Tuesday, August 30, 2016

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.
 
 
image
 
 
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
 
 
 
 
cwd_map_APRIL_2016
 
 
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.
 
 
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
 
 
*** 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.
 
 
 
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
 

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