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




You have been banned for the following reason: Voted to ban.



Date the ban will be lifted: Never








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?



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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










***************



Greetings Nebraska Hunters et al,


I kind greetings from Bacliff Texas. I signed up again here after a very long absence, to monitor what appears to be an increasing spread of CWD in Nebraska.


I am interested in what you hunters in Nebraska think about this CWD prion agent, and what your concerns might be, especially since it seems that CWD has mutated into a second strain. A disturbing factor indeed. also, new and emerging science has shown that the risk factor for transmission to humans is very real, and increasing with every new strain of CWD found.


ALSO, recently, a stern warning from Prof. Aguzzi about Aerosol and the TSE prion agent, in relations with CWD ;


In Chronic Wasting disease (CWD) of deer several careful studies have been performed that, together with our present finding, depose in favor of airborne transmission in this naturally occurring disease. Indeed, CWD prions can be transmitted experimentally via aerosol and the nasal route to transgenic cervidized mice.33 Although no anecdotal or epidemiological evidence has come forward that airborne transmission may be important for the spread of CWD, several lines of thought suggest that this possibility is not implausible. In deer, prions have been detected in urine, saliva, feces and blood of diseased animals. Moreover, it was claimed that pathological prion protein could be recovered from the environmental water in an endemic area.34 Since all fluids can act as sources for the generation of aerosols, any of the body fluids mentioned above may represent the point of origin for airborne transmission of CWD prions.


ALSO, recently science shows ;


Accelerated shedding of prions following damage to the olfactory epithelium


In this study we investigated the role of damage to the nasal mucosa in the shedding of prions into nasal fluids as a pathway for prion transmission. Here we demonstrate that prions can replicate to high levels in the olfactory sensory epithelium (OSE) in hamsters and that induction of apoptosis in olfactory receptor neurons (ORNs) in the OSE resulted in sloughing off of the OSE from nasal turbinates into the lumen of the nasal airway. In the absence of nasotoxic treatment olfactory marker protein (OMP), which is specific for ORNs, was not detected in nasal lavages. However, after nasotoxic treatment that leads to apoptosis of ORNs both OMP and prion proteins were present in nasal lavages. The cellular debris that was released from the OSE into the lumen of the nasal airway was positive for both OMP and the disease-specific isoform of the prion protein, PrPSc. Using the real time quaking-induced conversion assay to quantify prions, a 100- to 1,000-fold increase in prion seeding activity was observed in nasal lavages following nasotoxic treatment. Since neurons replicate prions to higher levels than other cell types and ORNs are the most environmentally exposed neurons, we propose that an increase in ORN apoptosis or damage to the nasal mucosa in a host with a pre-existing prion infection of the OSE could lead to a substantial increase in the release of prion infectivity into nasal fluids. This mechanism of prion shedding from the olfactory mucosa could contribute to prion transmission.


AS far as human risk factor from CWD, either from consumption, and or friendly fire or the pass it forward mode ‘iatrogenic’ , this risk factor is very real ;


EFSA Journal 2011 The European Response to BSE: A Success Story


This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;


Monday, October 10, 2011


EFSA Journal 2011 The European Response to BSE: A Success Story


snip...


EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential. ...end


I have followed this BSE TSE prion saga daily since December 14, 1997, when I watched my mother die from the Heidenhain Variant of Creutzfeldt Jakob Disease. I never did accept the UKBSEnvCJD only theory, and now science does not agree with it either. I don’t want to over state my concern here, but I am very concerned for Nebraska and the CWD ramifications there from, to animals, livestock, and humans.


I want to know how you as hunters are concerned with CWD, not only concern for yourself, but your family as well, your wife, your children, are you concerned for them as well, or not? remember, this is a disease that can incubate for decades, and more and more scientist seem to be very concerned for the potential transmission of CWD to humans, if it has not happened already and being masked as sporadic CJD.


ARE you concerned about the deer herd, or do you think CWD will just kill itself out?


OR, do you think CWD might kill the deer herds out?


WHAT are your concerns about CWD and GAME FARMS, and the environmental factors there from?


some of which have proven to be nothing more than a petri dish for TSE prion contamination. Some of these game farms use, or have used in the past high protein pellets containing SRMs (specified risk materials) i.e. ANIMAL TISSUE. oral transmission of CWD TSE tainted tissue is easily transmitted to deer. just this December the final report about the closing of a game farm in Wisconsin, and the purchase there from by the state, due to the incredible CWD infection rate there, and ramifications there from for years, if not decades to come. are you pro game farms, or not, and why?


WHAT about baiting and feeding? do you bait or feed, and if so, why, and if not, why not?


THESE are some of many of my questions I am curious about here.


I hope you don’t mind me asking these questions. I follow CWD from state to state, as it emerges.


I am NOT anti-hunter, I don’t care what you eat, I am a carnivore.


so please don’t shoot the messenger.


I will be glad to share some recent science with you as soon as I can post a few links here.


Nebraska has a CWD problem, it’s spreading, and I am just curious, what concerns the hunters have for it.


thank you,


kind regards, terry


LAYPERSON






***************



Join Date Jan 2012 Location 77518 Posts 0 Thanks 0 Thanked 0 Times in 0 Posts Nebraska cwd forum ??? hello there,


i was wondering if it is possible to speak about cwd here, and pass along some science links on the topic? i have been following CWD and other TSE since 1997 and am very concerned about the spread of CWD, and it looks like Nebraska is going to be another hot spot. i went to make a post with a few links, but i don't think that's possible to post links now. it would not be the first time i have been shut down about speaking about CWD, but i was wanting to know before making a post, just so i did not waste your time or mine. there is just some new science emerging on CWD i think everyone should know about. i am not anti-hunter, i am pro-hunter, i am a carnivore.


would it be possible to make a forum here for CWD or Animal disease ???


If not, can i post some scientific study links about cwd TSE prion disease to the hunting forum ???


thank you, kind regards, terry






***************



Terry,


Thank you for your inquiry on this matter. We don't see a problem with you posting or discussing the topic on CWD but we do ask you that you keep it under the Hunting section of the forum and just post a new thread. Also please take a look at the forum guidelines before posting so that you know what type of topics will be tolerated. Another thing you can find in the guidelines is that you can not post links, images, and attachments until you reach a minimum of 10 posts.




Thank you xxxxx




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Terry,


When you asked me if you could talk about CWD here I was under the impression you wanted to discuss the issue with other forum members. We don't have a problem with you discussing the issue with other member but just posting facts about it is just going to get other members upset with you and deter them from reading any of your posts. The long and lengthy posts you have made are to most people are very drawn out and will not get read. Please keep it a discussion or we may just have to pull the plug.




***************


You have been banned for the following reason: Voted to ban.


Date the ban will be lifted: Never






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




==============================end================================





> > > but just posting facts about it is just going to get other members upset




scientific facts are hard to digest sometimes. ignore them at your own, and others, peril. ...tss






2006



Chronic Wasting Disease 2006 Update Nebraska




My last posting before being banned due to discussing CWD in Nebraska the first time, in 2006 (I was trying to warn them back then, they shot the messenger then too) ;




posted August 09, 2006 09:17 PM


--------------------------------------------------------------------------------


Chronic Wasting Disease 2006 Update Nebraska


Summary of Chronic Wasting Disease in Nebraska


Chronic Wasting Disease testing during the 2005 deer hunting season produced 15 positives from 7,381 samples collected. Since testing began in 1997 there have been 65 positive mule deer and 29 positive white-tailed deer, out of 24,849 tested.


The locations of free ranging deer testing positive for the years 2002 - 2005 are shown below.








Captive Elk Herds Positive for CWD in Nebraska







Subject: SCRAPIE and CWD USA UPDATE July 19, 2006


Date: July 19, 2006 at 12:06 pm PST


SCRAPIE USA UPDATE MAY 31, 2006




Infected and Source Flocks


snip...end








AND THAT ENDED THAT. that was my last post before they banned me from speaking about CWD back then. ...




Due to a decision by the Commission, public posts to the Outdoor Forum are no longer allowed.


xxxx xxxxxxx



Information Systems Analyst Sr.


Nebraska Game and Parks Commission


2200 N. 33rd St.


(402) 471-5646


XXXXXXXXXXXXX






***************




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





Don’t Forget CWD



Sunday, January 22nd, 2012 | Posted by Dr. Dave Samuel




Nebraska just announced the finding of Chronic Wasting Disease in several counties in the center of the state. This shows the continued spread from western Nebraska. So what you say, “It’s obvious that CWD can’t spread to humans and it sure doesn’t seem to be hurting our deer herds.”


Maybe. Maybe on both counts. The release of information showing the spread of CWD in Nebraska (where I hunt every fall in the eastern part of the state) caused me to check out the website, http://transmissiblespongiformencephalopathy.blogspot.com/ . That blog lists a lot of other website with tons of information on CWD. CWD is not spread by bacteria but rather by prions that invade and destroy the brain. One very similar disease of humans is Creutzfeldt-Jacob Disease. This blog presents a lot of information on that disease relative to whether humans can get CWD from diseased deer or elk.



Bottom line is that we don’t know a lot about prions. We do know that prions survive in soil for years. We know that deer can be placed in an area where CWD lived and after being removed for over a year, deer placed there again get CWD.


We don’t know how long prions stay viable in the soil. My guess is . . . many, many years. Maybe decades. We know that deer have prions in nervous tissue but also in lymph tissue and even muscles. We know that prions are spread via saliva and urine. (In fact that is why many states are concerned about baiting for deer.) We don’t think prions can be spread via eating deer meat but we aren’t positive. Scary because another prion disease ‘mad cow disease’ can be spread from cows to humans leading to death.


I don’t want to play the ‘what if’ game, but ‘what if’ one hunter got CWD from eating deer meat and that hunter died? Let’s not go there. The ramifications are beyond comprehension.


Another aspect of this problem is found on the above website as well as http://chronic-wasting-disease.blogspot.com/ . I invite you to go to this website and after you peruse it you will see the relationship of CWD and deer farms. They discuss the Almond deer farm in Wisconsin. A buck shot there in 2002 had CWD and this led to all deer there being killed in 2006. Sixty of the 76 deer killed were CWD positive. In order to keep control of this situation and make sure the fence separating the contaminated farm from wild deer remained intact, the DNR bought the farm in 2011. Remember, this farm probably has CWD prions in the soil, so the potential for spread to wild deer is real. However, 1200 deer outside the farm have been tested and no CWD was found. The DNR wants to make sure the fences stay intact, so they bought it and will do research on CWD there. Seems like a good idea.


A total decontamination of the farm was conducted, but there is no way to know whether prions are still in the soil. They probably are. All timber along the fence is being cut to protect the fence. A second fence 12 feet from the first is being constructed. Apparently the Wisconsin DNR is very concerned about the spread of CWD.


If baiting for deer has been shown to exacerbate the spread of CWD then why do we find baiting being legalized in more and more states? The reason is simple. Hunters want baiting and they apply political pressure to keep baiting if they have it or to get baiting if they do not have it. The DNR in my home state of West Virginia would love to stop baiting for deer to prevent, or slow the spread of CWD from the eastern panhandle of the state, but the hunters won’t let that happen. A political hot potato.


Again, check out the above two web sites then tell me that CWD is not a potential problem for hunters and deer. This ain’t your average disease. So far, humans eating venison are OK and so far deer herds are OK too. But packing large numbers of deer in small areas is an experiment and only time will tell if ‘it’s not nice to fool with Mother Nature.’









Wednesday, January 04, 2012


CWD NEBRASKA NGPC 26 DEER CARCASSES TESTED POSITIVE BUFFALO, CUSTER AND HOLT COUNTIES DURING NOVEMBER HUNT






Friday, February 25, 2011


Soil clay content underlies prion infection odds






Monday, August 8, 2011


Susceptibility of Domestic Cats to CWD Infection


Oral.29: Susceptibility of Domestic Cats to CWD Infection






Tuesday, January 24, 2012


CWD found in two free-ranging deer from Macon County Missouri






Monday, January 16, 2012


9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD








> > > similar if less acute concerns exist for all nine deer farms in Wisconsin that have tested positive for CWD. < < <




WISCONSIN DEPT. OF NATURAL RESOURCES




NEWS RELEASE




Wisconsin Department of Natural Resources




West Central Region




1300 W. Clalremont Ave., PO Box 4001, Eau Claire, WI 54702-2786 Phone: (715) 839-3715 TDD: 711 dnr.wi.gov www.wisconsin.gov




DATE: Monday, July 18,2011




CONTACTS: Davin Lopez, ONR CWO coordinator, Madison. 608-267-2948 Kris Belling, DNR regional wildlife supervisor, Eau Claire, 715-839-3736




SUBJECT: Public input sought on future of CWO-tainted deer farm




BAD CLAlRE - Neighbors and others interested ill the deer farm formerly known as Buckhorn Flats are invited to a public meeting on the future ofthe property, now owned by the state Department of Natural Resources.




The open house meeting will mil 6-8 p.m. Thursday, July 28, in the auditorium at the Almond- Bancroft School at 1336 Elm Street in Almond, Background on the property, now called the Almond Deer Farm, will be provided, and the public is invited to ask questions and offer input 011 the management of the site,




The first case of CWD, 01' chronic wasting disease, among Wisconsin farm-raised deer was discovered on this property in September 2002. CWD, which affects deer and elk, is a contagious and always fatal brain disease for which there is no cure. The discovery o.f CWD on this property led .to the . depopulation of the entire deer herd on the farm.




In the end, 82 of the deer killed and removed tested positive for CWD. This is an 80 percent infection rate, the highest rate ofCWD infection recorded in North America, and possibly in the world.




The property is located along the east side of3rd Street, about one mile north and west of the Village of Almond in Portage County. The DNR purchased the 80~acre property this past spring for $465,000. There are 25 acres of cropland and 55 acres of woodland. About 65 acres are fenced, the area previously used as a deer farm. The property includes a single-family residence and a storage shed located outside of the fence.




Research indicates prions, proteins associated with the disease, can persist in soil for a minimum of three years and perhaps much longer. Prions that cause scrapie, a CWD-Iike disease in sheep and goats, have remained available and infectious for up to 16 years. DNR officials believe there is all unacceptable risk that CWD prions would infect wild white-tailed deer around this site if the fences would be removed. Since the previous owners were selling the property, and there is no continuing obligation to maintain the fence, wildlife officials concluded the best available option was to acquire the property.




similar if less acute concerns exist for all nine deer farms in Wisconsin that have tested positive for CWD. Because the question of how long a contaminated site is a risk to deer is of national and international 'interest there will be a number of opportunities for research at the Almond farm. Plans include building a second fence, if funding is available, to provide a secondary barrier and further reduce the risk of disease transmission to the wild deer herd. In addition, DNR officials must decide whether to maintain ownership of the house and lot.




The primary reason for DNR purchase ofthe property is to ensure that the deel-,fence remains intact, preventing wild deer from accessing the property and becoming infected. The pNR has an ethical and financial responsibility to maintain the fences until science offers a solution for assessing the risk 01' remediating the site. The fence will be inspected frequently.




-30-




The following counties are In the Wast Central Region: Adams, Buffalo, Chippewa, Clark, Dunn, Eau Claire, Jackson, Juneau, La Crosse, Marathon, Monroe, Pepin. Pierce, Portage, st. Croix, Trempealeau, Varnon and Wood. The Public Affairs Manager for DNR West Central Region Is Ed Culhane, 715-839-3715.




Tuesday, December 20, 2011




CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011








SNIP...SEE FULL TEXT ;








Sunday, January 22, 2012


Chronic Wasting Disease CWD cervids interspecies transmission






TSS


Labels:

Tuesday, January 24, 2012

CWD found in two free-ranging deer from Macon County Missouri

CWD found in two free-ranging deer from Macon County
 
 
Statewide


Published on: Jan. 24, 2012


Posted by Joe Jerek


JEFFERSON CITY Mo – The Missouri Department of Conservation (MDC) received two positive test results for Chronic Wasting Disease (CWD) from 1,077 tissue samples taken from free-ranging deer harvested by hunters in north-central Missouri during the 2011 fall firearms deer season. Both positive test results were from adult bucks harvested by Missouri hunters in Macon County, and are the first CWD-positive results for free-ranging deer in Missouri.


MDC plans to obtain more tissue samples for CWD testing by harvesting additional deer in the immediate area where the two infected deer were harvested.


“Teamwork among landowners, hunters and MDC staff allowed us to detect this infection early,” said MDC Deer Biologist Jason Sumners. “We will be working with local landowners to harvest additional deer for tissue sampling. This is a first step and one of our best hopes for containing, and perhaps even eliminating, what we believe to be a recent localized event.”


MDC staff have contacted the two Missouri hunters who harvested the CWD-positive bucks to inform them of the situation and answer questions.


CWD is a neurological disease that is limited to deer, elk, moose and other members of the deer family, known as “cervids.” CWD is spread by animal-to-animal contact or by animal contact with soil that contains prions from urine, feces or the decomposition of an infected animal. Deer and other cervids with signs of CWD show changes in natural behavior and can exhibit extreme weight loss, excessive salivation, stumbling and tremors. CWD can spread through natural movements of infected animals, transportation of infected live captive animals, or the transportation of infected carcasses.


The Missouri Department of Agriculture (MDA) says there is no evidence from existing research that CWD can spread to domestic livestock, such as sheep or cattle. The Missouri Department of Health and Senior Services (MDHSS) says there is no scientific evidence that CWD is transmissible to humans through contact with or the consumption of deer meat.


MDC conducted its tissue-sampling effort during the fall firearms season in November in response to two cases of CWD found in captive white-tailed deer at two private, captive-hunting preserves in Linn and Macon counties. A third captive deer at one of the preserves tested positive for CWD in December. The two earlier cases of CWD found at the private hunting preserves were detected in February 2010 and October 2011. The two free-ranging bucks that tested positive were harvested within two miles of the Macon County preserve.


CWD in deer can only be confirmed by laboratory testing of the brain stem or lymph tissue. Tissue samples collected by MDC were tested by the Southeast Cooperative Wildlife Disease Study Laboratory of the University of Georgia, Athens, with confirmation by the National Veterinary Services Laboratory in Ames, Iowa.


The disease was first recognized in 1967 in captive mule deer in Colorado. CWD has also been documented in both captive and free-ranging deer in neighboring Kansas and Nebraska. It has been documented in free-ranging deer in neighboring Illinois. CWD has also been documented in both captive and free-ranging members of the deer-family in Colorado, Minnesota, New York, South Dakota, Wisconsin and the Canadian provinces of Alberta and Saskatchewan. Maryland, New Mexico, North Dakota, Utah, Virginia, West Virginia and Wyoming also have documented cases of CWD in free-ranging members of the deer family. Michigan and Montana have documented cases of CWD in captive members of the deer family.


CWD is transmitted through prions, which are abnormal proteins that attack the nervous systems of these species. These prions accumulate in the brain, spinal cord, eyes, spleen, and lymph nodes of infected animals. While there is no scientific evidence that CWD is transmissible to humans or animals other than deer and other cervids, health officials caution that consumption of these parts is not recommended. They also advise people to not eat meat from animals known to be infected with CWD or that exhibit signs of any disease.


While CWD is new to free-ranging deer in Missouri, MDC has been testing for it for years. With the help of hunters, MDC has tested more than 34,000 free-ranging deer for CWD from all parts of the state since 2002.


Missouri also has a Cervid Health Committee to address the threat of CWD to Missouri’s free-ranging and captive cervids. The Committee is composed of wildlife biologists, veterinarians and other animal-health experts from MDC, MDA, MDHSS and the USDA.








Friday, October 21, 2011


Chronic Wasting Disease Found in Captive Deer Missouri








Friday, February 26, 2010


Chronic wasting disease found in Missouri deer







Sunday, January 22, 2012


Chronic Wasting Disease CWD cervids interspecies transmission







TSS

Labels:

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

Chronic Wasting Disease CWD cervids interspecies transmission



Wednesday, January 5, 2011


ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions


David W. Colby1,* and Stanley B. Prusiner1,2


+ Author Affiliations


1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu


SNIP...


Greetings,


I believe the statement and quote below is incorrect ;


"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."


Please see ;


Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.




"although the infection rate was low (4 of 13 animals [Hamir et al. 2001])."


shouldn't this be corrected, 86% is NOT a low rate. ...


kindest regards,


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518


MARCH 1, 2011


UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;


----- Original Message -----


From: David Colby


To: flounder9@verizon.net


Cc: stanley@XXXXXXXX


Sent: Tuesday, March 01, 2011 8:25 AM


Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations


Dear Terry Singeltary,


Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter.


Warm Regards, David Colby


--


David Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of Delaware


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SNIP...SEE FULL TEXT ;




UPDATED DATA ON 2ND CWD STRAIN


Wednesday, September 08, 2010


CWD PRION CONGRESS SEPTEMBER 8-11 2010




Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies Location: Virus and Prion Diseases of Livestock


Title: TRANSMISSION OF CHRONIC WASTING DISEASE AGENT OF MULE DEER (CWD**MD) TO SUFFOLK SHEEP BY INTRACEREBRAL ROUTE


Authors


Hamir, Amirali Kunkle, Robert Cutlip, Randall - ARS RETIRED Miller, Janice - ARS RETIRED Williams, Elizabeth - UNIVERSITY OF WYOMING Richt, Juergen


Submitted to: European Society of Veterinary Pathology Publication Type: Abstract Publication Acceptance Date: June 5, 2006 Publication Date: August 31, 2006 Citation: Hamir, A., Kunkle, R., Cutlip, R., Miller, J., Williams, E., Richt, J. 2006. Transmission of chronic wasting disease agent of mule deer (CWD**md) to Suffolk sheep by intracerebral route [abstract]. European Society of Veterinary Pathology 24th Annual Meeting. Paper No. P63. p. 171-172.


Technical Abstract: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) that has been identified in captive and free-ranging cervids in the U.S. since 1967. To determine the transmissibility of CWD to sheep, 8 Suffolk lambs [4 QQ and 4 QR at codon 171 of prion protein (PRNP) gene] were inoculated intracerebrally with a pooled brain suspension from 28 mule deer naturally affected with CWD (CWD**md). Two other lambs (1 QQ and 1 QR at codon 171 of the PRNP gene) were kept as non-inoculated controls. Within 36 months post inoculation (MPI), 2 animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in the sheep with the clinical signs of TSE and its tissues were positive for the abnormal prion protein (PrP**res) by immunohistochemistry and Western blot. Between 36 and 60 MPI, 3 other sheep were euthanized because of conditions unrelated to TSE. The remaining 3 sheep remained non-clinical at the termination of the study (72 MPI) and were euthanized at that time. One of the 3 animals revealed SE and its tissues were positive for PrP**res. Both sheep positive for PrP**res were homozygous QQ at codon 171. Retrospective examination of the PRNP genotype of the 2 TSE-positive animals revealed that the sheep with clinical prion disease (euthanized at 35 MPI) was heterozygous (AV) and the sheep with the sub-clinical disease (euthanized at 72 MPI) was homozygous (AA) at codon 136 of the PRNP. These findings demonstrate that transmission of the CWD**md agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a significant part in successful transmission and incubation period of CWD**md.




Transmission of chronic wasting disease of mule deer to Suffolk sheep following intracerebral inoculation


Amir N. Hamir,1 Robert A. Kunkle, Randall C. Cutlip, Janice M. Miller, Elizabeth S. Williams, Juergen A. Richt


Abstract. To determine the transmissibility of chronic wasting disease (CWD) to sheep, 8 Suffolk lambs of various prion protein genotypes (4 ARQ/ARR, 3 ARQ/ARQ, 1 ARQ/VRQ at codons 136, 154, and 171, respectively) were inoculated intracerebrally with brain suspension from mule deer with CWD (CWDmd). Two other lambs were kept as noninoculated controls. Within 36 months postinoculation (MPI), 2 inoculated animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in this sheep, and its tissues were determined to be positive for the abnormal prion protein (PrPres) by immunohistochemistry and Western blot. Three other inoculated sheep were euthanized (36 to 60 MPI) because of conditions unrelated to TSE. The 3 remaining inoculated sheep and the 2 control sheep did not have clinical signs of disease at the termination of the study (72 MPI) and were euthanized. Of the 3 remaining inoculated sheep, 1 was found to have SE, and its tissues were positive for PrPres. The sheep with clinical prion disease (euthanized at 35 MPI) was of the heterozygous genotype (ARQ/VRQ), and the sheep with subclinical disease (euthanized at 72 MPH) was of the homozygous ARQ/ARQ genotype. These findings demonstrate that transmission of the CWDmd agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a notable part in successful transmission and incubation period of CWDmd.


snip...


Thus far, among domestic animals, CWDmd has been transmitted by the intracerebral route to a goat18 and cattle.5–7 The present findings demonstrate that it is also possible to transmit CWDmd agent to sheep via the intracerebral route. However, the only sheep to develop clinical TSE within 35 MPI was genotypically AV at PRNP codon 136, suggesting that host genotype may play a notable part in successful transmission of the disease in this species. Although in Suffolk sheep the AV variant at codon 136 is very rare,17 selective breeding of Suffolk sheep with this codon has begun in the hope of testing this differential susceptibility hypothesis in a future study of CWDmd transmission to sheep.


Key words: Chronic wasting disease; immunohistochemistry; intracerebral transmission; prion protein; sheep; spongiform encephalopathy.




Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies Location: Virus and Prion Diseases of Livestock


Title: EXPERIMENTAL SECOND PASSAGE OF CHRONIC WASTING DISEASE (CWD(MULE DEER)) AGENT TO CATTLE


Authors


Hamir, Amirali Kunkle, Robert Miller, Janice - ARS RETIRED Greenlee, Justin Richt, Juergen


Submitted to: Journal of Comparative Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 25, 2005 Publication Date: January 1, 2006 Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Greenlee, J.J., Richt, J.A. 2006. Experimental second passage of chronic wasting disease (CWD(mule deer)) agent to cattle. Journal of Comparative Pathology. 134(1):63-69.


Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB. Technical Abstract: To compare clinicopathological findings of first and second passage of chronic wasting disease (CWD) in cattle, a group of calves (n=6) were intracerebrally inoculated with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and lost weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify CWD PrPres but also develop clinical CNS signs without manifestation of morphologic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, scrapie. The current study confirms previous work that indicates the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of neuropathologic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.




Wednesday, September 21, 2011


Evidence for distinct CWD strains in experimental CWD in ferrets




Wednesday, October 12, 2011


White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation




Wednesday, July 06, 2011


Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation




see incredible infection rate at one of these game farms Wisconsin shut down and bought out. 86% infection rate...


Monday, January 16, 2012


9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD




Tuesday, December 20, 2011


CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011




SNIP...SEE FULL TEXT ;




*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.




CWD END OF YEAR REVIEW 2011


EFSA Journal 2011 The European Response to BSE: A Success Story


This is an interesting editorial about the Mad Cow Disease debacle, and it’s ramifications that will continue to play out for decades to come ;


Monday, October 10, 2011


EFSA Journal 2011 The European Response to BSE: A Success Story


snip…


EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as “sporadic” CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.


snip…






see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;






Chronic Wasting Disease Susceptibility of Four North American Rodents


Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu


We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.




please see ;




Oral.29: Susceptibility of Domestic Cats to CWD Infection


Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason† Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu


Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.


www.landesbioscience.com Prion




see more recent science abstracts from the Prion 2011 on CWD here ;




PAGE 25


Transmission Studies


Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculam (?saline).


Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in all of these species with the shortest incubation period in the ferret.




Generation of a New Form of Human PrPScin Vitro by Interspecies Transmission from Cervid Prions*


Marcelo A. Barria‡, Glenn C. Telling§, Pierluigi Gambetti¶, James A. Mastrianni‖ and Claudio Soto‡,1


+ Author Affiliations


From the ‡Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Medical School at Houston, Houston, Texas 77030,


the §Departments of Microbiology, Immunology, and Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky Medical Center, Lexington, Kentucky 40506,


the ¶Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, and


the ‖Department of Neurology, The University of Chicago, Chicago, Illinois 60637


1 To whom correspondence should be addressed: University of Texas Medical School at Houston, 6431 Fannin St., Houston, TX 77030. Tel.: 713-500-7086; Fax: 713-500-0667; E-mail: claudio.soto@uth.tmc.edu.


Abstract


Prion diseases are infectious neurodegenerative disorders that affect humans and animals and that result from the conversion of normal prion protein (PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. Determining the risk of transmission of CWD to humans is of utmost importance, considering that people can be infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the misfolded form by CWD PrPSc, we performed experiments using the protein misfolding cyclic amplification technique, which mimics in vitro the process of prion replication. Our results show that cervid PrPSc can induce the conversion of human PrPC but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct biochemical pattern that differs from that of any of the currently known forms of human PrPSc. Our results also have profound implications for understanding the mechanisms of the prion species barrier and indicate that the transmission barrier is a dynamic process that depends on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans and that this ability progressively increases with CWD spreading.


snip...


Interestingly, when the Western blot profile of this newly generated form of human PrPSc (termed CWD-huPrPSc) was compared with known strains of human prions, it was clear that CWD-huPrPSc exhibited a different pattern (Fig. 4A). The electrophoretic migration of this protein after PK-digestion is similar to the type 1 strain of sCJD, but its glycosylation profile is clearly different, showing a highly predominant diglycosylated form (Fig. 4A and B). This result suggests that CWD hu-PrPSc corresponds to a new human prion strain. Interestingly, a detailed previous study from Gambetti’s group comparing the biochemical characteristics of PrPSc from cervids and humans showed that CWD PrPSc is similar to sCJDMM1 in terms of electrophoretic mobility (6). However, the misfolded protein associated with CWD is predominantly di-glycosylated, whereas PrPSc from type 1 sCJD is mostly monoglycosylated (6). Based on the fact that transmission of BSE prions to humans resulted in a new form of PrPSc very similar to the one in cattle (6;27), these authors predicted that if humans were infected by CWD it is likely that PrPSc would be of type 1 and with a predominance of the diglycosylated isoform (6). Our results agree with that prediction and suggest that the newly generated CWD-huPrPSc acquires the biochemical properties of the cervid infectious material (Fig. 4A and B).


snip...


Our results have far-reaching implications for human health, since they indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc, suggesting that CWD might be infectious to humans. Interestingly our findings suggest that unstable strains from CWD affected animals might not be a problem for humans, but upon strain stabilization by successive passages in the wild, this disease might become progressively more transmissible to man.


Reference List


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please see full text and many thanks to the Professor Soto and the other Authors of this study AND to The Journal Of Biological Chemistry for the free full text !!!


Amyloid Neurodegeneration Neurological Diseases Prions Protein Conformation Prion Diseases






see full text and more here ;




PLEASE NOTE ;


there are now two documented strains of CWD, and science is showing that indeed CWD could transmit to humans via transmission studies ;


P35


ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD


Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5


The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.




PPo3-7:


Prion Transmission from Cervids to Humans is Strain-dependent


Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA


Key words: CWD, strain, human transmission


Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.


Acknowledgement Supported by NINDS NS052319 and NIA AG14359.


PPo2-27:


Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions


Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA


Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.


PPo2-7:


Biochemical and Biophysical Characterization of Different CWD Isolates


Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany


Key words: CWD, strains, FT-IR, AFM


Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.




Saturday, November 12, 2011


Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease


Fri, 22 Sep 2006 09:05:59 –0500




Tuesday, May 31, 2011


Chronic Wasting Disease


DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011


Top Curr Chem (2011) DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011


Chronic Wasting Disease


Sabine Gilch, Nandini Chitoor, Yuzuru Taguchi, Melissa Stuart, Jean E. Jewell, and Hermann M. Schatzl


Abstract


Chronic wasting disease (CWD) is a prion disease of free-ranging and farmed ungulates (deer, elk, and moose) in North America and South Korea. First described by the late E.S. Williams and colleagues in northern Colorado and southern Wyoming in the 1970s, CWD has increased tremendously both in numerical and geographical distribution, reaching prevalence rates as high as 50% in freeranging and >90% in captive deer herds in certain areas of USA and Canada. CWD is certainly the most contagious prion infection, with significant horizontal transmission of infectious prions by, e.g., urine, feces, and saliva. Dissemination and persistence of infectivity in the environment combined with the appearance in wildliving and migrating animals make CWD presently uncontrollable, and pose extreme challenges to wild-life disease management. Whereas CWD is extremely transmissible among cervids, its trans-species transmission seems to be restricted, although the possible involvement of rodent and carnivore species in environmental transmission has not been fully evaluated. Whether or not CWD has zoonotic potential as had Bovine spongiform encephalopathy (BSE) has yet to be answered. Of note, variant Creutzfeldt–Jakob disease (vCJD) was only detected because clinical presentation and age of patients were significantly different from classical CJD. Along with further understanding of the molecular biology and pathology of CWD, its transmissibility and species restrictions and development of methods for preclinical diagnosis and intervention will be crucial for effective containment of this highly contagious prion disease.


snip...


8 Zoonotic Potential Deer hunting is a popular sport in the USA; venison is usually consumed by hunters and their families, and this raises reasonable concerns about the transmissibility of CWD to humans, as exemplified by the zoonotic transmission of BSE. Epidemiological studies have not revealed an increased incidence of CJD in CWD endemic areas. Suspicious case reports about persons having consumed venison and succumbed to neurological disorders turned out to be classical or familial CJD and a causal link to the consumption of contaminated meat could not be proven [109]. In vitro conversion assays were performed to assess the convertibility of human PrPc into PK resistant PrP using CWD derived from elk, mule deer, and white-tailed deer as a template. Only a very low conversion rate could be demonstrated, indicative of a considerable species barrier [110]. In a very recent study employing protein misfolding cyclic amplification (PMCA), a highly sensitive method for in vitro amplification conversion of human PrPc was successful, albeit with the restriction that CWD prions had to be adapted by PMCA or in vivo passage through cervidized tg mice. Passaged CWD template gave rise to a new form of human PrPSc, and its infectivity is currently under investigation. Of note, when field isolates of CWD Chronic Wasting Disease brains were used as a template, no conversion of human PrPc was achieved, which again questions the relevance of the in vitro data [111]. Studies using humanized tg mouse inoculated with CWD furthermore argue against transmissibility to humans since mice did not develop prion disease [112–114]. The best possible animal models to study transmission of animal prion diseases to humans probably are non-human primates. For instance, inoculation of BSE prions into Cynomolgus macaques provided the first hints that BSE might be transmissible to humans [115]. However, oral or i.c. challenge with CWD of macaques did not cause disease [116]. On the other hand, squirrel monkeys (Saimiri sciureus) were susceptible to i.c. inoculation with CWD prions [116, 117], and after oral exposure PrPSc was detectable in brain, spleen, and lymph nodes of 2/15 squirrel monkeys [116]. This shows that CWD can be transmitted to certain non-human primates, although results in Cynomolgus macaques might be of higher relevance since they are evolutionary closer relatives of humans than squirrel monkeys. Overall, there is no compelling evidence that CWD can be transmitted to humans with high efficiency.


snip...end




Monday, June 27, 2011


Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates




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.




PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;


Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey


Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.




NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;


Wednesday, March 18, 2009


Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II




Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey


Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD


Accepted 15 November 2010. Abstract Full Text PDF References .


Abstract


The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.




"These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent."


Potential Venison Exposure Among FoodNet Population Survey Respondents, 2006-2007


Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B. Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail: rmaddox@cdc.gov


The foodborne transmission of bovine spongiform encephalopathy to humans, resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be susceptible to animal prion diseases. However, it is not known whether foodborne exposure to the agent causing chronic wasting disease (CWD) in cervids can cause human disease. The United States Foodborne Diseases Active Surveillance Network (FoodNet) conducts surveillance for foodborne diseases through an extensive survey administered to respondents in selected states. To describe the frequency of deer and elk hunting and venison consumption, five questions were included in the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%) reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of Colorado. Respondents reporting hunting were significantly more likely to be male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and, in general, older respondents were significantly more likely to report hunting than younger respondents. Venison consumption was reported by more than half (67.4%) of the study population, and most venison consumers (94.1%) reported that at least half of their venison came from the wild. However, more than half (59.1%) of the consumers reported eating venison only one to five times in their life or only once or twice a year. These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent.




now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????


“Our conclusion stating that we found no strong evidence of CWD transmission to humans”


From: TSS (216-119-163-189.ipset45.wt.net)


Subject: CWD aka MAD DEER/ELK TO HUMANS ???


Date: September 30, 2002 at 7:06 am PST


From: "Belay, Ermias"


To:


Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"


Sent: Monday, September 30, 2002 9:22 AM


Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS


Dear Sir/Madam,


In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.


That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.


Ermias Belay, M.D. Centers for Disease Control and Prevention


-----Original Message-----


From:


Sent: Sunday, September 29, 2002 10:15 AM


To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV


Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS


Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS


Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease


2008 1: Vet Res. 2008 Apr 3;39(4):41


A prion disease of cervids: Chronic wasting disease


Sigurdson CJ.


snip...


*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,


snip...


full text ;




Monday, November 14, 2011


WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011




Wednesday, November 16, 2011


Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011




Sunday, November 13, 2011


COLORADO CWD CJD TSE PRION REPORTING 2011




Monday, May 23, 2011 CDC


Assesses Potential Human Exposure to Prion Diseases Travel Warning


Public release date: 23-May-2011


Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences


CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or "Mad Cow Disease"), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.


"While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases," commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta."But it's also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents."


Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.


CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.


Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.


The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.


The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.


According to Abrams, "The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health."


###


The article is "Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey" by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.


In an accompanying podcast CDC's Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast.




Thursday, December 29, 2011


Aerosols An underestimated vehicle for transmission of prion diseases?




please see more on Aerosols and TSE prion disease here ;




Sunday, July 27, 2008


DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability


-------- Original Message --------


Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability


Date: Fri, 16 May 2003 11:47:37 -0500


From: "Terry S. Singeltary Sr."


To: fdadockets@oc.fda.gov


Greetings FDA,


i would kindly like to comment on;


Docket 03D-0186


FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability


Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;


1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the _total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...


2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test to assure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthy ones as well. it this is not done, they system will fail...


3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.


4. THERE are and have been for some time many TSEs in the USA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.


5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread these TSE mad cow agents in the USA. I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in the USA, but this has yet to happen...


6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)


7. WE must learn from our past mistakes, not continue to make the same mistakes...


snip...


Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1


Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit, Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA 99164-7030, USA5


Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail ehoover@lamar.colostate.edu


Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.


snip...


These results indicate that mule deer fawns develop detectable PrP res after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node. He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings support oral exposure as a natural route of CWD infection in deer and support oral inoculation as a reasonable exposure route for experimental studies of CWD.


snip...




snip...see full text ;


-------- Original Message --------


Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability


Date: Fri, 16 May 2003 11:47:37 -0500


From: "Terry S. Singeltary Sr."


To: fdadockets@oc.fda.gov


Greetings FDA,


i would kindly like to comment on;


Docket 03D-0186


FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability




Article


Experimental oral transmission of chronic wasting disease to red deer


(Cervus elaphus elaphus): Early detection and late stage distribution


of protease-resistant prion protein


Aru Balachandran, Noel P. Harrington, James Algire, Andrei Soutyrine, Terry R. Spraker,


Martin Jeffrey, Lorenzo González, Katherine I. O'Rourke


Abstract - Chronic wasting disease (CWD), an important emerging prion disease of cervids, is readily transmitted by intracerebral or oral inoculation from deer-to-deer and elk-to-elk, suggesting the latter is a natural route of exposure. Studies of host range susceptibility to oral infection, particularly of those species found in habitats where CWD currently exists are imperative. This report describes the experimental transmission of CWD to red deer following oral inoculation with infectious CWD material of elk origin. At 18 to 20 months post-inoculation, mild to moderate neurological signs and weight loss were observed and animals were euthanized and tested using 3 conventional immunological assays. The data indicate that red deer are susceptible to oral challenge and that tissues currently used for CWD diagnosis show strong abnormal prion (PrPCWD) accumulation. Widespread peripheral PrPCWD deposition involves lymphoreticular tissues, endocrine tissues, and cardiac muscle and suggests a potential source of prion infectivity, a means of horizontal transmission and carrier state.


SNIP...


There is a strong correlation between the presence of PrPTSE and infectivity in prion diseases. Although the epidemiologic evidence strongly suggests that CWD is not transmissible to humans, this study and others suggest caution in this regard. The finding of PrPCWD in various organs, albeit in clinical CWD, suggests that humans who consume or handle meat from CWD-infected red deer may be at risk of exposure to CWD prions. This study found that red deer tissues other than nervous and lymphoid tissue can support CWD prion replication and accumulation. As a result, the consumption or handling of meat from CWD-infected red deer will put humans at risk of exposure to CWD prions. In spite of a well-documented species barrier, a cautious approach would involve preventing such tissues from entering the animal and human food chains. Future studies will require sensitive and quantitative techniques such as bioassays in transgenic mice that assess tissue infectivity and quantitative immunoassays adapted to PrPCWD detection in peripheral tissues.


SNIP...


The exact mode of transmission of CWD in nature remains unclear but is believed to involve direct animal-to-animal contact or environmental contamination. As TSE agents are extremely resistant in the environment (39), oral exposure is the most plausible pathway by which the CWD prion may be introduced to deer in nature and represents a significant obstacle to eradication of CWD from either farmed or free-ranging cervid populations. The distribution of PrPCWD in gut-associated lymphoid tissues, salivary glands, and nasal mucosa in the red deer of this study suggests potential routes of PrPCWD shedding into the environment via fluids such as saliva or feces. However, this study did not identify the point at which an animal may become infectious during the course of infection. An improved understanding of the mechanisms of shedding and transmission will be important in the future management of CWD.


SNIP...


In summary, this study demonstrates the potential for oral transmission of CWD to red deer and describes the pattern of PrPCWD accumulation for this species. The current surveillance testing regime for cervids would be expected to identify CWD-infected red deer should it occur in North America. These results confirm the usefulness of rapid tests such as ELISA but with generally slightly lower sensitivity when compared with IHC when testing tissues with patchy or sporadic PrPCWD deposition. The finding of PrPCWD in several extraneural tissues including cardiac muscle and the endocrine system suggests that further investigation and monitoring of the potential transmissibility to other species including humans is warranted.


SNIP...


(Traduit par Isabelle Vallières)


Can Vet J 2010;51:169-178


Ottawa Laboratory - Fallowfield, Canadian Food Inspection Agency, Ottawa, Ontario (Balachandran, Harrington, Algire,


Soutyrine); Veterinary Diagnostic Laboratory, Colorado State University, Fort Collins, Colorado, USA (Spraker); Veterinary


Laboratory Agency, Department for the Environment, Food & Rural Affairs, Lasswade, Midlothian, Scotland, United Kingdom


(Jeffrey, González); Animal Disease Research Unit, Agricultural Research Service, United States Department of Agriculture, Pullman,


Washington, USA (O'Rourke).


Address all correspondence to Dr. Aru Balachandran; e-mail: BalachandranA@inspection.gc.ca




Saturday, November 6, 2010


TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS


INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation




Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>


Prion disease update 2010 (11)


PRION DISEASE UPDATE 2010 (11)




Wednesday, January 18, 2012


BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE


February 1, 2012




Friday, January 6, 2012


OIE 2012 Training Manual on Wildlife Diseases and Surveillance and TSE Prion disease




Tuesday, January 17, 2012


Annual report of the Scientific Network on BSE-TSE EFSA-Q-2011-01110 Issued: 20 December 2011








2011 Monday, September 26, 2011


L-BSE BASE prion and atypical sporadic CJD







TSS

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