE,
atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine,
typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98
Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD
in cervid is slowly spreading without any stopping it in Canada and the USA and
now has mutated into many different strains. Transmissible Mink Encephalopathy
TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease
have been silently mutating and spreading in different species in North America
for decades.
The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion
Firewall, of which we now know without a doubt, that it was nothing but ink on
paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of
banned mad cow feed has been put out into commerce, never to return, as late as
December of 2013, serious, serious breaches in the FDA mad cow feed ban have
been documented. The 2004 enhanced BSE surveillance program was so flawed, that
one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown,
who is preparing a scientific paper based on the latest two mad cow cases to
estimate the maximum number of infected cows that occurred in the United States,
said he has "absolutely no confidence in USDA tests before one year ago" because
of the agency's reluctance to retest the Texas cow that initially tested
positive.
see ;
The BSE surveillance and testing have also been proven to be flawed, and
the GAO and OIG have both raised serious question as to just how flawed it has
been (see GAO and OIG reports). North America has more documented TSE prion
disease, in different documented species (excluding the Zoo BSE animals in the
EU), then any other place on the Globe. This does not include the very
likelihood that TSE prion disease in the domestic feline and canine have been
exposed to high doses of the TSE prion disease vid pet food. To date, it’s still
legal to include deer from cwd zone into pet food or deer food. Specified Risk
Material i.e. SRM bans still being breach, as recently as just last month.
nvCJD or what they now call vCJD, another case documented in Texas last
month, with very little information being released to the public on about this
case? with still the same line of thought from federal officials, ‘it can’t
happen here’, so another vCJD blamed on travel of a foreign animal disease from
another country, while ignoring all the BSE TSE Prion risk factors we have here
in the USA and Canada, and the time that this victim and others, do spend in the
USA, and exposed to these risk factors, apparently do not count in any way with
regard to risk factor. a flawed process of risk assessment.
sporadic CJD, along with new TSE prion disease in humans, of which the
young are dying, of which long duration of illness from onset of symptoms to
death have been documented, only to have a new name added to the pot of prion
disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a
familial type disease could be sporadic with no genetic link to any family
member? when the USA is the only documented Country in the world to have
documented two different cases of atypical H-type BSE, with one case being
called atypical H-G BSE with the G meaning Genetic, with new science now showing
that indeed atypical H-type BSE is very possible transmitted to cattle via oral
transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada,
USA, and the UK, with the same old excuse, better surveillance. You can only use
that excuse for so many years, for so many decades, until one must conclude that
CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a
blip or a reason of better surveillance, it is a mathematical rise in numbers.
More and more we are seeing more humans exposed in various circumstance in the
Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same
time in North America, more and more humans are becoming exposed to the TSE
prion disease via consumption of the TSE prion via deer and elk, cattle, sheep
and goats, and for those that are exposed via or consumption, go on to further
expose many others via the iatrogenic modes of transmission of the TSE prion
disease i.e. friendly fire. I pondered this mode of transmission via the victims
of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone
sub-clinical with sFFI or sGSS ? what if?
Two decades have passed since Dr. Ironside first confirmed his first ten
nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first
ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is
transmissible. yet all these TSE prion disease and victims in the USA and Canada
are being pawned off as a spontaneous event, yet science has shown, the
spontaneous theory has never been proven in any natural case of TSE prion
disease, and scientist have warned, that they have now linked some sporadic CJD
cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about
this in the public domain. We must make all human and animal TSE prion disease
reportable in every age group, in ever state and internationally, we must have a
serious re-evaluation and testing of the USA cattle herds, and we must ban
interstate movement of all cervids. Any voluntary effort to do any of this will
fail. Folks, we have let the industry run science far too long with regards to
the TSE prion disease. While the industry and their lobbyist continues to funnel
junk science to our decision policy makers, Rome burns. ...end
REFERENCES
Sunday, June 29, 2014
Transmissible Spongiform Encephalopathy TSE Prion Disease North America
2014
Tuesday, August 12, 2014
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST
2014
Singeltary Response to USDA, and USDA
RESPONSE TO SINGELTARY ON HARVARD BSE RISK ASSESSMENT
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE) Page 1 of 98
FSIS, USDA, REPLY TO SINGELTARY
*** 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.
NOW, what is the latest on human risk factors to CWD strains ???
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid
prion protein (PrP) sequence through passage in cervidized transgenic mice
efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
***These results indicate that the CWD prion may have the potential to
infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of
the ability of sheep, cattle and deer prion disease isolates to convert normal
human prion protein to its pathological isoform in a cell-free system
***However, they also show that there is no absolute barrier to conversion of
human prion protein in the case of chronic wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood,
and mother to offspring transmission
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
there is in fact evidence that the potential for cwd transmission to humans
can NOT be ruled out.
I thought your readers and hunters and those that consume the venison,
should have all the scientific facts, personally, I don’t care what you eat, but
if it effects me and my family down the road, it should then concern everyone,
and the potential of iatrogenic transmission of the TSE prion is real i.e.
‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there
from...like deer antler velvet and TSE prions and nutritional supplements there
from, all a potential risk factor that should not be ignored or silenced. ...
the prion gods at the cdc state that there is ;
''no strong evidence''
but let's see exactly what the authors of this cwd to human at the cdc
state ;
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD
transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article
and call me if you have questions or need more clarification (phone:
404-639-3091). Also, we do not claim that "no-one has ever been infected with
prion disease from eating venison." Our conclusion stating that we found no
strong evidence of CWD transmission to humans in the article you quoted or in
any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
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
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip...
full text ;
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb**************
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer
and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 –0500
EMC 1 Terry S. Singeltary Sr. Vol #: 1
*** We hypothesize that both BSE prions and CWD prions passaged through
felines will seed human recPrP more efficiently than BSE or CWD from the
original hosts, evidence that the new host will dampen the species barrier
between humans and BSE or CWD. The new host effect is particularly relevant as
we investigate potential means of trans-species transmission of prion disease.
Monday, August 8, 2011
*** Susceptibility of Domestic Cats to CWD Infection ***
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness.
*** Two of these cats have developed rear limb ataxia. Although the limited
data from this ongoing study must be considered preliminary, they raise the
potential for cervid-to-feline transmission in nature.
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado
State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN
USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
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 $
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose
DOCUMENT ID: APHIS-2006-0118-0411
***Singeltary submission
Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program
Standards
>>>The CWD herd certification program is a voluntary, cooperative
program that establishes minimum requirements for the interstate movement of
farmed or captive cervids, provisions for participating States to administer
Approved State CWD Herd Certification Programs, and provisions for participating
herds to become certified as having a low risk of being infected with
CWD<<<
Greetings USDA/APHIS et al,
I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting
Disease Herd Certification Program and Interstate Movement of Farmed or Captive
Deer, Elk, and Moose; Program Standards.
I believe, and in my opinion, and this has been proven by scientific facts,
that without a validated and certified test for chronic wasting disease cwd,
that is 100% sensitive, and in use, any voluntary effort will be futile. the
voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow
surveillance program has failed terribly, as well as the testing for bse tse
prion in cattle, this too has failed terrible. all this has been proven time and
time again via OIG reports and GOA reports.
I believe that until this happens, 100% cwd testing with validated test,
ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO
INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.
In my opinion, and the opinions of many scientists and DNR officials, that
these so called game farms are the cause of the spreading of chronic wasting
disease cwd through much negligence. the game farms in my opinion are not the
only cause, but a big factor. I kindly wish to submit the following to show what
these factors are, and why interstate movement of cervids must be banned.
...
snip...see full text and PDF ATTACHMENT HERE ;
Sunday, June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper
(Document ID APHIS-2012-0105-0001)
***Terry S. Singeltary Sr. submission
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE PRION
disease in cervids
***SINGELTARY SUBMISSION
The Scottish Parliament’s Rural Affairs, Climate Change and Environment
Committee has been looking into deer management, as you can see from the
following press release,
***and your email has been forwarded to the committee for information:
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population
Sunday, July 21, 2013
Welsh Government and Food Standards Agency Wales Joint Public Consultation
on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations
2013
*** Singeltary Submission WG18417
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 ***
=============================================================================
Ronnie Dunn Cross Examination, slaughtering cattle, or killing deer ?
IN THE UNITED STATES DISTRICT COURT FOR THE NORTHERN DISTRICT OF INDIANA
SOUTH BEND DIVISION UNITED STATES OF AMERICA, vs. RUSSELL G. BELLAR, Defendant.
___________________________
)))))))))
Cause No.: 3:04cr00068-AS South Bend, Indiana January 4, 2005 9:30 a.m.
TRANSCRIPT EXCERPT OF JURY TRIAL (TESTIMONY OF: RONNIE DUNN AND RUSTY CAMP)
BEFORE THE HONORABLE ALLEN SHARP
snip...
Ronnie Dunn Cross Examination
Q. Mr. Dunn, at one point I believe you told the federal agents that Mr.
Bellar told you that this was a private deer farm and shooting deer on that farm
was like slaughtering cattle; is that correct?
A. I don't know if I used the word "slaughter," but it was, yeah, like
that.
Q. You don't know if that was your word, "slaughtering cattle"?
A. I don't know that.
Q. Well, did he give you the idea of killing cattle?
A. Yes, it was the same principle.
snip...
see full text ;
BUCK FEVER
Thursday, September 18, 2014
*** Risk behaviors in a rural community with a known point-source exposure
to chronic wasting disease
Saturday, September 20, 2014
*** North Carolina Captive cervid licenses and permits Senate Bill 744
Singeltary Submission
Description The proposed changes to 15A NACA 10H .0301 would allow the
Commission to issue new captivity licenses and permits for the purpose of
holding cervids in captivity and allow certified herd owners to sell or transfer
cervids to any licensed facility. Also, mandatory testing for CWD will be raised
from all cervids that die at age 6 months or older to all cervids that die at
age 12 months or older.
Rule Text Click here http://www.ncwildlife.org/Portals/0/ProposedRegulations/15A%20NCAC%2010H%20.0301%20for%20web%20posting.pdf
North Carolina Captive cervid licenses and permits Senate Bill 744
Singeltary Submission
*** p.s. please add this to my submission, very important
information...
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
*** 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.
SNIP...SEE FULL TEXT ;
Saturday, September 20, 2014
*** North Carolina Captive cervid licenses and permits Senate Bill 744
Singeltary Submission
Thursday, September 11, 2014
Missouri Nixon's Veto Stands Overide Fails on Agriculture Legislation
How they voted: attempt to override veto of ag bill fails in the
House
Thursday, September 11, 2014
*** TEXAS ANIMAL HEALTH COMMISSION 390th COMMISSION MEETING AGENDA (CWD
movement restriction zone) September 16, 2014 8:30 A.M.
Wednesday, September 17, 2014
*** Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant
Health Inspection Service Veterinary Services ***
Friday, September 05, 2014
*** CFIA CWD and Grain Screenings due to potential risk factor of spreading
via contamination of grain, oil seeds, etc. ***
Wednesday, September 17, 2014
*** Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant
Health Inspection Service Veterinary Services ***
Sunday, September 21, 2014
INFORM: Cervid Health and States Indemnity FY 2015
Wednesday, September 17, 2014
Cost benefit analysis of the development and use of ante-mortem tests for
transmissible spongiform encephalopathies
Sunday, August 24, 2014
*** USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program
Goals TSE PRION October 17 – 23, 2013
*** 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.
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 CONFERENCE CHRONIC WASTING DISEASE CWD
*** 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
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute
and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental
routes, and there are also concerns about BSE infection remaining in the
environment after carcass burial or waste 3disposal. In two demonstration
experiments we are determining survival and migration of TSE infectivity when
buried for up to five years, as an uncontained point source or within bovine
heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters
containing either sandy or clay soil. Migration from the boluses is being
assessed from soil cores taken over time. With the exception of a very small
amount of infectivity found 25 cm from the bolus in sandy soil after 12 months,
no other infectivity has been detected up to three years. Secondly, ten bovine
heads were spiked with TSE infected mouse brain and buried in the two soil
types. Pairs of heads have been exhumed annually and assessed for infectivity
within and around them. After one year and after two years, infectivity was
detected in most intracranial samples and in some of the soil samples taken from
immediately surrounding the heads. The infectivity assays for the samples in and
around the heads exhumed at years three and four are underway. These data show
that TSE infectivity can survive burial for long periods but migrates slowly.
Risk assessments should take into account the likely long survival rate when
infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
*** Susceptibility of UK red deer (Cervus alaphus elaphus) to oral BSE
transmission Project Code: M03024 ***
02/08/2011
The project confirmed that U.K red deer are susceptible to both oral and
intra-cerebral inoculation with the cattle BSE agent. Six clinically positive
(from 26-42 months post inoculation) i.c inoculated and one (56 months post
inoculation) orally dosed deer that tested positive for TSE by
immunohistochemistry and Western blotting using several primary antibodies
demonstrated widespread accumulation of disease specific prion protein in the
central nervous system, peripheral nervous system and enteric nervous system but
none in lymphoreticular system. All showed several brain sites positive for
disease specific prion protein and presented immunohistochemistry and Western
blotting phenotypes with similarities to BSE in sheep, goats and cattle but
unlike those seen in chronic wasting disease (CWD) in elk or scrapie in sheep.
The vacuolar pathology and distribution of disease specific prion protein in red
deer resembled that of CWD in most major respects however we have shown that BSE
can be clearly differentiated from CWD by existing immunohistochemical and
biochemical methods that are in routine use.
The knowledge gained as a result of this work will permit rapid and
accurate diagnosis should a TSE ever be detected in European red deer and will
also enable effective disease control methods to be quickly put in place.
Results
We confirmed that U.K red deer are susceptible to both oral and
intra-cerebral inoculation with the cattle BSE agent. Six clinically positive
(from 26-42mpi) i.c inoculated and one (56mpi) orally dosed deer that tested
positive for TSE by IHC and WB using several primary antibodies demonstrated
widespread accumulation of disease specific PrP in CNS, PNS and ENS but none in
LRS. All showed several brain sites positive for disease specific PrP and
presented IHC and WB phenotypes with similarities to BSE in sheep, goats and
cattle but unlike those seen in CWD in elk or scrapie in sheep. The vacuolar
pathology and distribution of PrPd BSE in red deer resembled that of CWD in most
major respects however we have shown that BSE can be clearly differentiated from
CWD by existing immunohistochemical and biochemical methods that are in routine
use.
Final technical report MO3024 01/04/2003 – 31/03/2010 Susceptibility of UK
red deer (Cervus elaphus elaphus) to oral BSE transmission. Stuart Martin - VLA
Lasswade Pentlands Science Park Bush Loan Penicuik EH26 0PZ Page 2 of 21 Further
work undertaken August 2009 – March 2010. Genetic analysis - Wilfred Goldmann;
Roslin NPD.
Negative controls and the remaining 5 orally dosed deer culled at 72mpi
tested negative by IHC and Western blot however analysis of the PrP ORF of these
deer (kindly carried out by Wilfred Goldmann of the Roslin NPD) identified a Q
to E polymorphism at codon 226 that may influence the efficiency of oral
transmission (not published).
In the experimental BSE challenge of red deer six out of six deer succumbed
to BSE when challenged by intracerebral routes but only one of six deer
challenged by the oral route succumbed to infection. Deer killed at 190 days or
365 days post oral challenge showed no evidence of abnormal PrP accumulation
when tested by immunocytochemistry. The PrP gene of red deer includes a Q to E
polymorphism at codon 226. The table shows the distribution of these codon 226
polymorphisms within experimental challenge groups.
snip...
Research article Open Access
Immunohistochemical and biochemical characteristics of BSE and CWD in
experimentally infected European red deer (Cervus elaphus elaphus)
Stuart Martin*1, Martin Jeffrey1, Lorenzo González1, Sílvia Sisó1, Hugh W
Reid2, Philip Steele2, Mark P Dagleish2, Michael J Stack3, Melanie J Chaplin3
and Aru Balachandran4 Address: 1Veterinary Laboratories Agency (VLA-Lasswade),
Pentlands Science Park, Bush Loan, Penicuik, Midlothian, EH26 0PZ, UK, 2Moredun
Research Institute, Pentlands Science Park, Bush Loan, Penicuik, Midlothian,
EH26 0PZ, UK, 3VLA-Weybridge, Addlestone, Surrey, KT15 3NB, UK and 4Animal
Diseases Research Institute, Canadian Food Inspection Agency, Ottawa, Ontario,
K2H 8P9, Canada
Abstract
Background: The cause of the bovine spongiform encephalopathy (BSE)
epidemic in the United Kingdom (UK) was the inclusion of contaminated meat and
bone meal in the protein rations fed to cattle. Those rations were not
restricted to cattle but were also fed to other livestock including farmed and
free living deer. Although there are no reported cases to date of natural BSE in
European deer, BSE has been shown to be naturally or experimentally
transmissible to a wide range of different ungulate species. Moreover, several
species of North America's cervids are highly susceptible to chronic wasting
disease (CWD), a transmissible spongiform encephalopathy (TSE) that has become
endemic. Should BSE infection have been introduced into the UK deer population,
the CWD precedent could suggest that there is a danger for spread and
maintenance of the disease in both free living and captive UK deer populations.
This study compares the immunohistochemical and biochemical characteristics of
BSE and CWD in experimentally-infected European red deer (Cervus elpahus
elaphus).
Results: After intracerebral or alimentary challenge, BSE in red deer more
closely resembled natural infection in cattle rather than experimental BSE in
small ruminants, due to the lack of accumulation of abnormal PrP in lymphoid
tissues. In this respect it was different from CWD, and although the
neuropathological features of both diseases were similar, BSE could be clearly
differentiated from CWD by immunohistochemical and Western blotting methods
currently in routine use.
Conclusion: Red deer are susceptible to both BSE and CWD infection, but the
resulting disease phenotypes are distinct and clearly distinguishable.
SNIP...
Results
Clinical disease
All six deer challenged i.c. with BSE developed clinical disease between
794 and 1260 days post-inoculation with a mean incubation period of 1027 days. A
detailed description of the clinical signs was provided in an earlier report
[8]. Briefly, affected deer showed variable degrees of ataxia, anorexia,
circling and apparent blindness, together with failure of seasonal change of
coat, weight loss and 'panic attacks'. In addition, one of six red deer orally
dosed with BSE developed clinical disease 1740 days after challenge, and this
animal presented with a short clinical duration of two days; the other five deer
from this group remain healthy at the time of writing (65 months after
challenge). Sequential rectal biopsies taken at five different time points from
orally and i.c. inoculated deer were negative for PrPd.
All four deer orally challenged with CWD started to show behavioural
changes between 577 and 586 days post challenge;
these progressed to definite neurological disease between 742 and 760 days
post-challenge (Table 1).
Clinical signs were similar to the BSE challenged deer and included
nervousness, weight loss, excessive salivation, roughness of coat, and
progressive ataxia. All these CWD inoculated deer showed PrPd accumulation in
the secondary follicles of rectal biopsies taken at 7 months post
infection.
Conclusion
European red deer are susceptible to infection with the cattle BSE agent,
not only by the intra-cerebral but also by the oral route, and although the
clinical signs and spong- iform change are similar to those of CWD in the same
species, these two infections can be easily differentiated. The lack of lymphoid
involvement, the PrPd truncation pattern both "in vivo" and "in vitro", and the
predominantly intracellular accumulation of PrPd are features of deer BSE that
are in contrast with those of deer CWD. However, only one of six deer developed
disease after alimentary exposure to 25 g of a BSE brain pool homogenate after
an incubation period of nearly 5 years; this suggests a strong species barrier
but if a TSE in European red deer should ever be identified then BSE/CWD
discrimination would be an urgent priority. To determine whether there are
potential naturally occurring BSE-like strains and to determine the degree to
which there is strain variation, it would be necessary to examine many more
naturally occurring CWD cases. These results will support the ongoing European
surveillance for natural TSEs in red deer and the further assessment of
potential risk to human health.
Published: 27 July 2009 BMC Veterinary Research 2009, 5:26
doi:10.1186/1746-6148-5-26 Received: 12 February 2009 Accepted: 27 July 2009
This article is available from: http://www.biomedcentral.com/1746-6148/5/26
© 2009 Martin et al; licensee BioMed Central Ltd. This is an Open Access article
distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium,
provided the original work is properly cited.
Monday, May 05, 2014
*** Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing ***
snip...
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
*** Overall, therefore, it is considered there is a __greater than
negligible risk___ that (nonruminant) animal feed and pet food containing deer
and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In
Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #: 1
see my full text submission here ;
Sunday, December 15, 2013
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
Tuesday, September 16, 2014
mad cow scaremongers consumerfreedom.com December 20, 2003 article and a
2014 review
Wednesday, September 10, 2014
Creutzfeldt-Jakob disease (CJD) biannual update (August 2014), with updated
guidance on decontamination of gastrointestinal endoscopy equipment
Research and analysis
CWD STRAINS TO HUMANS ???
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).
as I said, what if ?
*** our results raise the possibility that CJD cases classified as VV1 may
include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne
infection by type 1 prions from animals, e.g., chronic wasting disease prions in
cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have
been reported (40, 41). The results of the present study emphasize the need for
traceback studies and careful re-examination of the biochemical properties of
sCJD-VV1 prions. ***
===========================================
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
WHAT IF ?
Saturday, April 19, 2014
Exploring the zoonotic potential of animal prion diseases: In vivo and in
vitro approaches
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010 ***
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
Tuesday, April 01, 2014
*** Questions linger in U.S. CJD cases 2005, and still do in 2014
Monday, March 29, 2010
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN
AND SPINAL CORD MATTER
URGENT, PLEASE NOTE ;
>>> Up until about 6 years ago, the pt worked at Tyson foods where
she worked on the assembly line, slaughtering cattle and preparing them for
packaging. She was exposed to brain and spinal cord matter when she would
euthanize the cattle. <<<
CJD NE TEXAS CLUSTER
Creutzfeldt-Jakob Disease in Northeast Texas
J.A. Rawlings,*1 K.A. Hendricks1, O.M. Nuno1, D.A. Brown1, D.A. Evans2,
Texas Department of Health, 1Austin and 2Tyler, Texas Creutzfeldt-Jacob Disease
(CJD), a transmissible spongiform encephalopathy, is caused by prions composed
of proteinaceous material devoid of nucleic acid. CJD occurs sporadically
(generally 1 case/1,000,000 population per year) in older patients (average age
of 65) and is characterized by rapidly progressive dementia, accompanied by
severe muscle spasms and incoordination. Death usually occurs within 3 to 12
months (average 7 months). CJD activity in Texas, which has a population of
nearly 19 million, appeared to be typical. The statewide death rate for 1995 and
1996 was just under 1/1,000,000. In April of 1997, the Texas Department of
Health became aware of an increased number of possible CJD cases in a 23-county
area of NE Texas with a population of just over one million. After review of
medical and pathology records, four patients were identified with definite
classic CJD and three were identified with probable CJD. Dates of death for the
eight patients were from April, 1996 through mid-July 1997. The patients were
from 46 through 65 years of age; four were male and three were female. A
case-control study to identify risks for CJD in NE Texas has been initiated. http://www.jifsan.umd.edu/tse/Rawlings.htm
we get them young cases of tse prion disease in Texas, that is not related
to anything $$$ money and politics will buy anything, especially junk science...
sporadic ffi and sporadic gss ;
NOT THIS CASE !!! but another one a while back in Texas...see ;
We report a case of a 33-year-old female who died of a prion disease for
whom the diagnosis of sFI or FFI was not considered clinically. Following death
of this patient, an interview with a close family member indicated the patient's
illness included a major change in her sleep pattern, corroborating the reported
autopsy diagnosis of sFI.
sporadic FFI or nvCJD Texas style ???
Creutzfeldt-Jakob Disease Surveillance in Texas
Sunday, July 11, 2010
CJD or prion disease 2 CASES McLennan County Texas population 230,213 both
cases in their 40s
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
Thursday, August 12, 2010
Seven main threats for the future linked to prions
***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...
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
*** 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...
***In addition, non-human primates are specifically susceptible for
atypical BSE as demonstrated by an approximately 50% shortened incubation time
for L-type BSE as compared to C-type. Considering the current scientific
information available, it cannot be assumed that these different BSE types pose
the same human health risks as C-type BSE or that these risks are mitigated by
the same protective measures.
Monday, May 19, 2014
Variant CJD: 18 years of research and surveillance
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health
Crisis
full text with source references ;
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
Views & Reviews
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in
the United States
Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and
Lawrence B. Schonberger, MD
+ Author Affiliations
From the Division of Viral and Rickettsial Diseases (Drs. Belay and
Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers
for Disease Control and Prevention, Atlanta, GA; and National Prion Disease
Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology,
Institute of Pathology, Case Western Reserve University, Cleveland, OH.
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600
Clifton Road, Mailstop A-39, Atlanta, GA 30333.
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.
JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL
TEXT
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as
well
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North
America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember,
the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been
documented in North America, along with the typical scrapie's, and atypical
Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these
TSE in different species have been rendered and fed to food producing animals
for humans and animals in North America (TSE in cats and dogs ?), and that the
trading of these TSEs via animals and products via the USA and Canada has been
immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances
and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD
only theory in 2009. With all the science to date refuting it, to continue to
validate this old myth, will only spread this TSE agent through a multitude of
potential routes and sources i.e. consumption, medical i.e., surgical, blood,
dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and
the urgent need to make all human TSE in the USA a reportable disease, in every
state, of every age group, and to make this mandatory immediately without
further delay. The ramifications of not doing so will only allow this agent to
spread further in the medical, dental, surgical arena's. Restricting the
reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO
age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al
and many more, that the world of TSE Transmissible Spongiform Encephalopathy is
far from an exact science, but there is enough proven science to date that this
myth should be put to rest once and for all, and that we move forward with a new
classification for human and animal TSE that would properly identify the
infected species, the source species, and then the route.
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
I kindly disagree with your synopsis for the following reasons ;
snip...
I would kindly like to add to my initial concerns, something I brought up
years ago, and I believe that still hold true today, more so even than when I
first stated these concerns in 2003 ;
routine passive mortality CJD surveillance USA ?
THIS has been proven not to be very useful in the U.K.;
THE EPIDEMIOLOGY OF CJD RG WILL 1984 (182 PAGES)
snip...
One reason for this was the _inaccuracy_ in coding of cases correctly
certified as CJD Coding is carried out by staff who are not medically qualified
and it is not surprising that coding errors occur in the processing of large
numbers of certificates. In 1982, 12,000 certificates per week were processed at
the office of population censuses and surveys by 15 coders and 6 checkers
(Alderson et al., 1983). The occurrence of both inter- and intra-observer coding
errors has been described (Curb et al., 1983) and the _inaccuracies_ of BOTH
certification and coding discovered in this study _support_ the introduction of
a more accurate system of death certificates and a more detailed and specific
coding system...
snip...
Draft Proposal For The Monitoring of Creutzfeldt-Kakob Disease 1989 Dr. R.
Will
snip...
IDENTIFICATION OF CASES
Cases of CJD may be identified from death certificates, but this alone is
unlikely to provide adequate monitoring. ERRORS are made in certification and
diagnosis; in the Oxford study death certificates were obtained on a series of
known confirmed cases and CJD was mentioned in only 66% of certificates. In
another series of 175 certified cases, 42 patients were judged not to have
suffered from CJD after examination of case notes (7)...
full text;
http://web.archive.org/web/20050526035006/http://www.bseinquiry.gov.uk/files/yb/1989/05/00005001.pdf
snip...see my full text submission here ;
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
2001-2002ish
greetings TSE PRION WORLD,
i am reminded of a few things deep throat told me years ago;
*** The most frightening thing I have read all day is the report of
Gambetti's finding of a new strain of sporadic cjd in young people.........
Dear God, what in the name of all that is holy is that!!! If the US has
different strains of scrapie..... why???? than the UK... then would the same
mechanisms that make different strains of scrapie here make different strains of
BSE... if the patterns are different in sheep and mice for scrapie..... could
not the BSE be different in the cattle, in the mink, in the humans....... I
really think the slides or tissues and everything from these young people with
the new strain of sporadic cjd should be put up to be analyzed by many, many
experts in cjd........ bse..... scrapie
Scrape the damn slide and put it into mice..... wait..... chop up the mouse
brain and and spinal cord........ put into some more mice..... dammit amplify
the thing and start the damned research..... This is NOT rocket science... we
need to use what we know and get off our butts and move.... the whining about
how long everything takes..... well it takes a whole lot longer if you whine for
a year and then start the research!!!
Not sure where I read this but it was a recent press release or something
like that: I thought I would fall out of my chair when I read about how there
was no worry about infectivity from a histopath slide or tissues because they
are preserved in formic acid, or formalin or formaldehyde..... for God's
sake........ Ask any pathologist in the UK what the brain tissues in the
formalin looks like after a year....... it is a big fat sponge... the agent
continues to eat the brain ...... you can't make slides anymore because the
agent has never stopped........ and the old slides that are stained with
Hemolysin and Eosin...... they get holier and holier and degenerate and
continue... what you looked at 6 months ago is not there........ Gambetti better
be photographing every damned thing he is looking at.....
***Okay, you need to know. You don't need to pass it on as nothing will
come of it and there is not a damned thing anyone can do about it. Don't even
hint at it as it will be denied and laughed at.......... USDA is gonna do as
little as possible until there is actually a human case in the USA of the
nvcjd........ if you want to move this thing along and shake the earth.... then
we gotta get the victims families to make sure whoever is doing the autopsy is
credible, trustworthy, and a saint with the courage of Joan of Arc........ I am
not kidding!!!! so, unless we get a human death from EXACTLY the same form with
EXACTLY the same histopath lesions as seen in the UK nvcjd........ forget any
action........ it is ALL gonna be sporadic!!! And, if there is a case.......
there is gonna be every effort to link it to international travel, international
food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex
partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a
long, lonely, dangerous twisted journey to the truth. They have all the cards,
all the money, and are willing to threaten and carry out those threats.... and
this may be their biggest downfall...***
Thanks as always for your help. (Recently had a very startling revelation
from a rather senior person in government here.......... knocked me out of my
chair........ you must keep pushing. If I was a power person.... I would be
demanding that there be at least a million bovine tested as soon as possible and
agressively seeking this disease. The big players are coming out of the wood
work as there is money to be made!!!
In short: "FIRE AT WILL"!!! for the very dumb.... who's "will"! "Will be
the burden to bare if there is any coverup!"
again it was said years ago and it should be taken seriously.... BSE will
NEVER be found in the US!
As for the BSE conference call... I think you did agreat service to freedom
of information and making some people feign integrity... I find it scary to see
that most of the "experts" are employed by the federal government or are
supported on the "teat" of federal funds. A scary picture! I hope there is a
confidential panel organized by the new government to really investigate this
thing.
You need to watch your back........ but keep picking at them....... like a
buzzard to the bone... you just may get to the truth!!! (You probably have more
support than you know. Too many people are afraid to show you or let anyone else
know. I have heard a few things myself... you ask the questions that everyone
else is too afraid to ask.)
================================================
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 SINGELTARY
HACKS IN (DEEP THROAT ABOVE HELPED ME GET IN)
Mad cow disease: Could it be here?
Man's stubborn crusade attracts experts' notice By Carol Christian | August
5, 2001
yes, cjd is popping up in more and more places it seems. I think in 55 year
and older, it's now 1 in 9,000.
see ;
lifetime risk of developing sporadic CJD is about 1 in 30,000, jumps to 1
in 9,000 in 50 years of age and above
IN REALITY, sporadic CJD is 1 in 9,000 in 50 years of age and above, and
that's with a inadequate or what I call passive surveillance system. see below
;
Dr. William Shulaw, a veterinarian with The Ohio State University extension
service, is involved in a nationwide program to eradicate scrapie, the form of
BSE found in sheep.
Shulaw said the chances of a person getting sporadic Creutzfeldt- Jakob
disease is about one in a million. But that's the total population, infants,
children, adults and the elderly.
Chances increase to one in 9,000 when the group is restricted to those age
50 and older.
NOW, remember, the federal government lied to us for 100 years about other
long incubating disease i.e. tobacco and asbestos, just to protect the industry.
...
just saying...
kind regards, terry
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
flounder9@verizon.net
Monday, June 02, 2014
Confirmed Human BSE aka mad cow Variant CJD vCJD or nvCJD Case in Texas
fact is, BSE cases in Europe of the past years have dropped dramatically
due to feed ban that was enforced, and extensive BSE testing, in large numbers.
just the opposite has happened in the USA. it’s all been documented. there is
ample evidence that there is as much of a chance (if not more), that this victim
contracted human mad cow disease from sources right here in the USA. this PR
push to alienate a USA source factor for human BSE in the USA is a PR stunt by
the USDA inc., and not justified now, in my opinion. compare BSE testing figures
in the EU compared to the USA, compare mad cow feed ban breaches, and you will
see. hell, the 2004 enhanced BSE surveillance program was flawed so bad, the top
Prion God at the NIH TSE prion expert Paul Brown, says he does not trust
anything from the USDA since Texas covered up a mad cow for 7 months, on a 48
hour confirmation turn around. it’s all documented below in link. USDA inc shut
down the mad cow testing after so many atypical BSE cases started showing up.
yes, another foreigner comes to the USA, or another USA citizens does some
traveling, and all of a sudden, it’s a foreign disease. evidently, these folks
never eat anything in the USA, and contracts nvcjd. right. just like the last
one in 2005. really? here are the facts of the TEXAS MAD COW, MAD COW FEED in
Texas, CJD CLUSTER in Texas, CJD CASE IN 38 YEAR OLD WOMAN THAT APPARENTLY
WORKED ON THE SLAUGHTER LINE FOR TYSON in Texas, AND OTHER STRANGE TSE PRION
DISEASE IN VERY YOUNG VICTIMS HERE IN TEXAS with long duration of illness from
onset of clinical symptoms to death, CALLED SPORADIC FFI (except it is not
linked to any genetic make up of that family), another nvcjd victim back in 2005
in Texas, apparently another UK victim that had moved to Texas, and never ate
anything. these are the facts as I have come to know them (official documents),
since hvcjd took my mom in December of 1997. just made a promise to mom, never
forget, and never let them forget, the rest of the story, the truth you don’t
hear about. ...our fine federal friends and the USDA inc, has lied to all of
us...
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
Monday, June 02, 2014 Confirmed Variant CJD Case in Texas
kind regards, terry
posted by Terry S. Singeltary Sr. at
7:05 PM
