NEBRASKA CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT
NEBRASKA
CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT MAP
NEBRASKA CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT
Chronic Wasting Disease (CWD) Chronic Wasting Disease (CWD) was first
discovered in Colorado in 1967 and in Nebraska in 2000 in Kimball County. Since
1997 Game and Parks staff have tested nearly 49,000 deer and found 289 that
tested positive. CWD is now found in 30 counties, some as far east as Grand
Island...
SNIP...
Reported locations CWD has been reported in the following Nebraska
counties:
Arthur Banner Boone Box Butte Buffalo Cherry Cheyenne Custer Dawes Deuel
Furnas Garden Grant Hall Harlan Hitchcock Holt Hooker Keith Kimball Lincoln Loup
Morrill Nance
Phelps Red Willow Scotts Bluff Sheridan Sioux Webster
SNIP...
What you should know CWD is prion disease that attacks the brain of an
infected deer and elk, eventually causing emaciation, listlessness, excessive
salivation and death. Infection rates in harvested animals in some deer
management units exceed 6 percent, but there have been no population declines in
Nebraska attributed to CWD at this time
Human health concerns for CWD remain modest, as no person is known to have
contracted CWD from eating an infected deer. However, given the number of human
deaths in Europe linked to bovine spongiform encephalopathy, also known as mad
cow disease, people should remain cautious in how they handle, process and
consume deer. Hunters and commercial processors should avoid any butchering or
processing of deer that spreads spinal cord or brain tissue to meat or to the
environment.
Deer health concerns remain a primary concern, and hunters can help prevent
the spread of CWD by using proper carcass disposal methods. CWD prions can
remain viable for months or even years in the soil. We advise hunters to field
dress animals at the place of kill and to dispose of the head (brain), spinal
column and other bones at a licensed landfill.
While the exact method of CWD transmission is unknown, we know that CWD is
transmitted from animal to animal. In all probability, the transmission is
through body fluids like feces, urine or saliva. Animals that are crowded or
confined have a greater chance of encountering the body fluids of other animals
and, therefore, a higher likelihood of becoming infected if CWD prions are
present.
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Voluntary CWD Plan
Program Guidelines for Nebraska Chronic Wasting Disease - Cervid Monitoring
Program Part 1 - Definitions
Affected Herd: Any herd in which an animal has been determined to be CWD
positive.
Animal: Any domesticated mule deer, white-tailed deer, or elk.
Commingling: Animals grouped together having physical contact, e.g.,
sharing common pastures. Commingling does not include limited contacts, such as
contact at auction/sales or during transportation as long as animals are in
separate compartments.
Chronic Wasting Disease (CWD): A non-febrile, transmissible, insidious,
degenerative disease affecting the central nervous system of deer and elk. CWD,
a transmissible spongiform encephalopathy, may cause, but is not limited to, the
following signs in affected animals:
weight loss, poor condition salivating, drooling behavioral abnormalities
abnormalities such as incoordination swaying of back end, weakness recumbency It
is important to note that not all CWD-affected animals show all clinical signs.
CWD-Positive Animal: An animal which has had a diagnosis of CWD confirmed
by the National Veterinary Services Laboratory (NVSL), United States Department
of Agriculture, Ames, Iowak, or any additional laboratory approved approved by
NVSL.
CWD Suspect: An animal which displays clinical signs suggestive of CWD, or
for which laboratory analysis is not conclusive.
Department: The Nebraska Department of Agriculture.
Enrolled Herd: A herd participating in the Program which has met the
requirements listed in Part 2 of these Guidelines.
Enrollment Date: The date on which the Department approved the application,
or the date the Department can verify that the requirements listed in Part 2 of
these guidelines have been met.
Herd Status: Classification of a herd with regard to CWD in the Nebraska
CWD Cervid Herd Monitoring Program.
Herd: Any group of animals maintained on common ground for any purpose, or
two or more groups of animals under common ownership or supervision,
geographically separated but which have an interchange of animals without regard
to whether the animals are infected or exposed.
Owner: An individual, partnership, company, corporation, or other legal
entity which has legal or rightful title to an animal or animals, regardless of
any liens held on the animal(s).
Premises: The ground, area, buildings, and equipment occupied by one or
more herds of animals.
Program: The Nebraska Chronic Wasting Disease (CWD) Cervid Herd Monitoring
Program.
Trace-Back Herd: A herd(s) where an affected animal has resided up to 36
months prior to death.
Trace-Forward Herd: A herd(s) which has received animals from an affected
herd within 36 months prior to the death of an affected animal.
Part 2 - Requirements for entry into the Program
Applicant must have a Domesticated Cervine Animal Facility Permit and a
herd identification number and be in compliance with Domesticated Cervine Animal
Act and Domesticated Cervine Animal Regulations.
There must be no indication of CWD in the herd in the past 12 months, as
attested to by the owner and his veterinarian or area veterinarian.
Program application form must be completed, signed and submitted to the
Department. Part 3 - Program Protocol
A. General Provisions
The herd owner or manager who participates in the Program shall agree to do
the following: Identify all animals 12 months of age or over within the herd, as
provided for in Title 23 Chapter 16, Domesticated Cervine Animal Regulations,
Section 006.
Report all death losses of animals over 16 months of age that die from any
cause and ensure that proper tissue samples are collected and submitted for
diagnostic purposes as provided for in Title 23, Chapter 16, Domesticated
Cervine Animal Regulations, Section 014.
Report to the Department any animals that escape from the herd enclosure,
as provided for in section Title 23, Chapter 16, Domesticated Cervine Animal
Regulations, Section 010.
Maintain a current herd inventory report which shall include the following
records on animals present in the herd:
Official and visible identification numbers. Sex, breed and age.
Disposition of animals - date and reason for removal from the herd. Primary and
secondary identification numbers and sex and birth dates of progeny. Date of
birth and date of entry for acquired animals, as well as herd of origin. Copies
of laboratory reports of CWD submissions. These records will be kept on each
animal for five years after removal from the herd for any reason.
Make all animals and records available as provided for in Title 23, Chapter
16, Domesticated Cervine Animal Regulations, Section 13. B. Inspections
Inspections of CWD Monitored Herds and their inventory records will be done as
provided for in Title 23, Chapter 16, Domesticated Cervine Animal Regulations,
Section 004. C. Program Status A herd will gain program status based on the
herd's enrollment date and the continuous number of years in the program. Once a
herd is approved to participate in the program, the herd will be considered an
enrolled herd with the date of approval being the enrollment date. The status
will be dependent on the herd being in compliance with the Program Guidelines
and being approved annually for advancement in the program. Non-Participant
refers to any herd which is not enrolled in the Program.
Enrolled herd refers to any herd that has been approved to participate in
the Program. Program Classification will be as follows:
Year 0 - herd is enrolled in the program, but has not completed one year of
herd surveillance. Year 1 - one year of surveillance and successful completion
of program requirements. Year 2 - two years of surveillance and successful
completion of program requirements. Years 3, 4, 5, etc. - for each successive
year of surveillance. D. Management of CWD Affected or Exposed Herds Affected
Herd - If an enrolled herd has a confirmed diagnosis of CWD, the Department will
issue a quarantine and the herd will be removed from the Monitored CWD Cervid
Herd Status Program.
Trace-back or Trace-forward Herd - If an epidemiologic investigation
reveals an enrolled herd to be a Trace-back or Trace-forward herd, the
Department may issue a hold order, quarantine, or suspend the CWD monitoring
program status, and will develop a herd plan based on the epidemiological
investigation. E. Acquisitions and Commingling Enrolled herds may acquire
animals from another enrolled herd with the same or higher management level.
Such animals will assume the level of the receiving herd. If the animal(s) is
received from a herd with a lower management level, the receiving herd will
maintain its management level, but the imported animal(s) will retain the level
of the herd of origin. (The herd status would reflect both levels.)
When establishing a new herd entirely from an enrolled herd, the herd of
origin's status level will transfer to the new herd if the new herd owner
notifies the Department and submits an application for participation in the
program within 90 days of the animals arrival on the farm and before any herd
additions. Applications received more than 90 days after arrival will be
reviewed by the Department. The enrollment date of the new herd will be the date
of the approval by the Department. F. Use of Semen and Embryos Enrolled herds
may not use germ plasm from any donor found to be CWD positive. Enrolled herds
may use semen from lower status or non-participating herds with no effect on
program status as long as the semen is not from infected herds or trace herds at
the time of collection. Embryo recipient animals must meet the programs
requirements for animal acquisitions. G. Animals Imported From Foreign Countries
Imported animals from foreign countries may enter the program at the appropriate
level if they have an equivalent certification program, or are recognized free
of CWD by APHIS standards. If animals at any time commingle with animals of a
lower program status before entering the recipient herd, they will enter at the
lowest status of the commingled herds. Part 4 - Herd Information The Department
will maintain an information database that will include all enrolled herds and
their respective herd status levels.
Interested parties may access this information during working hours by
telephone, 402-471-2351. The following information will be made available to the
public on herds participating in the program: Name, address, enrollment date and
herd status level.
Part 5 - Laboratory Submission of Samples
All tissues submitted for CWD diagnostic testing shall be submitted to the
National Veterinary Services Laboratory (NVSL), United States Department of
Agriculture, Ames, Iowa, and additional laboratories approved by NVSL.
CWD Testing Procedure for Removal of the Brain Stem & Cerebellum for
CWD Testing in Cervine Animals http://www.nda.nebraska.gov/animal/diseases/chronic_wasting/test.html
Retropharyngeal Lymph Node Collection Procedure
Nebraska Scrapie Eradication Program A Program for Nebraska Sheep and Goat
Producers History Disease Information Scrapie Eradication Program Voluntary
Flock Certification Program Nebraska Department of Agriculture Animal Health In
cooperation with United States Department of Agriculture University of Nebraska
Extension
History of Scrapie The disease known as Scrapie has been recognized for
more than 250 years. The unusual name was coined from sheep trying to relieve
the intense itching which results in "scraping" off the wool. In 1947, scrapie
was introduced into a Michigan flock through sheep imported from Britain.
Scrapie has spread throughout the U.S. since that time. In 2002, new cases of
scrapie totaled 259 and 5 goats were also found infected. Hundreds more cases
have been found since then.
The Cause Scrapie is a member of a family of diseases known as
Transmissible Spongiform Encephalopathys (TSEs). TSEs are caused by an
infectious protein called a prion. After prions are ingested, they enter the
lymphatic system and travel to lymph nodes. After many months, the prions are
found in the brain where they cause "holes" in the brain tissue giving it a
sponge-like appearance. Other TSE-type diseases are Bovine Spongiform
Encephalopathy (BSE) in cattle, Chronic Wasting Disease (CWD) in deer, and
Creutzfeldt - Jakob disease (CJD) in humans.
A Slow Developing Disease Sheep (and goats) are infected at a very young
age, but may not show symptoms of disease until two - six years of age. Goats
are susceptible to scrapie when raised together with sheep but do not appear to
spread the disease. Symptoms develop slowly and may go unrecognized at first.
Symptoms may include:
Weight loss, despite normal appetite; Behavioral changes; Excessive itching
and rubbing; Wool pulling or biting; Lip smacking; Loss of coordination;
Startling at sudden noise or movement; High-stepping gait (front legs);
Bunny-hop movement (rear legs); Tremors; Swaying of back-end; Down, unable to
stand; and Death. Since scrapie affects the central nervous system, it can be
confused with other diseases. Remember, symptoms of scrapie may take months to
develop and is always fatal.
Scrapie Diagnosis A positive diagnosis of scrapie in a flock is based on
symptoms, duration of illness, and submission of brain tissues from an affected
animal. The presence of prions in a microscopic section of brain tissue is the
only method to be certain that sheep are infected with scrapie. A test of lymph
tissue contained in the third-eyelid of sheep can be performed by a regulatory
veterinarian in some instances, but this test is not used for routine scrapie
diagnosis. If you suspect that one of your sheep may be infected with scrapie,
you should contact your local veterinarian for a diagnosis.
Scrapie and Genetics Research has shown that certain genes in the DNA of
sheep play a role in the development of scrapie. The testing for the resistance
or susceptibility of sheep to scrapie can be done with a blood sample drawn from
the sheep in question. An approved laboratory can determine the resistance or
susceptibility to scrapie by examining the DNA at Codon 171of the genetic
make-up. Letter designations are reported for each strand of the DNA. An "R" at
Codon 171 indicates resistance to scrapie, whereas, a "Q" or "H" indicates
susceptibility. Three combinations are possible since there are two strands of
DNA:
RR = Highly resistant QR = Moderate resistance QQ = Susceptible By knowing
the genetics of breeding animals, producers can actually breed more resistance
to scrapie into their flock. Producers who retain their own replacement ewe
lambs can begin influencing their flock resistance to scrapie by selecting rams
that have been DNA tested and certified by an approved lab as carrying the "RR"
gene at Codon 171. In a few years, the flock resistance to scrapie will be
greatly increased. There is no genetic test available for goats at this time.
Scrapie Eradication USDA's Animal Plant Health Inspection Service (APHIS)
launched a new and enhanced Scrapie Eradication Program in November of 2002. All
states agreed to be consistent with the program so producers could transport
sheep between states. Scrapie costs American sheep producers an estimated $25
million annually. Trade barriers exist with Scrapie-Free countries, such as
Australia and New Zealand. Rendering companies will not pick up dead sheep
because of scrapie concerns.
The Scrapie Eradication Program utilizes genetics in a flock based clean-up
plan. Slaughter surveillance of cull ewes will identify infected flocks.
Infected flocks will be DNA tested and the scrapie infected and susceptible
sheep removed.
USDA has funds available for the clean-up of infected flocks including the
costs associated with DNA testing, and the purchase of infected and susceptible
sheep at fair market value.
Other aspects of the eradication program include identification of sheep
and goats with official USDA scrapie tags in:
Breeding sheep and sheep older than 18 months at the time of sale; Purebred
goats and goats that have resided with sheep; and All unaltered sheep and goats
for exhibition. Producers must also keep good records including names and
addresses of purchases and sales of sheep from the flock. Voluntary Scrapie
Flock Certification Program With the implementation of the Voluntary Scrapie
Flock Certification Program in 1992 and modified in 1997, USDA provided
producers with the opportunity to protect their sheep from scrapie and to
enhance the marketability of their animals through certifying their origin in
scrapie-free flocks. The intent of the program is to monitor flocks over a
period of five years or more to identify flocks that are free of scrapie.
Because there is no live animal test for this disease and scrapie has a long
incubation period, a flock is considered free of disease if no sheep have been
diagnosed with scrapie over a period of time. The longer a flock is enrolled and
following the requirements of the program, the more likely the sheep in the
flock are free of scrapie.
The economic value of animals in enrolled flocks increases the longer they
are in the program, especially once the flock is certified. Animals from
certified flocks are a valuable source for replacement breeding animals,
especially when the genetics of the replacements are known.
When participating in the program, flock owners must:
Report any scrapie suspects immediately to animal health official;
Officially identify all sheep over one year of age or when a change of ownership
occurs (except slaughter) Maintain adequate records including all sales,
purchases, births and deaths for a minimum of five years; Agree to an annual
inspection by regulatory health officials for symptoms of scrapie, record
completeness, and verifying identification of the flock; and Purchase
replacement breeding animals from flocks of equal or higher status. A list of
flocks enrolled in the certification program and their status is available on
the USDA web site. Nebraska Efforts The Nebraska Bureau of Animal Industry (BAI)
working together with USDA/APHIS has begun efforts throughout the state to
eradicate scrapie.
Sheep producers within the state have been issued official identification
tags by USDA/APHIS to use when selling animals from their flocks. A statewide
effort to educate producers and give veterinarians new information about scrapie
has been started and will continue to expand as the program develops. Several
infected flocks in Nebraska have been cleaned up since the Scrapie Eradication
Program began in 2001. New interest has developed from producers in the
Voluntary Scrapie Flock Certification Program. Nebraska Sheep Statistics 1,685
Nebraska flocks 98,500 breeding sheep These numbers are based on flocks
registered with USDA/APHIS/VS. Genetic Testing for Scrapie available at:
Gene Check, Inc. 1629 Blue Spruce Drive, Ste 106 Fort Collins, CO 80524
800-822-6740 More Information Available on the Web at: United States Department
of Agriculture
Bovine Spongiform Encephalopathy (BSE) Prevention The Nebraska Department
of Agriculture, Animal Health is carefully monitoring the present situation with
Foreign Animal Diseases that have surfaced around the globe. It is imperative
that we stay abreast of animal health issues that could affect our state, as
well as in foreign countries. With this mission, it is equally important that we
educate producers and consumers across Nebraska on the issues and address
concerns related to their food production.
This site will link you to the United States Department of Agriculture's
(USDA) direct web sites which contain facts and address questions regarding BSE
(Mad Cow Disease). We urge you to use these resources to assist you as you
become informed on the situation.
The Nebraska Department of Agriculture, Animal Health, can be reached at
402-471-2351 for reporting or inquiring for further information.
Procedure for removal of the brain stem.
NDA Abbreviated Response Summary: Foreign Animal Disease Emergency Response
Levels
FAD Emergency Response – Level 3
FAD Emergency Response – Level 4
FAD Emergency Response – Level 5
General Information about BSE.
Producers (Ruminant Feeders)
Feed Manufacturers
Transporters
ruminant feed and BSE TSE Prion LOL!
Friday, January 29, 2016
NEBRASKA Three Positives for CWD Found in Recent Testing of Deer
Wednesday, January 25, 2012
*** Nebraska Fish and Game Association Censors Singeltary from speaking
about Chronic Wasting Disease (CWD) again ***
*** Nebraska Fish and Game Association Censors Singeltary from speaking
about Chronic Wasting Disease (CWD) again, what is Nebraska hiding ? ***
*** Elk and Deer Use of Mineral Licks: Implications for Disease
Transmission ***
01-19-2012, 06:58 PM Elk and Deer Use of Mineral Licks: Implications for
Disease Transmission
Wednesday, January 04, 2012
CWD NEBRASKA NGPC 26 DEER CARCASSES TESTED POSITIVE BUFFALO, CUSTER AND
HOLT COUNTIES DURING NOVEMBER HUNT
Tuesday, April 24, 2012
NEBRASKA CHRONIC WASTING DISEASE CWD SPREADING SLOWLY 2011 REPORT GAME FARM
RANCH UPDATE
There were 1,565 lymph node samples collected from deer taken during the
2011 November firearm deer season, with 26 samples testing positive for CWD. In
addition, samples were taken from 37 culled deer that showed clinical symptoms
for CWD, with one male mule deer from Garden County testing positive. Those
symptoms include a rough, emaciated appearance and a lack of fear of humans.
There were a record 51 positives from 3,645 samples in Nebraska in 2010.
However, the surveillance effort was reduced in 2011 due to a lack of funds. The
2011 effort focused on central Nebraska, the leading edge of the disease as it
spreads from west to east.
Wednesday, January 25, 2012
Nebraska Fish and Game Association Censors Singeltary from speaking about
Chronic Wasting Disease (CWD) again
snip...
2012
NOW, let me be perfectly clear. this time, it was the Nebraska Fish and
Game Association that allowed me back on board, to post about CWD, after I had
asked them to do so. what happened was, I got to speaking the truth about game
farms, and CWD spreading there from, and a certain few complained, and kept
complaining, they did not want anymore information (valid scientific peer review
journals) that might hurt their industry. SO, I thank NFGC again for giving me a
chance to try and educate hunters on CWD and the TSE prion disease. I think I
supplied enough information to help educate, the ones that wanted to be
educated, however, it’s the other folks I am concerned about. the ones that
don’t want to be educated on this CWD, the ones that don’t want to speak about
it, or learn about, and they don’t want others to either. these few folks are
the ones that will help continue the spread of CWD. these folks caused the
surpressing of CWD TSE prion information. to be good stewards of the woods and
hunt, you cannot stick your head in the sand. these few folks did, and in doing
so, they want everyone else’s head in the sand. and that’s been the problem all
along. ...good luck!
so much for freedom of speech. can’t say I did not try. ... TSS
snip...
Wednesday, March 02, 2011
CWD IN NEBRASKA IS INCREASING WITH 51 POSITIVE CASES IN 2010
Wednesday, February 04, 2009
Nebraska reports 22 cases of CWD in deer
Tuesday, December 18, 2007
NEBRASKA CWD tested 3,400 deer, with 17 testing positive 2007
Singeltary permanently banned from NEFGA for speaking about Chronic Wasting
Disease CWD TSE Prion...see;
Monday, March 17, 2014
NEBRASKA CHRONIC WASTING DISEASE CWD TSE PRION DISEASE 2013-2014 UPDATE MIA
?
Greetings again Nebraska CWD officials et al,
I thought I should update you a bit on CWD TSE Prion. I hope you don’t
mind. it’s been a while, so I thought it was time. lot going on.
I am still banned from posting on http://www.nefga.org/
you can see a bit of history here, and in the full history of me being
banned in the link below in the post, there is another link.
CWD GAME FARMS AND RANCHES IN NEBRASKA and RISK FACTOR THERE FROM
Although the Game and Parks Commission's wildlife management areas and U.S.
Forest Service pastures in the Bordeaux and Hat Creek units provide some
opportunities for elk hunters, most elk taken in Nebraska are killed on private
land. Obtaining private land access to hunt elk is difficult, but not
impossible, and a growing number of Nebraska landowners charge fees for hunting
privileges.
snip...see full text ;
The director and the moderators of this forum came together and voted to
ban you from this forum. We had a lot of members complain about the way you wet
about posting your threads.
I personally would like to say thanks for helping some of our members
realize the importance of CWD and the affects. Thank you for your time.
Best regards, xxxx
==============================
Terry,
First off, I would like to apologize for the harsh manner in which you have
been greeted on this site. As you said, I'm sure you are used to it but that is
no excuse. I know there have been problems in the past of people registering on
this forum to simply blow their own horn and promote their own cause. One guy
was trying to convince people common carp were the best game fish and threatened
to stock them into every public body of water he could reach! Notwithstanding,
the greeting you received was unnecessarily harsh and a poor representation of
the majority of people on this site.
Regarding CWD, I am not too familiar with the disease but I do try to keep
up on the current state it. I too am puzzled why the people with the largest
interest in deer are so resistant to learn more about this major issue. It
certainly seems like you know what you are talking about and as you have said
you have spent many years learning about and researching this topic.
One small piece of advice I may offer you is to introduce yourself and give
some background information about yourself. Where are you from? Do you hunt or
fish? Why are you interested in CWD/TSE? Do you work professionally with this
topic? Just some ideas. I understand you are trying to provide a large amount of
information and are unable to post links to articles, but the large blocks of
text pasted in your posts comes off as impersonal and abrasive to some,
especially from a new member.
I hope you stick around, I am always eager to learn especially when the
issue is something as large as this.
Regards xxxxxxx
***************
I was waaaay too far down the food chain to know him! The only vets I knew
were the IIC's (inspector in charge) if whatever establishment I was working at.
With the game and parks pushing increased white tail doe harvest in our state as
a result of politically motivated legislation (Senator Lautenbaugh's deer
depredation bill) passed 2 years ago, your information and "sounding the alarm"
is falling on deaf ears with those who have the clout to do anything about it.
It's your right to do what you're doing, but in my opinion it's a waste of time.
Where are you from, and do you eat the deer you kill?
***************
You're proceeding on the wrong assumption. A little background info. would
be in order. I'm a retired Federal Meat and Poultry Inspector for the USDA. I've
educated myself on the CWD issue, and have made my decision in regards to the
consumption (or lack thereof) of venison. You have obviously educated yourself
on this issue, and are free to divulge your information in this forum. I
honestly feel the vast majority of the members of this forum have already made
their decision in regards to this matter; and it is my personal opinion you are,
for lack of a better description, "beating a dead horse". Out of curiosity, have
you had any contact with our states game and parks commission with your
concerns, and if so, what has been their response? xxxx
*************** nobody's trolling here. i asked to come here to speak about
CWD. CWD in Nebraska is mounting, it's spreading, and humans are being exposed
to the CWD agent. if it was just the people that eat meat, were the only ones
that were exposed, that is one thing. but this is about your cervids and
environment, and, when you become exposed with the CWD agent, or any other TSE,
and then have medical or dental or donate blood, you then expose others. so,
it's just not about consumption. i knew there would be some that do not want to
hear it, that's o.k., your entitled to your opinion, but others here may want to
hear some of this, and try and do something to prevent the further exposure and
spreading of the CWD TSE agent. i assure you i am here to promote awareness
about CWD, to promote discussion and debate, nothing else. i am vested in
nothing but the truth, and have been all along. i don't advertise on any of my
blogs i post this CWD TSE science to. it's there for educational purposes. you
need to educate yourself folks, with all the science. and yes, i am anti, i am
anti stupid. i am anti corporate and political science. and the cut and paste
are just facts, they have links. when i can post the links, the posts will be
much shorter. but if it will make you feel better, i will go jump in a lake too,
if you just become more aware to what you are dealing with i.e. CWD TSE prion
disease. i had chicken last night, and a steak last week. oh, and yes somebody
does just show up out of no where, from another state, and talk about CWD. i
did, i do, and i have done it for years, from state to state as they fall with
CWD, or any other TSE in a species. i was asked to be moderator of one State
that fell, after being there for years, and i said the same thing, i can't
moderate a state that i don't live in. but they freely accept the science and
discussion and debate that comes from it. there are a few states that i have had
trouble with, simply because they did not want to hear it, and did not want
there hunters to hear it, because of the financial fallout. one of those states
has recently let me back in to speak and share science about CWD. look, this is
about more than money here, it's about your cervids, and your people. i have
been in the pits for years doing this, debated folks and scientist all over the
world, there is nothing you can say that will hurt my feelings. i am just the
messenger folks, you can hate me, throw all the stones you wish, but read the
science and educate yourself all you can. CWD and TSEs are here. they have even
now linked the TSE agent to Alzheimer's, ALS, Parkinson's disease. and there is
science now showing that Alzheimer's is transmissible. course there was science
showing that a decade ago i.e. transmission studies. what does all this mean? i
cannot answer that. i can tell you this, continue to ignore the CWD TSE agent
and you risk your herd and people. shoot the messenger if you must, (i am full
of holes), but don't ignore the science. ...
kind regards,
terry
*** 2016 CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
***
Subject: NWHC USGS CHRONIC WASTING
DISEASE CWD TSE PRION UPDATE
Chronic wasting disease update 2016
Chronic wasting disease (CWD) is a fatal, contagious,
neurodegenerative disease of cervids (Family Cervidae), including North American
deer (Odocoileus sp.), elk (Cervus canadensis) and moose (Alces alces). The
disease continues to be detected in new geographic locations and with increasing
prevalence in some areas where the disease has been monitored the longest. Since
the beginning of calendar year 2016, CWD has been documented in free-ranging
deer and elk populations in new geographic locations within in Alberta,
Nebraska, Texas and Wyoming, and was detected for the first time in Arkansas.
The disease was also detected in captive white-tailed deer (O. virginianus)
facilities in Texas and Wisconsin. A map of the current known distribution of
CWD in North America is available from the USGS National Wildlife Health Center
(NWHC). In addition, the first detection of CWD in wild reindeer (Rangifer
tarandus), and the first documented CWD cases in Europe were announced by the
Norwegian Veterinary Institute and the Norwegian Environment Agency.
The first detection of CWD in Arkansas, announced by
the Arkansas Game & Fish Commission (AGFC) in February 2016, was a
hunter-killed cow elk taken in 2015 in Newton County. Subsequent to this initial
detection AGFC has conducted outbreak surveillance to determine the geographic
distribution of CWD and the disease prevalence within the affected area. To
date, CWD has been detected in five contiguous northwestern Arkansas counties in
both white-tailed deer and elk, and 23% (62 of 266) of the randomly collected
deer samples have been positive. This high level of prevalence, as measured in
the initial round of sampling, suggests that CWD has been present and undetected
in this population for a protracted period of time. In a second phase of
sampling designed to determine geographic distribution, AGFC is collecting
samples from vehicle-killed deer, deer found dead, and animals exhibiting
clinical signs consistent with CWD.
On April 4 2016 the Norwegian Veterinary Institute
announced detection of CWD in a cow reindeer from the Nordfjella population in
southern Norway. Researchers with the Norwegian Institute for Nature Research
(NINA) were capturing reindeer for a telemetry project in March 2016 when they
observed the animal. The adult female, sick and in less than average physical
condition, died and was submitted for necropsy. Brain samples collected from the
reindeer tested positive for CWD by enzyme-linked immunosorbent assay (ELISA),
western blotting, and immunohistochemistry (IHC). Caribou (Rangifer tarandus)
were previously determined to be susceptible to CWD in a research setting and
scientists expressed concern over how the disease would manifest in a
highly-gregarious cervid species. The detection, from the area of Sogn and
Fjordane, is the first report of CWD in free-ranging reindeer and the first
report in Europe. Norway routinely samples reindeer as a part of their national
surveillance program for CWD and other transmissible spongiform encephalopathies
(TSEs).
Subsequent to intensified disease monitoring, the
Norway Environment Agency announced, on May 25, 2016, the detection of a
CWD-positive moose (Alces alces, commonly referred to as elk in Europe) from the
Selbu municipality of Sor-Trondelag. This region is approximately 300 kilometers
from where the initial CWD-positive reindeer was detected. On June 15, 2016, the
Norwegian Veterinary Institute announced a second CWD-positive moose, also from
the Selbu region. Both moose were necropsied at the Norwegian Veterinary
Institute in Trondheim and their brain tissue tested positive for CWD by ELISA
and western blot. Both moose were adult pregnant females. The first moose was
euthanized based on clinical signs consistent with CWD. The second, found dead
in a river, was in normal condition and necropsy revealed trauma as the cause of
death. At this point, the origin of CWD in Norway and any relationship between
the reindeer and elk cases is undetermined.
To view, search, and download historic and ongoing
wildlife morbidity and mortality event records nationwide visit the Wildlife
Health Information Sharing Partnership event reporting system (WHISPers) online
database: http://www.nwhc.usgs.gov/whispers/
To request diagnostic services or report wildlife
mortality: http://www.nwhc.usgs.gov/services/
2016 CHRONIC WASTING DISEASE CWD TSE PRION
UPDATE
TSE PRIONS AKA MAD COW TYPE DISEASE, LIONS AND TIGERS
AND BEARS, OH MY!
DEER BRAIN SURVEY
***5. Although the sample size would be too small to
provide scientifically valid evidence that there is no cervine spongiform
encephalopathy in the UK (4,000 odd brains would be necessary for that), a
negative result would aid our efforts to have trade in deer resumed.
...end...tss
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY &
HOUND STUDY
Date: Thu, 17 Oct 2002 17:04:51 –0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L
Greetings BSE-L,
is there any other CWD surveys/testing in the UK on
their deer? what sort of testing has been done to date on UK/EU deer? any input
would be helpful... thank you
DEER SPONGIFORM ENCEPHALOPATHY SURVEY
CVO BSE 1 28
DEER BRAIN SURVEY
1. The Parliamentary Secretary will wish to be aware
of a survey of deer brains for signs of a spongiform encephalopathy.
2. The purpose of the study will be to gather
evidence of freedom from any spongiform encephalopathy in the UK deer-
population to support our efforts to resume trade in deer with countries with
which BSE has disrupted it.
3. This will be a low key study with no publicity to
avoid unnecessary media interest. It will be carried out in two stages:
(i) A small scale examination of around 30 deer
brains to establish the normal histology of the healthy brain; and
(ii) A larger scale random examination of 300 or more
adult deer brains drawn from both deer farms and parks to establish whether
there is any evidence of a cervine spongiform encephalopathy.
4. The industry have agreed to cooperate with the
study and will supply the necessary brain material. No compensation will be
paid. The only cost to Government will be for the laboratory examinations which
will be borne within existing resources.
*** 5. Although the sample size would be too small to
provide scientifically valid evidence that there is no cervine spongiform
encephalopathy in the UK (4,000 odd brains would be necessary for that), a
negative result would aid our efforts to have trade in deer resumed.
ROBERT LOWSON
Animal Health (Disease Control) Division
081 330 8042 - GTN 3836
Fax: 081 330 7862
Room 28A TOLB
20 November 1991
Mr Tanner - PS/Mr Maclean
c.c. PS/Minister Dr P Dawson Mr Lawrence PS/Permanent
Secretary Mr Dugdalé Dr Matthews Mr Capstick Mr Bradley — CVL Mr Maslin Mr
MeldrumL Mr Wilesmith - CVL Mr Thomson SOAFD Mr Haddon Mr Bell Mr Shannon DANI
Mr X Taylor Mr Robertson Mr Podmore WOAD
91/11.20/4.1
***5. Although the sample size would be too small to
provide scientifically valid evidence that there is no cervine spongiform
encephalopathy in the UK (4,000 odd brains would be necessary for that), a
negative result would aid our efforts to have trade in deer resumed.
...end...tss
Tuesday, August 02, 2016
Chronic wasting disease of deer – is the battle to
keep Europe free already lost?
Tuesday, April 12, 2016
The first detection of Chronic Wasting Disease (CWD)
in Europe free-ranging reindeer from the Nordfjella population in South-Norway.
Tuesday, June 14, 2016
*** Chronic Wasting Disease (CWD) in a moose from
Selbu in Sør-Trøndelag Norway ***
Thursday, July 07, 2016
Norway reports a third case Chronic Wasting Disease
CWD TSE Prion in 2nd Norwegian moose
14/06/2016 - Norway reports a third case
Saturday, July 16, 2016
Chronic wasting Disease in Deer (CWD or Spongiform
Encephalopathy) The British Deer Society 07/04/2016
Red Deer Ataxia or Chronic Wasting Disease CWD TSE
PRION?
could this have been cwd in the UK back in 1970’S ???
SEE FULL TEXT ;
Sunday, August 28, 2016
CONFIDENTIAL
Transmissible Spongiform Encephalopathy TSE Prion and
how Politics and Greed by the Industry spread madcow type diseases from species
to species and around the globe
TSE PRIONS AKA MAD COW TYPE DISEASE, LIONS AND TIGERS
AND BEARS, OH MY!
Please be assured, the USA does NOT have any clue as
to what the real perspective on the TSE prion disease in domestic feline and
canine, much less our big wild cats, OR any other species including humans for
that matter, but one thing for sure, the studies and history of the mad cow
debacle below are deeply concerning with regards, to humans and wild big cats
like mountain lions, cougars, lynx, Jaguar, and such, that feed on cervids that
are infected with CWD. one thing for sure, don’t kid yourselves, all are very
much susceptible to the TSE Prion disease, and if you don’t look, you don’t
find, problems solved$$$
WDA 2016 NEW YORK
We found that CWD adapts to a new host more readily
than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions.
In addition, we investigated the role of specific regions of the bovine, deer
and human PrP protein in resistance to conversion by prions from another
species. We have concluded that the human protein has a region that confers
unusual susceptibility to conversion by CWD prions.
Student Presentations Session 2
The species barriers and public health threat of CWD
and BSE prions
Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr.
Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University
Chronic wasting disease (CWD) is spreading rapidly
through cervid populations in the USA. Bovine spongiform encephalopathy (BSE,
mad cow disease) arose in the 1980s because cattle were fed recycled animal
protein. These and other prion diseases are caused by abnormal folding of the
normal prion protein (PrP) into a disease causing form (PrPd), which is
pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD
spreads among cervids very efficiently, but it has not yet infected humans. On
the other hand, BSE was spread only when cattle consumed infected bovine or
ovine tissue, but did infect humans and other species. The objective of this
research is to understand the role of PrP structure in cross-species infection
by CWD and BSE. To study the propensity of each species’ PrP to be induced to
misfold by the presence of PrPd from verious species, we have used an in vitro
system that permits detection of PrPd in real-time. We measured the conversion
efficiency of various combinations of PrPd seeds and PrP substrate combinations.
We observed the cross-species behavior of CWD and BSE, in addition to
feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily
than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions.
In addition, we investigated the role of specific regions of the bovine, deer
and human PrP protein in resistance to conversion by prions from another
species. We have concluded that the human protein has a region that confers
unusual susceptibility to conversion by CWD prions. CWD is unique among prion
diseases in its rapid spread in natural populations. BSE prions are essentially
unaltered upon passage to a new species, while CWD adapts to the new species.
This adaptation has consequences for surveillance of humans exposed to
CWD.
Wildlife Disease Risk Communication Research
Contributes to Wildlife Trust Administration Exploring perceptions about chronic
wasting disease risks among wildlife and agriculture professionals and
stakeholders
Ms. Alyssa Wetterau1, Dr. Krysten Schuler1, Dr.
Elizabeth Bunting1, Dr. Hussni Mohammed1 1Cornell University
Chronic wasting disease (CWD) is a fatal disease of
North American Cervidae. New York State (NYS, USA) successfully managed an
outbreak of CWD in 2005 in both captive and wild white-tailed deer (Odocoileus
virginianus) with no reoccurrence of the disease as of 2015. To attain maximum
compliance and efficacy of management actions for prevention of CWD entry,
understanding the varied risk perceptions will allow for targeted, proactive
communication efforts to address divergences between expert-derived risk
assessments and stakeholder risk perceptions. We examined perceived risks
associated with CWD introduction and exposure among agricultural and wildlife
agency professionals within and outside of NYS, as well as stakeholder groups
(e.g., hunters and captive cervid owners). We measured perceived risk using a
risk assessment questionnaire online via Qualtrics survey software and evaluated
similarities within, as well as differences in, perception among participant
groups. New York State biologists employed by the Department of Environmental
Conservation and independent non-NYS wildlife and agricultural professionals
thought CWD risks associated with captive cervids were high; captive cervid
owners thought risks for wild and captive cervids were low. Agriculture and
wildlife professional groups agreed on general risk perceptions. We ranked 15
individual risk hazards into high and low medium categories based on all
responses. Differences between groups were most evident in hypothetical disease
pathways. Any pathway involving inter-state import of live cervids received high
ranking for all groups except captive cervid owners. Comparatively low risk
perceptions by captive cervid operators may stem from misinformation, lack of
understanding of testing programs, and indemnity payments for animal
depopulation. Communication and education directed at areas of disagreement may
facilitate effective disease prevention and management.
* No evaluation of determination of CWD risk is
required for alternative livestock or captive wildlife shipped directly to
slaughter or to a biosecure facility approved by the Division and the Dept. of
Agriculture.
*** We found that CWD adapts to a new host more
readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD
prions. In addition, we investigated the role of specific regions of the bovine,
deer and human PrP protein in resistance to conversion by prions from another
species. We have concluded that the human protein has a region that confers
unusual susceptibility to conversion by CWD prions. CWD is unique among prion
diseases in its rapid spread in natural populations. BSE prions are essentially
unaltered upon passage to a new species, while CWD adapts to the new species.
This adaptation has consequences for surveillance of humans exposed to CWD. ***
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai
Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5,
Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease
Pathology Surveillance Center, 5Department of Neurology, 6National Center for
Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106,
USA.
4Department of Biological Sciences and Center for
Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta,
Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX
77010
Chronic wasting disease (CWD) is a widespread and
highly transmissible prion disease in free-ranging and captive cervid species in
North America. The zoonotic potential of CWD prions is a serious public health
concern, but the susceptibility of human CNS and peripheral organs to CWD prions
remains largely unresolved. We reported earlier that peripheral and CNS
infections were detected in transgenic mice expressing human PrP129M or PrP129V.
Here we will present an update on this project, including evidence for strain
dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as
the characteristics of experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH,
United States
Abstract
Prion disease is transmissible and invariably fatal.
Chronic wasting disease (CWD) is the prion disease affecting deer, elk and
moose, and it is a widespread and expanding epidemic affecting 22 US States and
2 Canadian provinces so far. CWD poses the most serious zoonotic prion
transmission risks in North America because of huge venison consumption (>6
million deer/elk hunted and consumed annually in the USA alone), significant
prion infectivity in muscles and other tissues/fluids from CWD-affected cervids,
and usually high levels of individual exposure to CWD resulting from consumption
of the affected animal among often just family and friends. However, we still do
not know whether CWD prions can infect humans in the brain or peripheral tissues
or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have
no essays to reliably detect CWD infection in humans. We hypothesize that:
(1) The classic CWD prion strain can infect humans at
low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is
dependent on the cervid prion strain and influenced by the host (human) prion
protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD
infection in humans;and
(4) CWD transmission to humans has already occurred.
We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and
complementary in vitro approaches.
Aim 1 will prove that the classical CWD strain may
infect humans in brain or peripheral lymphoid tissues at low levels by
conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing
common human PrP variants using a number of CWD isolates at varying doses and
routes. Experimental "human CWD" samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the
cervid-to-human prion transmission barrier is dependent on prion strain and
influenced by the host (human) PrP sequence by examining and comparing the
transmission efficiency and phenotypes of several atypical/unusual CWD
isolates/strains as well as a few prion strains from other species that have
adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse
lines as in Aim 1.
Aim 3 will establish reliable essays for detection
and surveillance of CWD infection in humans by examining in details the
clinical, pathological, biochemical and in vitro seeding properties of existing
and future experimental "human CWD" samples generated from Aims 1-2 and compare
them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD)
prions.
Aim 4 will attempt to detect clinical CWD-affected
human cases by examining a significant number of brain samples from
prion-affected human subjects in the USA and Canada who have consumed venison
from CWD-endemic areas utilizing the criteria and essays established in Aim 3.
The findings from this proposal will greatly advance our understandings on the
potential and characteristics of cervid prion transmission in humans, establish
reliable essays for CWD zoonosis and potentially discover the first case(s) of
CWD infection in humans.
Public Health Relevance There are significant and
increasing human exposure to cervid prions because chronic wasting disease (CWD,
a widespread and highly infectious prion disease among deer and elk in North
America) continues spreading and consumption of venison remains popular, but our
understanding on cervid-to-human prion transmission is still very limited,
raising public health concerns. This proposal aims to define the zoonotic risks
of cervid prions and set up and apply essays to detect CWD zoonosis using mouse
models and in vitro methods. The findings will greatly expand our knowledge on
the potentials and characteristics of cervid prion transmission in humans,
establish reliable essays for such infections and may discover the first case(s)
of CWD infection in humans.
Funding Agency Agency National Institute of Health
(NIH)
Institute National Institute of Neurological
Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of
Neurodegeneration Study Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
===========================================================
We hypothesize that:
(1) The classic CWD prion strain can infect humans at
low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is
dependent on the cervid prion strain and influenced by the host (human) prion
protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD
infection in humans;and
(4) *** CWD transmission to humans has already
occurred. *** We will test these hypotheses in 4 Aims using transgenic (Tg)
mouse models and complementary in vitro approaches.
============================================================
Key Molecular Mechanisms of TSEs
Zabel, Mark D.
Colorado State University-Fort Collins, Fort Collins,
CO, United States Abstract Prion diseases, or transmissible spongiform
encephalopathies (TSEs), are fatal neurodegenerative diseases affecting humans,
cervids, bovids, and ovids. The absolute requirement of PrPC expression to
generate prion diseases and the lack of instructional nucleic acid define prions
as unique infectious agents. Prions exhibit species-specific tropism, inferring
that unique prion strains exist that preferentially infct certain host species
and confront transmission barriers to heterologous host species. However,
transmission barriers are not absolute. Scientific consensus agrees that the
sheep TSE scrapie probably breached the transmission barrier to cattle causing
bovine spongiform encephalopathy that subsequently breached the human
transmission barrier and likely caused several hundred deaths by a new-variant
form of the human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact
to human health, emotion and economies can still be felt in areas like farming,
blood and organ donations and the threat of a latent TSE epidemic. This
precedent raises the real possibility of other TSEs, like chronic wasting
disease of cervids, overcoming similar human transmission barriers. A
groundbreaking discovery made last year revealed that mice infected with
heterologous prion strains facing significant transmission barriers replicated
prions far more readily in spleens than brains6. Furthermore, these splenic
prions exhibited weakened transmission barriers and expanded host ranges
compared to neurogenic prions. These data question conventional wisdom of
avoiding neural tissue to avoid prion xenotransmission, when more promiscuous
prions may lurk in extraneural tissues. Data derived from work previously funded
by NIH demonstrate that Complement receptors CD21/35 bind prions and high
density PrPC and differentially impact prion disease depending on the prion
isolate or strain used. Recent advances in live animal and whole organ imaging
have led us to generate preliminary data to support novel, innovative approaches
to assessing prion capture and transport. We plan to test our unifying
hypothesis for this proposal that CD21/35 control the processes of peripheral
prion capture, transport, strain selection and xenotransmission in the following
specific aims. 1. Assess the role of CD21/35 in splenic prion strain selection
and host range expansion. 2. Determine whether CD21/35 and C1q differentially
bind distinct prion strains 3. Monitor the effects of CD21/35 on prion
trafficking in real time and space 4. Assess the role of CD21/35 in incunabular
prion trafficking
Public Health Relevance Transmissible spongiform
encephalopathies, or prion diseases, are devastating illnesses that greatly
impact public health, agriculture and wildlife in North America and around the
world. The impact to human health, emotion and economies can still be felt in
areas like farming, blood and organ donations and the threat of a latent TSE
epidemic. This precedent raises the real possibility of other TSEs, like chronic
wasting disease (CWD) of cervids, overcoming similar human transmission
barriers. Early this year Canada reported its first case of BSE in over a decade
audits first case of CWD in farmed elk in three years, underscoring the need for
continued vigilance and research. Identifying mechanisms of transmission and
zoonoses remains an extremely important and intense area of research that will
benefit human and other animal populations.
Funding Agency Agency National Institute of Health
(NIH)
Institute National Institute of Allergy and
Infectious Diseases (NIAID)
Type High Priority, Short Term Project Award (R56)
Project # 1R56AI122273-01A1
Application # 9211114
Study Section Cellular and Molecular Biology of
Neurodegeneration Study Section (CMND)
Program Officer Beisel, Christopher E
Project Start 2016-02-16
Project End 2017-01-31
Budget Start 2016-02-16
Budget End 2017-01-31
Support Year 1
Fiscal Year 2016
Total Cost
Indirect Cost Institution Name Colorado State
University-Fort Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
PMCA Detection of CWD Infection in Cervid and
Non-Cervid Species
Hoover, Edward Arthur
Colorado State University-Fort Collins, Fort Collins,
CO, United States Abstract Chronic wasting disease (CWD) of deer and elk is an
emerging highly transmissible prion disease now recognized in 18 States, 2
Canadian provinces, and Korea. We have shown that Infected deer harbor and shed
high levels of infectious prions in saliva, blood, urine, and feces, and in the
tissues generating those body fluids and excreta, thereby leading to facile
transmission by direct contact and environmental contamination. We have also
shown that CWD can infect some non-cervid species, thus the potential risk CWD
represents to domestic animal species and to humans remains unknown. Whether
prions borne in blood, saliva, nasal fluids, milk, or excreta are generated or
modified in the proximate peripheral tissue sites, may differ in subtle ways
from those generated in brain, or may be adapted for mucosal infection remain
open questions. The increasing parallels in the pathogenesis between prion
diseases and human neurodegenerative conditions, such as Alzheimer's and
Parkinson's diseases, add relevance to CWD as a transmissible protein misfolding
disease. The overall goal of this work is to elucidate the process of CWD prion
transmission from mucosal secretory and excretory tissue sites by addressing
these questions: (a) What are the kinetics and magnitude of CWD prion shedding
post-exposure? (b) Are excreted prions biochemically distinct, or not, from
those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the
source of excreted prions? and (d) Are excreted prions adapted for horizontal
transmission via natural/trans-mucosal routes? The specific aims of this
proposal are: (1) To determine the onset and consistency of CWD prion shedding
in deer and cervidized mice; (2); To compare the biochemical and biophysical
properties of excretory vs. CNS prions; (3) To determine the capacity of
peripheral tissues to support replication of CWD prions; (4) To determine the
protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To
compare the mucosal infectivity of excretory vs. CNS prions. Understanding the
mechanisms that enable efficient prion dissemination and shedding will help
elucidate how horizontally transmissible prions evolve and succeed, and is the
basis of this proposal. Understanding how infectious misfolded proteins (prions)
are generated, trafficked, shed, and transmitted will aid in preventing,
treating, and managing the risks associated with these agents and the diseases
they cause.
Public Health Relevance Chronic wasting disease (CWD)
of deer and elk is an emergent highly transmissible prion disease now recognized
throughout the USA as well as in Canada and Korea. We have shown that infected
deer harbor and shed high levels of infectious prions in saliva, blood, urine,
and feces thereby leading to transmission by direct contact and environmental
contamination. In that our studies have also shown that CWD can infect some
non-cervid species, the potential risk CWD may represents to domestic animal
species and humans remains unknown. The increasing parallels in the development
of major human neurodegenerative conditions, such as Alzheimer's and Parkinson's
diseases, and prion diseases add relevance to CWD as a model of a transmissible
protein misfolding disease. Understanding how infectious misfolded proteins
(prions) are generated and transmitted will aid in interrupting, treating, and
managing the risks associated with these agents and the diseases they cause.
Funding Agency Agency National Institute of Health
(NIH)
Institute National Institute of Neurological
Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 4R01NS061902-07
Application # 9010980
Study Section Cellular and Molecular Biology of
Neurodegeneration Study Section (CMND)
Program Officer Wong, May Project Start 2009-09-30
Project End 2018-02-28
Budget Start 2016-03-01
Budget End 2017-02-28
Support Year 7
Fiscal Year 2016
Total Cost $409,868
Indirect Cost $134,234 Institution Name Colorado
State University-Fort Collins
Department Microbiology/Immun/Virology
Type Schools of Veterinary Medicine
DUNS # 785979618 City Fort Collins
State CO
Country United States
Zip Code 80523
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL
CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** 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).***
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO
HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai
Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case
Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples,
Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the
potential to infect human CNS and peripheral lymphoid tissues and that there
might be asymptomatic human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the
potential to infect human CNS and peripheral lymphoid tissues and that there
might be asymptomatic human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion
transmission
Kristen Davenport, Davin Henderson, Candace
Mathiason, and Edward Hoover Prion Research Center; Colorado State University;
Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE
characteristics to more efficiently convert bovine rPrP than feline rPrP.
Additionally, human rPrP was competent for conversion by CWD and fCWD.
***This insinuates that, at the level of
protein:protein interactions, the barrier preventing transmission of CWD to
humans is less robust than previously estimated.
================
***This insinuates that, at the level of
protein:protein interactions, the barrier preventing transmission of CWD to
humans is less robust than previously estimated.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION
update January 2, 2014
*** 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.
*** 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).***
*** 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.
***********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 ;
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
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion
2016 Tokyo ***
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** 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.
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie
prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline
Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine
Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5,
Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier
Andréoletti1, Affiliations Contributions Corresponding author Journal name:
Nature Communications Volume: 5, Article number: 5821 DOI:
doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014
Published 16 December 2014 Article tools Citation Reprints Rights &
permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is
the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic
potential of scrapie prions remains unknown. Mice genetically engineered to
overexpress the human prion protein (tgHu) have emerged as highly relevant
models for gauging the capacity of prions to transmit to humans. These models
can propagate human prions without any apparent transmission barrier and have
been used used to confirm the zoonotic ability of BSE. Here we show that a panel
of sheep scrapie prions transmit to several tgHu mice models with an efficiency
comparable to that of cattle BSE. The serial transmission of different scrapie
isolates in these mice led to the propagation of prions that are phenotypically
identical to those causing sporadic CJD (sCJD) in humans. These results
demonstrate that scrapie prions have a zoonotic potential and raise new
questions about the possible link between animal and human prions.
Subject terms: Biological sciences• Medical research
At a glance
*** In complement to the recent demonstration that
humanized mice are susceptible to scrapie, we report here the first observation
of direct transmission of a natural classical scrapie isolate to a macaque after
a 10-year incubation period. Neuropathologic examination revealed all of the
features of a prion disease: spongiform change, neuronal loss, and accumulation
of PrPres throughout the CNS.
*** This observation strengthens the questioning of
the harmlessness of scrapie to humans, at a time when protective measures for
human and animal health are being dismantled and reduced as c-BSE is considered
controlled and being eradicated.
*** Our results underscore the importance of
precautionary and protective measures and the necessity for long-term
experimental transmission studies to assess the zoonotic potential of other
animal prion strains.
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl
1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic
potential
Juan Maria Torres a, Olivier Andreoletti b, J
uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal (
CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes
Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie
MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy
(BSE) contaminated bovine tissues is considered as the origin of variant
Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only
recognized zoonotic prion. Despite the variety of Transmissible Spongiform
Encephalopathy (TSE) agents that have been circulating for centuries in farmed
ruminants there is no apparent epidemiological link between exposure to ruminant
products and the occurrence of other form of TSE in human like sporadic
Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the
diversity of circulating TSE agents has never been systematically assessed. The
major issue in experimental assessment of TSEs zoonotic potential lies in the
modeling of the ‘species barrier‘, the biological phenomenon that limits TSE
agents’ propagation from a species to another. In the last decade, mice
genetically engineered to express normal forms of the human prion protein has
proved essential in studying human prions pathogenesis and modeling the capacity
of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions
circulating in farmed ruminants, we study their transmission ability in
transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing
different forms of the human PrPC (129Met or 129Val) are used to determine the
role of the Met129Val dimorphism in susceptibility/resistance to the different
agents.
These transmission experiments confirm the ability of
BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129
homozygotes may be susceptible to BSE in sheep or goat to a greater degree than
the BSE agent in cattle and that these agents can convey molecular properties
and neuropathological indistinguishable from vCJD. However homozygous 129V mice
are resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie
prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle
BSE. While the efficiency of transmission at primary passage was low, subsequent
passages resulted in a highly virulent prion disease in both Met129 and Val129
mice. Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
why do we not want to do TSE transmission studies on
chimpanzees $
5. A positive result from a chimpanzee challenged
severly would likely create alarm in some circles even if the result could not
be interpreted for man. I have a view that all these agents could be transmitted
provided a large enough dose by appropriate routes was given and the animals
kept long enough. Until the mechanisms of the species barrier are more clearly
understood it might be best to retain that hypothesis.
snip...
R. BRADLEY
1978 SCRAPIE IN CONFIDENCE SCJD
1979
SILENCE ON CJD AND SCRAPIE
1980
SILENCE ON CJD AND SCRAPIE
*** 1981 NOVEMBER
Thursday, August 04, 2016
*** MEETING ON THE FEASIBILITY OF CARRYING OUT
EPIDEMIOLOGICAL STUDIES ON CREUTZFELDT JAKOB DISEASE 1978 THE SCRAPIE FILES IN
CONFIDENCE CONFIDENTIAL SCJD
2016
SCRAPIE AND CWD ZOONOSIS
PRION 2016 CONFERENCE TOKYO
Saturday, April 23, 2016
*** SCRAPIE WS-01: Prion diseases in animals and
zoonotic potential 2016 ***
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl
1933-690X
Transmission of scrapie prions to primate after an
extended silent incubation period
***Moreover, sporadic disease has never been observed
in breeding colonies or primate research laboratories, most notably among
hundreds of animals over several decades of study at the National Institutes of
Health25, and in nearly twenty older animals continuously housed in our own
facility.***
Transmission of scrapie prions to primate after an
extended silent incubation period
Emmanuel E. Comoy , Jacqueline Mikol , Sophie
Luccantoni-Freire , Evelyne Correia , Nathalie Lescoutra-Etchegaray , Valérie
Durand , Capucine Dehen , Olivier Andreoletti , Cristina Casalone , Juergen A.
Richt , Justin J. Greenlee , Thierry Baron , Sylvie L. Benestad , Paul Brown
& Jean-Philippe Deslys
Abstract
Classical bovine spongiform encephalopathy (c-BSE) is
the only animal prion disease reputed to be zoonotic, causing variant
Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures
for animal and human health against animal prion diseases. Recently, partial
transmissions to humanized mice showed that the zoonotic potential of scrapie
might be similar to c-BSE. We here report the direct transmission of a natural
classical scrapie isolate to cynomolgus macaque, a highly relevant model for
human prion diseases, after a 10-year silent incubation period, with features
similar to those reported for human cases of sporadic CJD. Scrapie is thus
actually transmissible to primates with incubation periods compatible with their
life expectancy, although fourfold longer than BSE. Long-term experimental
transmission studies are necessary to better assess the zoonotic potential of
other prion diseases with high prevalence, notably Chronic Wasting Disease of
deer and elk and atypical/Nor98 scrapie.
snip...
In addition to previous studies on scrapie
transmission to primate1,8,9 and the recently published study on transgenic
humanized mice13, our results constitute new evidence for recommending that the
potential risk of scrapie for human health should not be dismissed. Indeed,
human PrP transgenic mice and primates are the most relevant models for
investigating the human transmission barrier. To what extent such models are
informative for measuring the zoonotic potential of an animal TSE under field
exposure conditions is unknown. During the past decades, many protective
measures have been successfully implemented to protect cattle from the spread of
c-BSE, and some of these measures have been extended to sheep and goats to
protect from scrapie according to the principle of precaution. Since cases of
c-BSE have greatly reduced in number, those protective measures are currently
being challenged and relaxed in the absence of other known zoonotic animal prion
disease. We recommend that risk managers should be aware of the long term
potential risk to human health of at least certain scrapie isolates, notably for
lymphotropic strains like the classical scrapie strain used in the current
study. Relatively high amounts of infectivity in peripheral lymphoid organs in
animals infected with these strains could lead to contamination of food products
produced for human consumption. Efforts should also be maintained to further
assess the zoonotic potential of other animal prion strains in long-term
studies, notably lymphotropic strains with high prevalence like CWD, which is
spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was
first detected in the past two decades and now represents approximately half of
all reported cases of prion diseases in small ruminants worldwide, including
territories previously considered as scrapie free. Even if the prevailing view
is that sporadic CJD is due to the spontaneous formation of CJD prions, it
remains possible that its apparent sporadic nature may, at least in part, result
from our limited capacity to identify an environmental origin.
***Moreover, sporadic disease has never been observed
in breeding colonies or primate research laboratories, most notably among
hundreds of animals over several decades of study at the National Institutes of
Health25, and in nearly twenty older animals continuously housed in our own
facility.***
2015
O.05: Transmission of prions to primates after
extended silent incubation periods: Implications for BSE and scrapie risk
assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand,
Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and
Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative
proteinopathies reputed to be transmissible under field conditions since
decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans
evidenced that an animal PD might be zoonotic under appropriate conditions.
Contrarily, in the absence of obvious (epidemiological or experimental) elements
supporting a transmission or genetic predispositions, PD, like the other
proteinopathies, are reputed to occur spontaneously (atpical animal prion
strains, sporadic CJD summing 80% of human prion cases). Non-human primate
models provided the first evidences supporting the transmissibiity of human
prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques
brought major information for BSE risk assessment for human health (Chen, 2014),
according to their phylogenetic proximity to humans and extended lifetime. We
used this model to assess the zoonotic potential of other animal PD from bovine,
ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a
natural classical scrapie isolate to macaque after a 10-year silent incubation
period,
***with features similar to some reported for human
cases of sporadic CJD, albeit requiring fourfold long incubation than BSE.
Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and
L-type BSE),
***thus questioning the origin of human sporadic
cases. We will present an updated panorama of our different transmission studies
and discuss the implications of such extended incubation periods on risk
assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic
cases***
===============
***our findings suggest that possible transmission
risk of H-type BSE to sheep and human. Bioassay will be required to determine
whether the PMCA products are infectious to these animals.
==============
Friday, August 26, 2016
Journal Journal of Toxicology and Environmental
Health, Part A Volume 79, 2016 - Issue 16-17 Prion Research in Perspective IV
CANADA BSE CWD SCRAPIE CJD TSE Prion Disease
Thursday, August 18, 2016
*** PROCEEDINGS ONE HUNDRED AND Nineteenth ANNUAL
MEETING of the USAHA BSE, CWD, SCRAPIE, PORCINE TSE PRION October 22 28, 2015
***
Saturday, July 09, 2016
Texas Intrastate – within state movement of all
Cervid or Trucking Chronic Wasting Disease CWD TSE Prion Moratorium
Monday, July 18, 2016
Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in
Deer Herds, Farmers Sampling Own Herds, Rapid Testing, False Negatives, a Recipe
for Disaster
http://chronic-wasting-disease.blogspot.com/2016/07/texas-parks-wildlife-dept-tpwd-hiding.html
Friday, July 01, 2016
*** TEXAS Thirteen new cases of chronic wasting
disease (CWD) were confirmed at a Medina County captive white-tailed deer
breeding facility on June 29, 2016***
*** How Did CWD Get Way Down In Medina County, Texas?
DISCUSSION Observations of natural outbreaks of
scrapie indicated that the disease spread from flock to flock by the movement of
infected, but apparently normal, sheep which were incubating the disease.
There was no evidence that the disease spread to
adjacent flocks in the absent of such movements or that vectors or other host
species were involved in the spread of scrapie to sheep or goats; however, these
possibilities should be kept open...
Tuesday, August 02, 2016
TEXAS TPWD Sets Public Hearings on Deer Movement Rule
Proposals in Areas with CWD Rule Terry S. Singeltary Sr. comment submission
Thursday, August 25, 2016
TPWD Action Disease Detection and Response – Chronic
Wasting Disease TPW Commission Adopts New CWD Zones, Deer Movement Rules August
25, 2016
This map shows the recently imposed Surveillance Zone
for CWD in portions of Bandera, Medina and Uvalde counties.
http://chronic-wasting-disease.blogspot.com/2016/08/tpwd-action-disease-detection-and.html
Wednesday, August 10, 2016
Arkansas Chronic Wasting Disease CWD TSE Prion
Potentially Trucked in from Missouri, what about Florida and ?
Wednesday, July 27, 2016
Arkansas CWD 101 positive cases documented to date,
Biologists to take additional samples in in southern Pope County, Aug. 1-5
Tuesday, May 03, 2016
Arkansas Chronic Wasting Disease CWD TSE Prion and
Elk Restoration Project and Hunkering Down in the BSE Situation Room USDA 1998
Friday, August 05, 2016
MINNESOTA CHRONIC WASTING DISEASE SURVEILLANCE AND
TESTING CWD TSE PRION UPDATE
Monday, August 01, 2016
Florida Fish and Wildlife Conservation Commission CWD
TSE Prion Surveillance Monitoring Programs and Testing
Friday, July 29, 2016
IOWA CHRONIC WASTING DISEASE CWD TSE PRION TOTAL TO
DATE 304 CASES WILD AND CAPTIVE REPORT UPDATE JULY 2016
Tuesday, July 19, 2016
MONTANA CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
STILL SHOWS ONLY 9 CAPTIVE CASES CONFIRMED FROM Philipsburg Kesler Game game
since 1999
Sunday, July 17, 2016
Virginia Chronic Wasting Disease CWD As of March 2016
has diagnosed 13 CWD-positive white-tailed deer
Sunday, July 17, 2016
West Virginia Chronic Wasting Disease CWD has been
found in 195 white-tailed deer As of June 2016
Tuesday, July 12, 2016
Colorado Chronic Wasting Disease CWD TSE Prion
discovered in one deer in Montrose County
Friday, April 22, 2016
COLORADO CHRONIC WASTING DISEASE CWD TSE PRION
SURVEILLANCE AND TESTING PROGRAM IS MINIMAL AND LIMITED
*** SEE CWD HIGH INFECTION RATE MAPS FOR COLORADO !
***
Wednesday, February 10, 2016
*** Wisconsin Two deer that escaped farm had chronic
wasting disease CWD ***
Sunday, January 17, 2016
*** Wisconsin Captive CWD Lotto Pays Out Again
indemnity payment of $298,770 for 228 white-tailed deer killed on farm ***
Sunday, May 08, 2016
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION
SPIRALING FURTHER INTO THE ABYSS UPDATE
Tuesday, May 03, 2016
Wednesday, May 11, 2016
PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE
GEARS UP FOR ADDITIONAL CONTROL MEASURES
Friday, April 22, 2016
Missouri MDC finds seven new cases of ChronicWasting
Disease CWD during past‐season testing
Thursday, April 14, 2016
*** Louisiana Chronic Wasting Disease CWD TSE Prion
Surveillance and Testing Program? ***
KANSAS CWD CASES ALARMING
Wednesday, March 02, 2016 Kansas Chronic Wasting
Disease CWD TSE Prion 52 cases 2015 updated report 'ALARMING'
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive
for CWD in the Oswego zone of Kendall County
I could go on, for more see ;
Thursday, March 31, 2016
*** Chronic Wasting Disease CWD TSE Prion Roundup USA
April 1, 2016 ***
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from
CWD infected farm in Korea Prion 2016 Tokyo ***
What is the risk of chronic wasting disease being
introduced into Great Britain? An updated Qualitative Risk Assessment March
2016
Summary
The previous assessment concentrated on the incursion
of disease from North America through the imports of animal feed or the movement
of contaminated clothing, footwear and equipment. The results suggested that
import of pet feed was a non-negligible risk, but given the unlikely contact of
resident deer in GB with such non-ruminant feed, this was considered overall a
negligible to very low risk. The movement of contaminated clothing, footwear or
equipment (particularly hunting equipment) could pose a very low risk, although
the volume of contaminated soil which would need to be ingested to give rise to
an infection is likely to be higher than would be present. There is a variable
level uncertainty in all these assessments.
The new assessment focuses on an additional potential
route of entry: the importation of natural deer urine lures. The main
conclusions from this assessment are:
In areas of North America where CWD has been
reported, given that CWD is excreted in faeces, saliva, urine and blood, and
survives in the environment for several years there is a medium probability that
the deer urine in North America contains CWD (high uncertainty; depends on the
source of deer used for production).
The risk of a deer in GB being infected per 30 ml
bottle of urine imported from the USA is very low, albeit with high uncertainty.
Overall it is concluded that the risk of at least one infection of deer in the
UK with CWD per year from deer urine lures imported from the USA is medium. This
assumes a high number of 30 ml bottles imported per year from all areas of the
USA.
None of the species affected by CWD in North
America are present in GB. For a British species to become infected with CWD
following exposure, the dose and inherent susceptibility of the species will be
important. Based on current scientific evidence Red deer (Cervus elaphus
elaphus) are susceptible to CWD, Fallow deer (Dama dama) are likely to be less
susceptible and Roe deer (Capreolus capreolus) have a gene conferring
susceptibility. Therefore, it is likely that given exposure to an infectious
dose of CWD, deer in GB could become infected with CWD.
Overall, the probability of importing CWD into GB
from North America and causing infection in British deer is uncertain but likely
to be negligible to very low via movement of deer hunters, other tourists and
British servicemen and very low via imported (non-
2
ruminant) animal feed and medium for the use of
lures. However, if it was imported and (a) deer did become infected with CWD,
the consequences would be severe as eradication of the disease is impossible, it
is clinically indistinguishable from BSE infection in deer (Dalgleish et al.,
2008) and populations of wild and farmed deer would be under threat.
The USA has implemented a Herd Certification
Programme for farmed and captive cervids. So far, 29 States are approved for HCP
status (APHIS, 2015). The list includes States such as Colorado, where CWD is
present, therefore it is recommended that any sourcing of such natural urine
lures should be not only from States with an HCP programme, but also from a herd
which is registered as being regularly tested free of CWD.
Animal urine is not considered a commodity which is
subject to animal by-products legislation for imports. Internet sales are common
and although a license would be required, there are no conditions for the safe
sourcing of such products. Deer urine lures are also available in Europe and may
be produced from carcases of hunted deer. The use of deer urine produced from a
species not present in Europe (such as white tailed deer) is questioned for its
value with native GB deer according to the British Deer Society survey.
Background
Thursday, April 07, 2016
What is the risk of chronic wasting disease being
introduced into Great Britain? An updated Qualitative Risk Assessment March 2016
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting
Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment
October 2012
snip...
In the USA, under the Food and Drug Administration’s
BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk,
tallow, and gelatin) from deer and elk is prohibited for use in feed for
ruminant animals. With regards to feed for non-ruminant animals, under FDA law,
CWD positive deer may not be used for any animal feed or feed ingredients. For
elk and deer considered at high risk for CWD, the FDA recommends that these
animals do not enter the animal feed system. However, this recommendation is
guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD
and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month
period prior to slaughter were in a captive herd that contained a CWD-positive
animal.
Therefore, in the USA, materials from cervids other
than CWD positive animals may be used in animal feed and feed ingredients for
non-ruminants.
The amount of animal PAP that is of deer and/or elk
origin imported from the USA to GB can not be determined, however, as it is not
specified in TRACES. It may constitute a small percentage of the 8412 kilos of
non-fish origin processed animal proteins that were imported from US into GB in
2011.
Overall, therefore, it is considered there is a
__greater than negligible risk___ that (nonruminant) animal feed and pet food
containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate
given the lack of data on the amount of deer and/or elk protein possibly being
imported in these products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas,
population declines of deer of up to 30 to 50% have been observed (Almberg et
al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA,
2011).
The clinical signs of CWD in affected adults are
weight loss and behavioural changes that can span weeks or months (Williams,
2005). In addition, signs might include excessive salivation, behavioural
alterations including a fixed stare and changes in interaction with other
animals in the herd, and an altered stance (Williams, 2005). These signs are
indistinguishable from cervids experimentally infected with bovine spongiform
encephalopathy (BSE).
Given this, if CWD was to be introduced into
countries with BSE such as GB, for example, infected deer populations would need
to be tested to differentiate if they were infected with CWD or BSE to minimise
the risk of BSE entering the human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to
be as high as 30% and can approach 100% among captive animals in endemic areas
(Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium
probability that the soil and surrounding environment is contaminated with CWD
prions and in a bioavailable form. In rural areas where CWD has not been
reported and deer are present, there is a greater than negligible risk the soil
is contaminated with CWD prion.
snip...
In summary, given the volume of tourists, hunters and
servicemen moving between GB and North America, the probability of at least one
person travelling to/from a CWD affected area and, in doing so, contaminating
their clothing, footwear and/or equipment prior to arriving in GB is greater
than negligible. For deer hunters, specifically, the risk is likely to be
greater given the increased contact with deer and their environment. However,
there is significant uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer
may have a higher probability of exposure to CWD transferred to the environment
than wild deer given the restricted habitat range and higher frequency of
contact with tourists and returning GB residents.
snip...
What is the risk of chronic wasting disease being
introduced into Great Britain? A Qualitative Risk Assessment October 2012
I strenuously once again urge the FDA and its
industry constituents, to make it MANDATORY that all ruminant feed be banned to
all ruminants, and this should include all cervids, as well as non-ruminants
such as cats and dogs as well, as soon as possible for the following reasons...
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United
States? ***
31 Jan 2015 at 20:14 GMT
Terry Singeltary Sr. comment ;
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory
Program Standards Singeltary Comment Submission
*** Infectious agent of sheep scrapie may persist in
the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul
Brown3
Using in vitro prion replication for high sensitive
detection of prions and prionlike proteins and for understanding mechanisms of
transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related
Brain disorders, Department of Neurology, University of Texas Medical School at
Houston.
Prion and prion-like proteins are misfolded protein
aggregates with the ability to selfpropagate to spread disease between cells,
organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o
n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded
form of the prion protein (PrPSc), which propagates by transmitting its
misfolding to the normal prion protein (PrPC). The availability of a procedure
to replicate prions in the laboratory may be important to study the mechanism of
prion and prion-like spreading and to develop high sensitive detection of small
quantities of misfolded proteins in biological fluids, tissues and environmental
samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and
efficient methodology to mimic prion replication in the test tube. PMCA is a
platform technology that may enable amplification of any prion-like misfolded
protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able
to detect the equivalent of one single molecule of infectious PrPSc and
propagate prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the
role of environmental prion contamination on the horizontal spreading of TSEs.
These experiments have focused on the study of the interaction of prions with
plants and environmentally relevant surfaces. Our results show that plants (both
leaves and roots) bind tightly to prions present in brain extracts and excreta
(urine and feces) and retain even small quantities of PrPSc for long periods of
time. Strikingly, ingestion of prioncontaminated leaves and roots produced
disease with a 100% attack rate and an incubation period not substantially
longer than feeding animals directly with scrapie brain homogenate. Furthermore,
plants can uptake prions from contaminated soil and transport them to different
parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a
variety of environmentally relevant surfaces, including stones, wood, metals,
plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit
prion disease when these materials were directly injected into the brain of
animals and strikingly when the contaminated surfaces were just placed in the
animal cage. These findings demonstrate that environmental materials can
efficiently bind infectious prions and act as carriers of infectivity,
suggesting that they may play an important role in the horizontal transmission
of the disease.
========================
Since its invention 13 years ago, PMCA has helped to
answer fundamental questions of prion propagation and has broad applications in
research areas including the food industry, blood bank safety and human and
veterinary disease diagnosis.
see ;
with CWD TSE Prions, I am not sure there is any
absolute yet, other than what we know with transmission studies, and we know tse
prion kill, and tse prion are bad. science shows to date, that indeed soil,
dirt, some better than others, can act as a carrier. same with objects, farm
furniture. take it with how ever many grains of salt you wish, or not. if load
factor plays a role in the end formula, then everything should be on the table,
in my opinion. see ;
***Recently, we have been using PMCA to study the
role of environmental prion contamination on the horizontal spreading of TSEs.
These experiments have focused on the study of the interaction of prions with
plants and environmentally relevant surfaces. Our results show that plants (both
leaves and roots) bind tightly to prions present in brain extracts and excreta
(urine and feces) and retain even small quantities of PrPSc for long periods of
time. Strikingly, ingestion of prioncontaminated leaves and roots produced
disease with a 100% attack rate and an incubation period not substantially
longer than feeding animals directly with scrapie brain homogenate. Furthermore,
plants can uptake prions from contaminated soil and transport them to different
parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a
variety of environmentally relevant surfaces, including stones, wood, metals,
plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit
prion disease when these materials were directly injected into the brain of
animals and strikingly when the contaminated surfaces were just placed in the
animal cage. These findings demonstrate that environmental materials can
efficiently bind infectious prions and act as carriers of infectivity,
suggesting that they may play an important role in the horizontal transmission
of the disease.
Since its invention 13 years ago, PMCA has helped to
answer fundamental questions of prion propagation and has broad applications in
research areas including the food industry, blood bank safety and human and
veterinary disease diagnosis.
see ;
Oral Transmissibility of Prion Disease Is Enhanced by
Binding to Soil Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are
a group of incurable neurological diseases likely caused by a misfolded form of
the prion protein. TSEs include scrapie in sheep, bovine spongiform
encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer
and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting
disease are unique among TSEs because they can be transmitted between animals,
and the disease agents appear to persist in environments previously inhabited by
infected animals. Soil has been hypothesized to act as a reservoir of
infectivity and to bind the infectious agent. In the current study, we orally
dosed experimental animals with a common clay mineral, montmorillonite, or whole
soils laden with infectious prions, and compared the transmissibility to unbound
agent. We found that prions bound to montmorillonite and whole soils remained
orally infectious, and, in most cases, increased the oral transmission of
disease compared to the unbound agent. The results presented in this study
suggest that soil may contribute to environmental spread of TSEs by increasing
the transmissibility of small amounts of infectious agent in the
environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act
as a reservoir for scrapie transmission
The sources of dust borne prions are unknown but it
seems reasonable to assume that faecal, urine, skin, parturient material and
saliva-derived prions may contribute to this mobile environmental reservoir of
infectivity. This work highlights a possible transmission route for scrapie
within the farm environment, and this is likely to be paralleled in CWD which
shows strong similarities with scrapie in terms of prion dissemination and
disease transmission. The data indicate that the presence of scrapie prions in
dust is likely to make the control of these diseases a considerable
challenge.
>>>Particle-associated PrPTSE molecules may
migrate from locations of deposition via transport processes affecting soil
particles, including entrainment in and movement with air and overland flow.
<<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A.
Pedersen*
Several reports have shown that prions can persist in
soil for several years. Significant interest remains in developing methods that
could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary
research suggests that serine proteases and the microbial consortia in
stimulated soils and compost may partially degrade PrPTSE. Transition metal
oxides in soil (viz. manganese oxide) may also mediate prion inactivation.
Overall, the effect of prion attachment to soil particles on its persistence in
the environment is not well understood, and additional study is needed to
determine its implications on the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient
horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient
prion binding, inferring a durable environmental reservoir, and an efficient
mechanism for indirect horizontal CWD transmission.
>>>Another alternative would be an absolute
prohibition on the movement of deer within the state for any purpose. While this
alternative would significantly reduce the potential spread of CWD, it would
also have the simultaneous effect of preventing landowners and land managers
from implementing popular management strategies involving the movement of deer,
and would deprive deer breeders of the ability to engage in the business of
buying and selling breeder deer. Therefore, this alternative was rejected
because the department determined that it placed an avoidable burden on the
regulated community.<<<
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act
as a reservoir for scrapie transmission
Objects in contact with classical scrapie sheep act
as a reservoir for scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C.
Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A.
Simmons1
1 Animal Sciences Unit, Animal and Plant Health
Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant
Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services,
Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of
Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK,
5 School of Veterinary Medicine and Science, University of Nottingham, Sutton
Bonington, UK
Classical scrapie is an environmentally transmissible
prion disease of sheep and goats. Prions can persist and remain potentially
infectious in the environment for many years and thus pose a risk of infecting
animals after re-stocking. In vitro studies using serial protein misfolding
cyclic amplification (sPMCA) have suggested that objects on a scrapie affected
sheep farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible
disease because it has been reported in naïve, supposedly previously unexposed
sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19,
20). Although the vector for disease transmission is not known, soil is likely
to be an important reservoir for prions (2) where – based on studies in rodents
– prions can adhere to minerals as a biologically active form (21) and remain
infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD)
has re-occurred in mule deer housed in paddocks used by infected deer 2 years
earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring
scrapie infection was greater through exposure to contaminated wooden, plastic,
and metal surfaces via water or food troughs, fencing, and hurdles than through
grazing. Drinking from a water trough used by the scrapie flock was sufficient
to cause infection in sheep in a clean building. Exposure to fences and other
objects used for rubbing also led to infection, which supported the hypothesis
that skin may be a vector for disease transmission (9). The risk of these
objects to cause infection was further demonstrated when 87% of 23 sheep
presented with PrPSc in lymphoid tissue after grazing on one of the paddocks,
which contained metal hurdles, a metal lamb creep and a water trough in contact
with the scrapie flock up to 8 weeks earlier, whereas no infection had been
demonstrated previously in sheep grazing on this paddock, when equipped with new
fencing and field furniture. When the contaminated furniture and fencing were
removed, the infection rate dropped significantly to 8% of 12 sheep, with soil
of the paddock as the most likely source of infection caused by shedding of
prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of
contamination of field furniture sufficient to cause infection was dependent on
two factors: stage of incubation period and time of last use by scrapie-infected
sheep. Drinking from a water trough that had been used by scrapie sheep in the
predominantly pre-clinical phase did not appear to cause infection, whereas
infection was shown in sheep drinking from the water trough used by scrapie
sheep in the later stage of the disease. It is possible that contamination
occurred through shedding of prions in saliva, which may have contaminated the
surface of the water trough and subsequently the water when it was refilled.
Contamination appeared to be sufficient to cause infection only if the trough
was in contact with sheep that included clinical cases. Indeed, there is an
increased risk of bodily fluid infectivity with disease progression in scrapie
(24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light
and heat under natural conditions do not inactivate prions (26), furniture in
contact with the scrapie flock, which was assumed to be sufficiently
contaminated to cause infection, did not act as vector for disease if not used
for 18 months, which suggest that the weathering process alone was sufficient to
inactivate prions.
PrPSc detection by sPMCA is increasingly used as a
surrogate for infectivity measurements by bioassay in sheep or mice. In this
reported study, however, the levels of PrPSc present in the environment were
below the limit of detection of the sPMCA method, yet were still sufficient to
cause infection of in-contact animals. In the present study, the outdoor objects
were removed from the infected flock 8 weeks prior to sampling and were positive
by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also
yielded 2 positive reactions out of 139 in samples from the scrapie-free farm,
the sPMCA assay could not detect PrPSc on any of the objects above the
background of the assay. False positive reactions with sPMCA at a low frequency
associated with de novo formation of infectious prions have been reported (27,
28). This is in contrast to our previous study where we demonstrated that
outdoor objects that had been in contact with the scrapie-infected flock up to
20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis
[4 out of 15 reactions (12)] and was significantly more positive by the assay
compared to analogous samples from the scrapie-free farm. This discrepancy could
be due to the use of a different sPMCA substrate between the studies that may
alter the efficiency of amplification of the environmental PrPSc. In addition,
the present study had a longer timeframe between the objects being in contact
with the infected flock and sampling, which may affect the levels of extractable
PrPSc. Alternatively, there may be potentially patchy contamination of this
furniture with PrPSc, which may have been missed by swabbing. The failure of
sPMCA to detect CWD-associated PrP in saliva from clinically affected deer
despite confirmation of infectivity in saliva-inoculated transgenic mice was
associated with as yet unidentified inhibitors in saliva (29), and it is
possible that the sensitivity of sPMCA is affected by other substances in the
tested material. In addition, sampling of amplifiable PrPSc and subsequent
detection by sPMCA may be more difficult from furniture exposed to weather,
which is supported by the observation that PrPSc was detected by sPMCA more
frequently in indoor than outdoor furniture (12). A recent experimental study
has demonstrated that repeated cycles of drying and wetting of
prion-contaminated soil, equivalent to what is expected under natural weathering
conditions, could reduce PMCA amplification efficiency and extend the incubation
period in hamsters inoculated with soil samples (30). This seems to apply also
to this study even though the reduction in infectivity was more dramatic in the
sPMCA assays than in the sheep model. Sheep were not kept until clinical
end-point, which would have enabled us to compare incubation periods, but the
lack of infection in sheep exposed to furniture that had not been in contact
with scrapie sheep for a longer time period supports the hypothesis that prion
degradation and subsequent loss of infectivity occurs even under natural
conditions.
In conclusion, the results in the current study
indicate that removal of furniture that had been in contact with
scrapie-infected animals should be recommended, particularly since cleaning and
decontamination may not effectively remove scrapie infectivity (31), even though
infectivity declines considerably if the pasture and the field furniture have
not been in contact with scrapie-infected sheep for several months. As sPMCA
failed to detect PrPSc in furniture that was subjected to weathering, even
though exposure led to infection in sheep, this method may not always be
reliable in predicting the risk of scrapie infection through environmental
contamination. These results suggest that the VRQ/VRQ sheep model may be more
sensitive than sPMCA for the detection of environmentally associated scrapie,
and suggest that extremely low levels of scrapie contamination are able to cause
infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible
spongiform encephalopathy, sheep, field furniture, reservoir, serial protein
misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep
act as a reservoir for scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in
the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul
Brown3
>>>Another alternative would be an absolute
prohibition on the movement of deer within the state for any purpose. While this
alternative would significantly reduce the potential spread of CWD, it would
also have the simultaneous effect of preventing landowners and land managers
from implementing popular management strategies involving the movement of deer,
and would deprive deer breeders of the ability to engage in the business of
buying and selling breeder deer. Therefore, this alternative was rejected
because the department determined that it placed an avoidable burden on the
regulated community.<<<
Circulation of prions within dust on a scrapie
affected farm
Kevin C Gough1, Claire A Baker2, Hugh A Simmons3,
Steve A Hawkins3 and Ben C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that
affect humans and animals. Scrapie of sheep/goats and Chronic Wasting Disease
(CWD) of deer/elk are contagious prion diseases where environmental reservoirs
have a direct link to the transmission of disease. Using protein misfolding
cyclic amplification we demonstrate that scrapie PrPSc can be detected within
circulating dusts that are present on a farm that is naturally contaminated with
sheep scrapie. The presence of infectious scrapie within airborne dusts may
represent a possible route of infection and illustrates the difficulties that
may be associated with the effective decontamination of such scrapie affected
premises.
snip...
Discussion
We present biochemical data illustrating the airborne
movement of scrapie containing material within a contaminated farm environment.
We were able to detect scrapie PrPSc within extracts from dusts collected over a
70 day period, in the absence of any sheep activity. We were also able to detect
scrapie PrPSc within dusts collected within pasture at 30 m but not at 60 m
distance away from the scrapie contaminated buildings, suggesting that the
chance of contamination of pasture by scrapie contaminated dusts decreases with
distance from contaminated farm buildings. PrPSc amplification by sPMCA has been
shown to correlate with infectivity and amplified products have been shown to be
infectious [14,15]. These experiments illustrate the potential for low dose
scrapie infectivity to be present within such samples. We estimate low ng levels
of scrapie positive brain equivalent were deposited per m2 over 70 days, in a
barn previously occupied by sheep affected with scrapie. This movement of dusts
and the accumulation of low levels of scrapie infectivity within this
environment may in part explain previous observations where despite stringent
pen decontamination regimens healthy lambs still became scrapie infected after
apparent exposure from their environment alone [16]. The presence of sPMCA
seeding activity and by inference, infectious prions within dusts, and their
potential for airborne dissemination is highly novel and may have implications
for the spread of scrapie within infected premises. The low level circulation
and accumulation of scrapie prion containing dust material within the farm
environment will likely impede the efficient decontamination of such scrapie
contaminated buildings unless all possible reservoirs of dust are removed.
Scrapie containing dusts could possibly infect animals during feeding and
drinking, and respiratory and conjunctival routes may also be involved. It has
been demonstrated that scrapie can be efficiently transmitted via the nasal
route in sheep [17], as is also the case for CWD in both murine models and in
white tailed deer [18-20].
The sources of dust borne prions are unknown but it
seems reasonable to assume that faecal, urine, skin, parturient material and
saliva-derived prions may contribute to this mobile environmental reservoir of
infectivity. This work highlights a possible transmission route for scrapie
within the farm environment, and this is likely to be paralleled in CWD which
shows strong similarities with scrapie in terms of prion dissemination and
disease transmission. The data indicate that the presence of scrapie prions in
dust is likely to make the control of these diseases a considerable
challenge.
***Moreover, sporadic disease has never been observed
in breeding colonies or primate research laboratories, most notably among
hundreds of animals over several decades of study at the National Institutes of
Health25, and in nearly twenty older animals continuously housed in our own
facility.***
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine
Spongiform Encephalopathy BSE, TSE, Prion Zoonosis Science History
see history of NIH may destroy human brain
collection
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases
FY2015 CWD TSE PRION Detections in Farmed Cervids and Wild ***
Sunday, July 17, 2016
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL
REPORT UPDATE JULY 17 2016 ***
***at present, no cervid PrP allele conferring
absolute resistance to prion infection has been identified.
P-145 Estimating chronic wasting disease resistance
in cervids using real time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A
Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A
Richt2
1 Department of Microbiology and Immunology,
Midwestern University, United States; 2Department of Diagnostic Medicine and
Pathobiology, Kansas State University; 3Prion Research Center; Colorado State
University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife
Research Unit; 5Agricultural Research Service, United States Department of
Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference
Laboratory for Scrapie and CWO
In mammalian species, the susceptibility to prion
diseases is affected, in part, by the sequence of the host's prion protein
(PrP). In sheep, a gradation from scrapie susceptible to resistant has been
established both in vivo and in vitro based on the amino acids present at PrP
positions 136, 154, and 171, which has led to global breeding programs to reduce
the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly
characterized as a delayed progression of chronic wasting disease (CWD); at
present, no cervid PrP allele conferring absolute resistance to prion infection
has been identified. To model the susceptibility of various naturally-occurring
and hypothetical cervid PrP alleles in vitro, we compared the amplification
rates and efficiency of various CWD isolates in recombinant PrPC using real time
quaking-induced conversion. We hypothesized that amplification metrics of these
isolates in cervid PrP substrates would correlate to in vivo susceptibility -
allowing susceptibility prediction for alleles found at 10 frequency in nature,
and that there would be an additive effect of multiple resistant codons in
hypothetical alleles. Our studies demonstrate that in vitro amplification
metrics predict in vivo susceptibility, and that alleles with multiple codons,
each influencing resistance independently, do not necessarily contribute
additively to resistance. Importantly, we found that the white-tailed deer 226K
substrate exhibited the slowest amplification rate among those evaluated,
suggesting that further investigation of this allele and its resistance in vivo
are warranted to determine if absolute resistance to CWD is possible.
***at present, no cervid PrP allele conferring
absolute resistance to prion infection has been identified.
PRION 2016 CONFERENCE TOKYO
Tuesday, August 9, 2016
*** Concurrence with OIE Risk Designations for Bovine
Spongiform Encephalopathy [Docket No. APHIS-2015-0055]
Saturday, July 23, 2016
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION
SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
*** Atypical Bovine Spongiform Encephalopathy BSE TSE
Prion UPDATE JULY 2016
Saturday, July 16, 2016
*** Importation of Sheep, Goats, and Certain Other
Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10
WITH great disgust and concern, I report to you that
the OIE, USDA, APHIS, are working to further legalize the trading of
Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.
THIS is absolutely insane. it’s USDA INC.
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in
agriculture and we talk mad cow disease USDA and what really happened those mad
cows in Texas ***
Monday, June 20, 2016
*** Specified Risk Materials SRMs BSE TSE Prion
Program ***
Thursday, April 14, 2016
Arizona 22 year old diagnosed with Creutzfeldt Jakob
Disease CJD
Thursday, January 15, 2015
41-year-old Navy Commander with sporadic
Creutzfeldt–Jakob disease CJD TSE Prion: Case Report
Saturday, January 17, 2015
*** Becky Lockhart 46, Utah’s first female House
speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT
DECEMBER 14, 2015
Sunday, August 21, 2016
Kay Ellen Roedl Schwister Deceased August 7, 2016 at
the age of 53 with Creutzfeldt-Jakob disease CJD TSE Prion spontaneous sporadic,
zoonosis, or iatrogenic?
Monday, August 22, 2016
CREUTZFELDT JAKOB DISEASE USA 2015 SPORADIC CJD TOTAL
FIGURES REACHES HIGHEST ANNUAL COUNT TO DATE AT 239 CONFIRMED CASES
*** Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle ***
Over the next 8-10 weeks, approximately 40% of all
the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly
(>95%) downer or dead dairy cattle...
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. ...
”The occurrence of CWD must be viewed against the
contest of the locations in which it occurred. It was an incidental and
unwelcome complication of the respective wildlife research programmes. Despite
it’s subsequent recognition as a new disease of cervids, therefore justifying
direct investigation, no specific research funding was forthcoming. The USDA
veiwed it as a wildlife problem and consequently not their province!” ...page
26.
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK
DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ??? this recall was not for
the welfare of the animals. ...tss
you can check and see here ; (link now dead, does not
work...tss)
see listings of schools from state to state, county
to county, was your child exposed ;
try this link ;
Thursday, August 25, 2016
FSIS Green Bay Dressed Beef Recalls Beef Products Due
To Possible Specified Risk Materials Contamination the most high risk materials
for BSE TSE PRION AKA MAD COW TYPE DISEASE
Sunday, July 24, 2016
Chronic Wasting Disease Prions in Elk Antler Velvet
and Marketing of this Product in Nutritional Supplements for Humans?
Research Project: TRANSMISSIBLE SPONGIFORM
ENCEPHALOPATHIES: THE ROLE OF GENETICS, STRAIN VARIATION, AND ENVIRONMENTAL
CONTAMINATION IN DISEASE CONTROL
Monday, August 29, 2016
NWHC USGS CHRONIC WASTING DISEASE CWD TSE PRION
UPDATE
Terry S. Singeltary Sr. flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
2:07 PM
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