North Dakota Mule Deer from 3F2 Tests Positive for CWD Monday, December 9, 2013 TSE PRION DISEASE
Mule Deer from 3F2 Tests Positive for CWD
Monday, December 9, 2013 A mule deer taken from unit 3F2 during the deer
gun season has tested positive for chronic wasting disease.
Dr. Dan Grove, North Dakota Game and Fish Department wildlife veterinarian,
said a hunter shot the adult buck in western Grant County and submitted the head
for testing as part of the hunter-harvested surveillance program. Testing was
performed at Michigan State University. Game and Fish is awaiting verification
of initial tests results from a national lab in Ames, Iowa. The MSU lab still
has some 3F2 samples to test, as well as all samples from the eastern third of
the state.
Grove said according to the hunter, the animal looked healthy, with no
visible signs of having any health issues.
This is the fourth deer, and first buck, to test positive for CWD since
2009, and all were from taken from unit 3F2 in southwestern North Dakota. All
four were within the same general area.
The hunter-harvested surveillance program annually collects samples taken
from hunter-harvested deer in specific regions of the state. In addition to unit
3F2, samples during the 2013 deer gun season were collected from units in the
eastern third of the state.
CWD affects the nervous system of members of the deer family and is always
fatal. Scientists have found no evidence that CWD can be transmitted naturally
to humans or livestock.
The North Dakota Game and Fish Department (NDGFD)
Dear Hunter, October 22, 2013
The North Dakota Game and Fish Department (NDGFD) needs hunters’ assistance
this fall in deer hunting unit 3F2 (Sioux County, southern Morton and Grant
Counties, and eastern Hettinger and Adams Counties) to determine the extent of
CWD in wild deer populations in this area.
In March 2010, Chronic Wasting Disease (CWD) was discovered in a mule deer
buck in western Sioux County, North Dakota. In November 2010 and 2011, two
additional mule deer does were found in the same area. The area where these deer
were found encompasses parts of the Standing Rock Indian Reservation, and is
very close to the South Dakota border of Corson and Perkins Counties. This was
the first time that CWD had been found in North Dakota. The North Dakota Game
and Fish Department is coordinating efforts to test wild deer in this area.
Please carefully review the information below and help us by supplying the head
of any deer taken in the described area for testing.
Thank you.
To determine the extent of CWD in free-roaming wildlife in Sioux County,
southern Morton and Grant Counties, and eastern Hettinger and Adams Counties of
North Dakota, rifle hunters who harvest any deer in deer hunting unit 3F2 are
being asked to submit the head. These heads should be submitted to one of the
following drop-off locations:
North Dakota
Bismarck – NDGFD Main Office
Bismarck - M&M Sausage and Meats
Bismarck – West Dakota Meats
Elgin – Gunny’s Bait and Tackle
Elgin – Melvin’s Taxidermy
Glen Ullin – Kuntz’s Butcher Shop
Hettinger – Dakota Packing
Mandan – Butcher Block Meats
New Leipzig – Hertz Hardware
NDGFD will be collecting heads of harvested deer in this area only during
the month of November. Please submit heads as soon as possible. Fresh tissue is
better for the testing process.
Hunters should:
1. Remove the head at the middle of the neck and take it to one of the
drop-off locations. It is the responsibility of the hunter to remove the head.
Drop off stations may Animal Head Submissions not be able to assist you with
this process. Please follow the instructions below and as posted at the drop-off
locations to submit your deer head for testing.
2. Antlerless Deer: Deposit the head along with the NDGFD-issued license
head tag, properly notched and affixed to the ear. The carcass tag must remain
affixed to the carcass.
3. Antlered Deer: Animals that are to be mounted can be caped by a
taxidermist and the antlers can be removed with a v-cut that will not destroy
the tissue needed for CWD testing. Hunters who choose to mount their own deer
can remove the antlers in a similar fashion. After antlers have been removed,
the head can be submitted at one of the drop-off locations for testing. All
skull caps removed in the field must be cleaned of all brain material and soft
tissue before leaving the unit. The properly affixed and notched NDGFD-issued
license head tag must stay with the antlers. The carcass tag must be affixed to
the carcass. Identification tags are available at all drop-off locations to
re-label the head once the antlers have been removed for testing purposes.
Please use a permanent marker and print the requested information on the tag
provided at the drop-off location and attach the tag to one ear of the animal by
cutting a small hole through the center of the ear and inserting one leg of the
wire through the hole and twisting the two legs of the wire together. You will
need to provide your LICENSE NUMBER, HUNTING UNIT, HARVEST DATE and NAME on the
identification tag. This process is very important because we will need to know
the hunter’s Name and License Number to be able to contact the hunter with test
results. Without this information we will not test the animal.
Heads placed in barrels or collection areas at the drop-off locations will
be picked up on a weekly basis. Samples will be collected and sent to the lab
for CWD testing. This study is designed to monitor our free-roaming deer
populations to determine to what extent this disease occurs in the wild.
Recent research in Colorado suggests that CWD infected carcasses may be an
avenue for the spread of CWD to other areas of the state or to other states.
Transporting carcasses and discarding remnants of nervous tissue outside the
unit has the potential to spread the disease.
It is necessary that we take the precaution of limiting the movement of
potentially infected tissue outside the unit CWD was initially found.
Therefore, NDGFD has enacted regulations to prohibit the transport of whole
carcasses out of deer hunting unit 3F2. Whole carcasses may only be removed from
the area if the hunter is taking them to a licensed processor to be processed.
Heads may be removed and transported to one of the Drop Off sites listed in this
letter, or they may be taken to a licensed taxidermist. Removing the intact
carcass and head from the area for any other purpose is prohibited. Boned out
meat may be removed from the unit.
Current Board of Animal Health (BOAH) regulations require that captive elk
and deer are contained in enclosures that have fences adequate to prevent deer
and elk movement in or out. NDGFD has worked, and will continue to work, with
the BOAH to prevent exposure of free-roaming deer and elk to CWD. Monitoring of
both captive and wild deer and elk for CWD will continue for years to come. This
continued monitoring depends on hunters like you for cooperation in submitting
deer heads for testing. Once test results are back from this year’s sample of
hunter-harvested animals, monitoring methods and results will be evaluated to
determine need and methods for future CWD testing programs. Transportation and
Disposal of Carcasses
According to public health officials and the Center for Disease Control in
Atlanta, Georgia, there is no evidence that this disease can be naturally
transmitted to humans, domestic livestock or wildlife (outside the deer, elk,
and moose family). Nonetheless, it makes good common sense to take the following
simple precautions when handling carcasses of deer in areas of concern. It is
recommended that rubber gloves be worn when field dressing carcasses. Minimize
handling of brain and spinal tissues and wash hands afterward. Hunters should
bone out carcasses or at least avoid consuming brain, spinal cord, eyes, spleen
and lymph nodes of harvested animals. Hunters should take extra precautions
while handling wild animals whose behavior might suggest illness or disease.
Hunters should avoid shooting an animal that appears injured or unhealthy.
Test Results
All hunters providing samples will be notified by the NDGFD of their sample
test results. If any animal tests positive for CWD, NDGFD will notify that
particular hunter immediately by personal contact. Testing of North Dakota deer
will be conducted at the Michigan State University Diagnostic Center for
Population Animal Health. Although testing procedures and the speed that results
are received have improved, I regrettably cannot give you a definite amount of
time that it will take for you to receive test results. The CWD Surveillance
Program and testing procedures are neither designed nor intended to provide
hunters with meat quality assurance for individual animals. If you see or kill a
deer that appears unhealthy or in very poor condition or have any other
questions, contact the NDGFD office in Bismarck at 701-328-6300 or the District
Game Warden with information regarding the animal and its location.
Sincerely,
Terry Steinwand
Director
Wednesday, November 23, 2011
North Dakota Another 3F2 Mule Deer Tests Positive for CWD News Release
Archives - November 2011
Monday, December 13, 2010
North Dakota Another Deer From 3F2 Tests Positive for CWD
2013
Wednesday, September 04, 2013
***cwd - cervid captive livestock escapes, loose and on the run in the
wild...
Saturday, October 19, 2013
***ACA Council Meets to Endorse Several Proposed USAHA Resolutions (CWD TSE
PRION DISEASE)
Monday, December 02, 2013
WISCONSIN CHRONIC WASTING DISEASE CWD DISCOVERED MARATHON COUNTY HUNTING
PRESERVE
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population
Friday, November 29, 2013
Identification of Misfolded Proteins in Body Fluids for the Diagnosis of
Prion Diseases
International Journal of Cell Biology
Saturday, February 04, 2012
Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing
Protocol Needs To Be Revised
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population
cwd to humans ???
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 ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease
Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic
Association Volume 111, Issue 6 , Pages 858-863, June 2011.
Travel History, Hunting, and Venison Consumption Related to Prion Disease
Exposure, 2006-2007 FoodNet Population Survey
Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH ,
Lawrence B. Schonberger, MD , Ermias D. Belay, MD
Accepted 15 November 2010. Abstract Full Text PDF References .
Abstract
The transmission of bovine spongiform encephalopathy (BSE) to human beings
and the spread of chronic wasting disease (CWD) among cervids have prompted
concerns about zoonotic transmission of prion diseases. Travel to the United
Kingdom and other European countries, hunting for deer or elk, and venison
consumption could result in the exposure of US residents to the agents that
cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007
population survey was used to assess the prevalence of these behaviors among
residents of 10 catchment areas across the United States. Of 17,372 survey
respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5%
reported travel to any of the nine European countries considered to be
BSE-endemic since 1980. The proportion of respondents who had ever hunted deer
or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More
than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents
who traveled spent more time in the United Kingdom (median 14 days) than in any
other BSE-endemic country. Of the 11,635 respondents who had consumed venison,
59.8% ate venison at most one to two times during their year of highest
consumption, and 88.6% had obtained all of their meat from the wild. The survey
results were useful in determining the prevalence and frequency of behaviors
that could be important factors for foodborne prion transmission.
"These findings indicate that a high percentage of the United States
population engages in hunting and/or venison consumption. If CWD continues to
spread to more areas across the country, a substantial number of people could
potentially be exposed to the infectious agent."
Potential Venison Exposure Among FoodNet Population Survey Respondents,
2006-2007
Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B.
Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases,
National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for
Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail:
rmaddox@cdc.gov
The foodborne transmission of bovine spongiform encephalopathy to humans,
resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be
susceptible to animal prion diseases. However, it is not known whether foodborne
exposure to the agent causing chronic wasting disease (CWD) in cervids can cause
human disease. The United States Foodborne Diseases Active Surveillance Network
(FoodNet) conducts surveillance for foodborne diseases through an extensive
survey administered to respondents in selected states. To describe the frequency
of deer and elk hunting and venison consumption, five questions were included in
the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten
states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New
Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%)
reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a
CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern
Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of
Colorado. Respondents reporting hunting were significantly more likely to be
male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and,
in general, older respondents were significantly more likely to report hunting
than younger respondents. Venison consumption was reported by more than half
(67.4%) of the study population, and most venison consumers (94.1%) reported
that at least half of their venison came from the wild. However, more than half
(59.1%) of the consumers reported eating venison only one to five times in their
life or only once or twice a year. These findings indicate that a high
percentage of the United States population engages in hunting and/or venison
consumption. If CWD continues to spread to more areas across the country, a
substantial number of people could potentially be exposed to the infectious
agent.
Monday, May 23, 2011 CDC
Assesses Potential Human Exposure to Prion Diseases Travel Warning
Public release date: 23-May-2011
Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier
Health Sciences
CDC assesses potential human exposure to prion diseases Study results
reported in the Journal of the American Dietetic Association Philadelphia, PA,
May 23, 2011 – Researchers from the Centers for Disease Control and Prevention
(CDC) have examined the potential for human exposure to prion diseases, looking
at hunting, venison consumption, and travel to areas in which prion diseases
have been reported in animals. Three prion diseases in particular – bovine
spongiform encephalopathy (BSE or "Mad Cow Disease"), variant Creutzfeldt-Jakob
disease (vCJD), and chronic wasting disease (CWD) – were specified in the
investigation. The results of this investigation are published in the June issue
of the Journal of the American Dietetic Association.
"While prion diseases are rare, they are generally fatal for anyone who
becomes infected. More than anything else, the results of this study support the
need for continued surveillance of prion diseases," commented lead investigator
Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious
Diseases, CDC, Atlanta."But it's also important that people know the facts about
these diseases, especially since this study shows that a good number of people
have participated in activities that may expose them to infection-causing
agents."
Although rare, human prion diseases such as CJD may be related to BSE.
Prion (proteinaceous infectious particles) diseases are a group of rare brain
diseases that affect humans and animals. When a person gets a prion disease,
brain function is impaired. This causes memory and personality changes,
dementia, and problems with movement. All of these worsen over time. These
diseases are invariably fatal. Since these diseases may take years to manifest,
knowing the extent of human exposure to possible prion diseases could become
important in the event of an outbreak.
CDC investigators evaluated the results of the 2006-2007 population survey
conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This
survey collects information on food consumption practices, health outcomes, and
demographic characteristics of residents of the participating Emerging
Infections Program sites. The survey was conducted in Connecticut, Georgia,
Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties
in the San Francisco Bay area, seven counties in the Greater Denver area, and 34
counties in western and northeastern New York.
Survey participants were asked about behaviors that could be associated
with exposure to the agents causing BSE and CWD, including travel to the nine
countries considered to be BSE-endemic (United Kingdom, Republic of Ireland,
France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the
cumulative length of stay in each of those countries. Respondents were asked if
they ever had hunted for deer or elk, and if that hunting had taken place in
areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming
or southwestern Nebraska). They were also asked if they had ever consumed
venison, the frequency of consumption, and whether the meat came from the wild.
The proportion of survey respondents who reported travel to at least one of
the nine BSE endemic countries since 1980 was 29.5%. Travel to the United
Kingdom was reported by 19.4% of respondents, higher than to any other
BSE-endemic country. Among those who traveled, the median duration of travel to
the United Kingdom (14 days) was longer than that of any other BSE-endemic
country. Travelers to the UK were more likely to have spent at least 30 days in
the country (24.9%) compared to travelers to any other BSE endemic country. The
prevalence and extent of travel to the UK indicate that health concerns in the
UK may also become issues for US residents.
The proportion of survey respondents reporting having hunted for deer or
elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic
areas. Venison consumption was reported by 67.4% of FoodNet respondents, and
88.6% of those reporting venison consumption had obtained all of their meat from
the wild. These findings reinforce the importance of CWD surveillance and
control programs for wild deer and elk to reduce human exposure to the CWD
agent. Hunters in CWD-endemic areas are advised to take simple precautions such
as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or
spinal cord tissues, minimizing the handling of brain and spinal cord tissues,
and wearing gloves when field-dressing carcasses.
According to Abrams, "The 2006-2007 FoodNet population survey provides
useful information should foodborne prion infection become an increasing public
health concern in the future. The data presented describe the prevalence of
important behaviors and their associations with demographic characteristics.
Surveillance of BSE, CWD, and human prion diseases are critical aspects of
addressing the burden of these diseases in animal populations and how that may
relate to human health."
###
The article is "Travel history, hunting, and venison consumption related to
prion disease exposure, 2006-2007 FoodNet population survey" by Joseph Y.
Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger,
MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic
Association, Volume 111, Issue 6 (June 2011) published by Elsevier.
In an accompanying podcast CDC's Joseph Y. Abrams discusses travel,
hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast.
also, they did not call this CWD postive meat back for the well being of
the ELK ;
Wednesday, March 18, 2009
Noah’s Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat
derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS
AND FIELD CORRECTIONS: FOODS CLASS II
___________________________________
PRODUCT
a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each
package is approximately 2 lbs., and each case is approximately 16 lbs.; Item
number 755125, Recall # F-129-9;
b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;
c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;
d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;
e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall #
F-133-9;
f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9;
CODE
Elk Meats with production dates of December 29, 30, and 31
RECALLING FIRM/MANUFACTURER
Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009
and press release on February 9, 2009.
Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is
ongoing.
REASON
Elk products contain meat derived from an elk confirmed to have Chronic
Wasting Disease (CWD).
VOLUME OF PRODUCT IN COMMERCE
Unknown
DISTRIBUTION
NV, CA, TX, CO, NY, UT, FL, OK
___________________________________
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
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
Thursday, November 21, 2013
***Assessing the susceptibility of transgenic mice over-expressing deer
prion protein to bovine spongiform encephalopathy ***
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, *humans*, domestic cats,
blood, and mother to offspring transmission
Sunday, July 21, 2013
*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for
humans?
DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever
many grains of salt you wish. ...tss)
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 a least a million bovine tested as soon as possible and
aggressively seeking this disease. The big players are coming out of the
woodwork 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 a
great 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.)
[COLOR= ]
[/COLOR] [COLOR= ] In Confidence - Perceptions of unconventional slow virus
diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
[/COLOR]
CJD QUESTIONNAIRE USA
Tuesday, October 29, 2013
VARIANT CJD PRESENTS DIFFERENTLY IN OLDER PATIENTS
Wednesday, October 09, 2013
*** WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY,
£41,078,281 in compensation REVISED
FARMERS AND FARMERS WIVES WITH DOCUMENTED BSE HERDS, DIAGNOSED WITH
SPORADIC CJD ???
The chances of a person or domestic animal contracting CWD are “extremely
remote,” Richards said. The possibility can’t be ruled out, however. “One could
look at it like a game of chance,” he explained. “The odds (of infection)
increase over time because of repeated exposure. That’s one of the downsides of
having CWD in free-ranging herds: We’ve got this infectious agent out there that
we can never say never to in terms of (infecting) people and domestic
livestock.”
P35
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A
WISCONSIN STRAIN OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of
Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2
Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary
Research Institute, 4.Center for Prions and Protein Folding Diseases, 5
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
T6G 2P5
The identification and characterization of prion strains is increasingly
important for the diagnosis and biological definition of these infectious
pathogens. Although well-established in scrapie and, more recently, in BSE,
comparatively little is known about the possibility of prion strains in chronic
wasting disease (CWD), a disease affecting free ranging and captive cervids,
primarily in North America. We have identified prion protein variants in the
white-tailed deer population and demonstrated that Prnp genotype affects the
susceptibility/disease progression of white-tailed deer to CWD agent. The
existence of cervid prion protein variants raises the likelihood of distinct CWD
strains. Small rodent models are a useful means of identifying prion strains. We
intracerebrally inoculated hamsters with brain homogenates and phosphotungstate
concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD
endemic area) and experimentally infected deer of known Prnp genotypes. These
transmission studies resulted in clinical presentation in primary passage of
concentrated CWD prions. Subclinical infection was established with the other
primary passages based on the detection of PrPCWD in the brains of hamsters and
the successful disease transmission upon second passage. Second and third
passage data, when compared to transmission studies using different CWD inocula
(Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin
white-tailed deer population is different than the strain(s) present in elk,
mule-deer and white-tailed deer from the western United States endemic region.
*** 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.
P35
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A
WISCONSIN STRAIN OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of
Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2
Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary
Research Institute, 4.Center for Prions and Protein Folding Diseases, 5
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
T6G 2P5
The identification and characterization of prion strains is increasingly
important for the diagnosis and biological definition of these infectious
pathogens. Although well-established in scrapie and, more recently, in BSE,
comparatively little is known about the possibility of prion strains in chronic
wasting disease (CWD), a disease affecting free ranging and captive cervids,
primarily in North America. We have identified prion protein variants in the
white-tailed deer population and demonstrated that Prnp genotype affects the
susceptibility/disease progression of white-tailed deer to CWD agent. The
existence of cervid prion protein variants raises the likelihood of distinct CWD
strains. Small rodent models are a useful means of identifying prion strains. We
intracerebrally inoculated hamsters with brain homogenates and phosphotungstate
concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD
endemic area) and experimentally infected deer of known Prnp genotypes. These
transmission studies resulted in clinical presentation in primary passage of
concentrated CWD prions. Subclinical infection was established with the other
primary passages based on the detection of PrPCWD in the brains of hamsters and
the successful disease transmission upon second passage. Second and third
passage data, when compared to transmission studies using different CWD inocula
(Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin
white-tailed deer population is different than the strain(s) present in elk,
mule-deer and white-tailed deer from the western United States endemic region.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
Liuting Qing and Qingzhong Kong
Case Western Reserve University; Cleveland, OH USA
Chronic wasting disease (CWD) is a widespread prion disease in
free-ranging and captive cervid species in North America, and there is evidence
suggesting the existence of multiple CWD strains. The susceptibility of human
CNS and peripheral organs to the various CWD prion strains remains largely
unclear. Current literature suggests that the classical CWD strain is unlikely
to infect human brain, but the potential for peripheral infection by CWD in
humans is unknown. We detected protease-resistant PrpSc in the spleens of a few
humanized transgenic mice that were intracerebrally inoculated with natural CWD
isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated
mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral
challenge with such PrpSc-positive humanized mouse spleen already led to prion
disease in most animals. ***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
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki
Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and
Mark W. Head1
1National CJD Research and Surveillance Unit; Centre for Clinical Brain
Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh,
UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food
Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious
Pathogen Research Section; Central Research Laboratory; Japan Blood Products
Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku
University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division;
The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush;
Midlothian; Edinburgh, UK
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic
prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans.
In contrast, classical scrapie in sheep is thought to offer little or no danger
to human health. However, a widening range of prion diseases have been
recognized in cattle, sheep and deer. The risks posed by individual animal prion
diseases to human health cannot be determined a priori and are difficult to
assess empirically. The fundamemal event in prion disease pathogenesis is
thought to be the seeded conversion of normal prion protein (PrPC) to its
pathological isoform (PrPSc). Here we report the use of a rapid molecular
conversion assay to test whether brain specimens from different animal prion
diseases are capable of seeding the conversion of human PrPC ro PrPSc.
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE,
classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain
homogenates were tested for their ability to seed conversion of human PrPC to
PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed
human PrPSc was detected by protease digestion and western blotting using the
antibody 3F4.
Results. C-type BSE and vCJD were found to efficiently convert PrPC to
PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion
diseases tested only chronic wasting disease appeared to have the capability ro
convert human PrPC to PrPSc. The results were consistent whether the human PrPC
came from human brain, humanised transgenic mouse brain or from cultured human
cells and the effect was more pronounced for PrPC with methionine at codon 129
compared with that with valine.
Conclusion. Our results show that none of the tested animal prion disease
isolates are as efficient as C-type BSE and vCJD in converting human prion
protein in this in vitro assay. ***However, they also show that there is no
absolute barrier ro 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
Sunday, July 21, 2013
*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for
humans?
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2
Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch
Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and
Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany
†Presenting author; Email: dausm@rki.de
Chronic wasting disease (CWD) is a contagious, rapidly spreading
transmissible spongiform encephalopathy (TSE) occurring in cervids in North
America. Despite efficient horizontal transmission of CWD among cervids natural
transmission of the disease to other species has not yet been observed. Here, we
report a direct biochemical demonstration of pathological prion protein PrPTSE
and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected
cervids. The presence of PrPTSE was detected by Western- and postfixed frozen
tissue blotting, while the seeding activity of PrPTSE was revealed by protein
misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal
muscles of CWD-infected WTD was estimated to be approximately 2000- to
10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE
was located in muscle- associated nerve fascicles but not, in detectable
amounts, in myocytes.
***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.
PPo3-7:
Prion Transmission from Cervids to Humans is Strain-dependent
Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi
Gambetti and Liuting Qing Department of Pathology; Case western Reserve
University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial
Sloan-Kettering Cancer Center; New York, NY USA
Key words: CWD, strain, human transmission
Chronic wasting disease (CWD) is a widespread prion disease in cervids
(deer and elk) in North America where significant human exposure to CWD is
likely and zoonotic transmission of CWD is a concern. Current evidence indicates
a strong barrier for transmission of the classical CWD strain to humans with the
PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD
strains. What remain unknown is whether individuals with the PrP-129VV/MV
genotypes are also resistant to the classical CWD strain and whether humans are
resistant to all natural or adapted cervid prion strains. 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. Preliminary results on CWD transmission in transgenic mice
expressing human PrP-129V will also be discussed.
Acknowledgement Supported by NINDS NS052319 and NIA AG14359.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A.
Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and
related Brain disorders; Dept of Neurology; University of Texas Houston Medical
School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular
Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky
Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve
University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago;
Chicago, IL USA
Prion diseases are infectious neurodegenerative disorders affecting humans
and animals that result from the conversion of normal prion protein (PrPC) into
the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of
cervids is a prion disorder of increasing prevalence within the United States
that affects a large population of wild and captive deer and elk. CWD is highly
contagious and its origin, mechanism of transmission and exact prevalence are
currently unclear. The risk of transmission of CWD to humans is unknown.
Defining that risk is of utmost importance, considering that people have been
infected by animal prions, resulting in new fatal diseases. To study the
possibility that human PrPC can be converted into the infectious form by CWD
PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification
(PMCA) technique, which mimic in vitro the process of prion replication. Our
results show that cervid PrPSc can induce the pathological conversion of human
PrPC, but only after the CWD prion strain has been stabilized by successive
passages in vitro or in vivo. Interestingly, this newly generated human PrPSc
exhibits a distinct biochemical pattern that differs from any of the currently
known forms of human PrPSc, indicating that it corresponds to a novel human
prion strain. ***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
Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany
Key words: CWD, strains, FT-IR, AFM
Chronic wasting disease (CWD) is one of three naturally occurring forms of
prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie
in sheep. CWD is contagious and affects captive as well as free ranging cervids.
As long as there is no definite answer of whether CWD can breach the species
barrier to humans precautionary measures especially for the protection of
consumers need to be considered. In principle, different strains of CWD may be
associated with different risks of transmission to humans. Sophisticated strain
differentiation as accomplished for other prion diseases has not yet been
established for CWD. However, several different findings indicate that there
exists more than one strain of CWD agent in cervids. We have analysed a set of
CWD isolates from white-tailed deer and could detect at least two biochemically
different forms of disease-associated prion protein PrPTSE. Limited proteolysis
with different concentrations of proteinase K and/or after exposure of PrPTSE to
different pH-values or concentrations of Guanidinium hydrochloride resulted in
distinct isolate-specific digestion patterns. Our CWD isolates were also
examined in protein misfolding cyclic amplification studies. This showed
different conversion activities for those isolates that had displayed
significantly different sensitivities to limited proteolysis by PK in the
biochemical experiments described above. We further applied Fourier transform
infrared spectroscopy in combination with atomic force microscopy. This
confirmed structural differences in the PrPTSE of at least two disinct CWD
isolates. The data presented here substantiate and expand previous reports on
the existence of different CWD strains.
http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHP
SESSID=a30a38202cfec579000b77af81be3099
2012
Envt.06:
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human
Primates
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2
Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6
and Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food
Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS
USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa,
ON Canada
†Presenting author; Email: emmanuel.comoy@cea.fr
The constant increase of chronic wasting disease (CWD) incidence in North
America raises a question about their zoonotic potential. A recent publication
showed their transmissibility to new-world monkeys, but no transmission to
old-world monkeys, which are phylogenetically closer to humans, has so far been
reported. Moreover, several studies have failed to transmit CWD to transgenic
mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the
only animal prion disease for which a zoonotic potential has been proven. We
described the transmission of the atypical BSE-L strain of BSE to cynomolgus
monkeys, suggesting a weak cattle-to-primate species barrier. We observed the
same phenomenon with a cattleadapted strain of TME (Transmissible Mink
Encephalopathy). Since cattle experimentally exposed to CWD strains have also
developed spongiform encephalopathies, we inoculated brain tissue from
CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice
overexpressing bovine or human PrP. Since CWD prion strains are highly
lymphotropic, suggesting an adaptation of these agents after peripheral
exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid
brains using the oral route. Nearly four years post-exposure, monkeys exposed to
CWD-related prion strains remain asymptomatic. In contrast, bovinized and
humanized transgenic mice showed signs of infection, suggesting that CWD-related
prion strains may be capable of crossing the cattle-to-primate species barrier.
Comparisons with transmission results and incubation periods obtained after
exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted
TME) will also be presented, in order to evaluate the respective risks of each
strain.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2
Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch
Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and
Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany
†Presenting author; Email: dausm@rki.de
Chronic wasting disease (CWD) is a contagious, rapidly spreading
transmissible spongiform encephalopathy (TSE) occurring in cervids in North
America. Despite efficient horizontal transmission of CWD among cervids natural
transmission of the disease to other species has not yet been observed. Here, we
report a direct biochemical demonstration of pathological prion protein PrPTSE
and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected
cervids. The presence of PrPTSE was detected by Western- and postfixed frozen
tissue blotting, while the seeding activity of PrPTSE was revealed by protein
misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal
muscles of CWD-infected WTD was estimated to be approximately 2000- to
10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE
was located in muscle- associated nerve fascicles but not, in detectable
amounts, in myocytes. 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.
Wednesday, December 4, 2013
Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine
Products; Final Rule Federal Register / Vol. 78 , No. 233 / Wednesday, December
4, 2013
TO ALL IMPORTING COUNTRIES THAT IMPORTS FROM THE USA, BE WARNED, NEW MAD
COW BSE REGULATIONS USDA, AND OIE, not worth the paper the regulations were
wrote on, kind of like the mad cow feed ban of August 1997, nothing but ink on
paper $$$
full text ;
Sunday, August 11, 2013
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
From:noreply@parliament.uk
Sent: Tuesday, December 03, 2013 4:49 AM
To:Terry Singeltary Sr
Subject: Written submission to House of Commons Science and Technology
Committee inquiry
Thank you for your written submission to the House of Commons Science and
Technology Committee inquiry on Blood, tissue and organ screening. We will be in
touch if we have any further questions.
From:Terry S. Singeltary Sr. Sent:
Monday, December 02, 2013 9:18 PM
To:CJDVOICE CJDVOICE Cc:bloodcjd bloodcjd
Subject: [BLOODCJD] A parliamentary inquiry has been launched today into
the safety of blood, tissue and organ screening following fears that vCJD – the
human form of ‘mad cow’ disease – may be being spread by medical procedures
Monday, December 02, 2013
A parliamentary inquiry has been launched today into the safety of blood,
tissue and organ screening following fears that vCJD – the human form of ‘mad
cow’ disease – may be being spread by medical procedures
Wednesday, November 27, 2013
NHS failed to sterilise surgical instruments contaminated with 'mad cow'
disease
IATROGENIC
all iatrogenic cjd is, is sporadic CJD, until route and source of the
iatrogenic event that took place, is detected, documented, placed in the
academic domain as fact, and recorded, which happens very seldom due to a lot of
factors, besides the incubation period, and that be mainly industry. kind of
like asbestos and tobacco and the industry there from, they knew in the early
1900’s that they both were killing, and they both had long incubation, and
somebody chose not to do anything about if for decades and decades. kind of like
what we have here with the TSE prion disease. $$$
> In 12 of 15 hospitals with neurosurgical incidents, a decision was
made to notify patients of their potential exposure.
SO, X number of patients, from 3 hospitals, where
''exposure to potentially CJD-contaminated instruments ''
took place on these patients, the final decision NOT to tell those folks
about the potential exposure to the CJD TSE prion
insane, thus, the TSE prion agent continues to spread. ...please see
further comments here ;
Saturday, November 16, 2013
Management of neurosurgical instruments and patients exposed to
creutzfeldt-jakob disease 2013 December
Infect Control Hosp Epidemiol.
Thursday, November 14, 2013
Prion diseases in humans: Oral and dental implications
Saturday, November 2, 2013
Recommendation of the Swiss Expert Committee for Biosafety on the
classification of activities using prion genes and prion protein January 2013
Friday, November 29, 2013
Identification of Misfolded Proteins in Body Fluids for the Diagnosis of
Prion Diseases
International Journal of Cell Biology
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
TSS
posted by Terry S. Singeltary Sr. at
3:03 PM
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