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DNR to Continue Surveillance for Chronic Wasting Disease CWD TSE Prion

flounder9

Member
DNR to Continue Surveillance for Chronic Wasting Disease

Posted: 12/06/2013

DNR wildlife staff will again be in the field during Iowa’s shotgun deer seasons, collecting samples to test for Chronic Wasting Disease (CWD) in Iowa’s wild deer herd. The effort will concentrate on portions of Northeast Iowa near Wisconsin and Illinois as well as in Wapello, Davis, Pottawattamie and Cerro Gordo counties, following positive tests from captive facilities in or near those counties last year.

Many of the samples will be collected during the first half of December, as more than 120,000 hunters take part in Iowa’s shotgun deer seasons and deer harvested during those seasons are major sources of samples. Sampling—which involves removing and testing the brain stem and lymph nodes--has been done on free ranging deer across Iowa for years. Many hunters voluntarily contribute samples of their harvested deer for these testing efforts. Most samples are obtained by wildlife staff, checking with hunters in the field or at home processing points.

DNR has historically focused its sampling efforts heaviest in northeast Iowa, after Wisconsin and Illinois yielded positive cases in recent years. After the positive findings in captive herds in 2012, DNR focused additional testing in those counties identified above. Sampling in northeast Iowa for the 2013-2014 seasons will continue at a slightly lower intensity in order to accommodate the additional testing in Davis, Wapello, Pottawattamie and Cerro Gordo Counties.

Since 2002, more than 47 thousand wild deer in Iowa have been tested, with no positive CWD result in the wild herd detected to date. “We are hopeful CWD has not spread into Iowa’s deer herd. The only way to know this is to continue to collect samples and do the testing. We will work through all hunting seasons, with the peak being the shotgun seasons in December,” said Dr. Dale Garner, Wildlife Bureau Chief.

Iowa DNR’s website provides information about CWD and other information on infectious disease at:

http://www.iowadnr.gov/Hunting/DeerHunting/CWDEHDInformation.aspx


http://www.iowadnr.gov/insidednr/socialmediapressroom/newsreleases/vw/1/itemid/1725



this is good news that the DNR has decided to continue surveillance for CWD and testing. however, I think testing needs to be increased across the board, in every state, especially around, and inside game farms/ranches/mills etc. ...tss


Thursday, September 19, 2013

Illinois Chronic Wasting Disease: 2012-2013 Surveillance and Management Report

http://chronic-wasting-disease.blogspot.com/2013/09/illinois-chronic-wasting-disease-2012.html



Wednesday, August 21, 2013

IOWA DNR EMERGENCY CONSENT ORDER IN THE MATTER OF TOM & LINDA BRAKKE D/B/A PINE RIDGE HUNTING LODGE UPDATE AUGUST 21, 2013

http://chronic-wasting-disease.blogspot.com/2013/08/iowa-dnr-emergency-consent-order-in.html



Wednesday, September 04, 2013

***cwd - cervid captive livestock escapes, loose and on the run in the wild...

http://chronic-wasting-disease.blogspot.com/2013/09/cwd-cervid-captive-livestock-escapes.html



Saturday, October 19, 2013

***ACA Council Meets to Endorse Several Proposed USAHA Resolutions (CWD TSE PRION DISEASE)

http://chronic-wasting-disease.blogspot.com/2013/10/aca-council-meets-to-endorse-several.html



Monday, December 02, 2013

WISCONSIN CHRONIC WASTING DISEASE CWD DISCOVERED MARATHON COUNTY HUNTING PRESERVE

http://chronic-wasting-disease.blogspot.com/2013/12/wisconsin-chronic-wasting-disease-cwd.html



Friday, November 22, 2013

Wasting disease is threat to the entire UK deer population

http://chronic-wasting-disease.blogspot.com/2013/11/wasting-disease-is-threat-to-entire-uk.html



Friday, November 29, 2013

Identification of Misfolded Proteins in Body Fluids for the Diagnosis of Prion Diseases

International Journal of Cell Biology

http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/identification-of-misfolded-proteins-in.html



Saturday, February 04, 2012

Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-16-age-limit-on-testing-dead.html



kind regards,

terry



Sunday, December 08, 2013

IOWA DNR to Continue Surveillance for Chronic Wasting Disease CWD TSE PRION DISEASE

http://chronic-wasting-disease.blogspot.com/2013/12/iowa-dnr-to-continue-surveillance-for.html
 
FYI

A Wilton, Iowa man DIED from Crutzfeldt-Jacobs disease two weeks ago. As you know, that is the HUMAN form of CWD. I dunno how he got the disease or of any other cases of the human form of the disease in the midwest.
 
HUMAN FORM OF CWD, what might that look like ?

FYI

A Wilton, Iowa man DIED from Crutzfeldt-Jacobs disease two weeks ago. As you know, that is the HUMAN form of CWD. I dunno how he got the disease or of any other cases of the human form of the disease in the midwest.



say there Hunt Iowa, Iowa hunters et al,


let me try and explain this mess. I may have to get long winded a bit. I tend to get this way every year around December 14 i.e. mom dod 12/14/97 confirmed hvCJD, and I sometimes wonder if all this was even worth it. seems I might take one step forward with all this, and then 10 backwards because of the industries and politics involved, oh Lord, and to even mention Alzheimer’s, Parkinsons, ALS, and some of the other neurological disease, that the prion may play a role in, and you will be labeled as being MAD. or not.

sporadic creutzfeldt jakob disease, as with what Mr. Belknap was diagnosed with, was not documented as you put ‘HUMAN form of CWD’.
what the obituary stated was simply creutzfeldt jakob disease, meaning here in the USA and by NPDPS and the CJD Foundation, the diagnosis was sporadic CJD.

with that said, it very well could be from Chronic Wasting Disease CWD transmitting to humans in the case of Mr. Belknap, either directly or indirectly via the medical, surgical, dental, i.e. friendly fire mode i.e. iatrogenic CJD. all iatrogenic CJD is, is sporadic CJD, before the route and source of the iatrogenic event which took place, confirmed, documented, and then put into the academic domain as such, which very rarely happens. please be advised, the prion gods have stated, that cwd in cervids, transmitted to humans, would not necessarily look like nvCJD or vCJD (the same) in humans from bovine spongiform encephalopathy, and it might very well look like sporadic CJD. there are many sub-types of the sporadic CJD, with atypical sub-types mounting, the victims are becoming much younger, their symptoms now match that of nvCJD, with duration of illness, from first onset of symptoms to death, being much longer than the typical sporadic CJD. have I confused you yet, well, that’s what they want. this all really is not rocket science. I cannot stress enough the risk factors from iatrogenic CJD, from humans consuming CWD positive, sub-clinical cervids, and products there from, that are then exposed, but yet never go clinical in their lifetime and die do to something else, BUT YET, during that lifespan, these same CWD exposed people go on to have many medical, surgical, dental procedures that go on to expose many, many, more people for years, decades to come. you must remember, this is not just science, this is a big game of political science, in which the political part is winning. $$$ USDA INC, CFIA, MAFF/DEFRA, OIE, WTO $$$


Charles B. Belknap

Charles Bruce Belknap, age 75, of Wilton, IA, died on Wednesday, November 6, 2013 at Carrington Place, Muscatine, IA, following a battle with Creutzfeldt - Jakob Disease (CJD).

According to Charlie’s wishes, his brain will be donated to the National Prion Disease Pathology Surveillance Center and CJD Foundation, to further learn about this rare disease, in hopes of helping other families.


http://www.bentleyfuneralhome.com/ObituaryView.aspx?OID=693


cwd to humans ???

the prion gods at the cdc state that there is ;

''no strong evidence''

but let's see exactly what the authors of this cwd to human at the cdc state ;

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

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

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

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

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

From: "Belay, Ermias"

To:

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

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

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

Dear Sir/Madam,

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

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

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

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

From:

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

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

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

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

Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease

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

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

snip...

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

snip...

full text ;

http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html


http://chronic-wasting-disease.blogspot.com/2006_12_01_archive.html


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.

http://www.adajournal.org/article/S0002-8223(11)00278-1/abstract


"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.

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf


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.

http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php

also, they did not call this CWD postive meat back for the well being of the ELK ;

Wednesday, March 18, 2009

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

___________________________________

PRODUCT

a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;

b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;

c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;

d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;

e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;

f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9;

CODE

Elk Meats with production dates of December 29, 30, and 31

RECALLING FIRM/MANUFACTURER

Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009.

Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing.

REASON

Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD).

VOLUME OF PRODUCT IN COMMERCE

Unknown

DISTRIBUTION

NV, CA, TX, CO, NY, UT, FL, OK

___________________________________

http://www.fda.gov/bbs/topics/ENFORCE/2009/ENF01099.html


CJD REPORT 1994 increased risk for consumption of veal and venison and lamb

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994

Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)

These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...

Table 9 presents the results of an analysis of these data.

There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).

Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.

There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).

The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

snip...

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

snip...

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

snip...

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

snip...see full report ;

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf


Thursday, October 10, 2013

CJD REPORT 1994 increased risk for consumption of veal and venison and lamb

http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html

CJD9/10022

October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.

http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf



UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


Thursday, November 21, 2013

***Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy ***

http://chronic-wasting-disease.blogspot.com/2013/11/assessing-susceptibility-of-transgenic.html



PRION2013 CONGRESSIONAL ABSTRACTS CWD

Sunday, August 25, 2013

***Chronic Wasting Disease CWD risk factors, *humans*, domestic cats, blood, and mother to offspring transmission

http://chronic-wasting-disease.blogspot.com/2013/08/prion2013-chronic-wasting-disease-cwd.html



Sunday, July 21, 2013

*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?

http://chronic-wasting-disease.blogspot.com/2013/07/as-chronic-wasting-disease-cwd-rises-in.html



DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)

The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why???? than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!!

Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....

Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!

And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...

Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and aggressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"

again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.

You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)


[COLOR= ]


[/COLOR]
[COLOR= ] In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

[SIZE=+0]3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a very low profile indeed. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be avoided in the US at all costs. ...[/SIZE]

http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf



[/COLOR]


CJD QUESTIONNAIRE USA

http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html


http://cjdquestionnaire.blogspot.com/


Tuesday, October 29, 2013

VARIANT CJD PRESENTS DIFFERENTLY IN OLDER PATIENTS

http://creutzfeldt-jakob-disease.blogspot.com/2013/10/variant-cjd-presents-differently-in.html



Wednesday, October 09, 2013

*** WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY, £41,078,281 in compensation REVISED

FARMERS AND FARMERS WIVES WITH DOCUMENTED BSE HERDS, DIAGNOSED WITH SPORADIC CJD ???

http://creutzfeldt-jakob-disease.blogspot.com/2013/10/why-ukbsenvcjd-only-theory-is-so.html


http://bseinquiry.blogspot.com/2008/05/sporadic-cjd-in-farmers-farmers-wives.html




The chances of a person or domestic animal contracting CWD are “extremely remote,” Richards said. The possibility can’t be ruled out, however. “One could look at it like a game of chance,” he explained. “The odds (of infection) increase over time because of repeated exposure. That’s one of the downsides of having CWD in free-ranging herds: We’ve got this infectious agent out there that we can never say never to in terms of (infecting) people and domestic livestock.”



https://www.avma.org/News/JAVMANews/Pages/121201a.aspx








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.



http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf






*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.



http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf






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.



http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf





HUMAN FORM OF CWD, what might that look like ? continued part 2
 
HUMAN FORM OF CWD, what might that look like ? part II

say there Hunt Iowa, Iowa hunters et al,


let me try and explain this mess. I may have to get long winded a bit. I tend to get this way every year around December 14 i.e. mom dod 12/14/97 confirmed hvCJD, and I sometimes wonder if all this was even worth it. seems I might take one step forward with all this, and then 10 backwards because of the industries and politics involved, oh Lord, and to even mention Alzheimer’s, Parkinsons, ALS, and some of the other neurological disease, that the prion may play a role in, and you will be labeled as being MAD. or not.

sporadic creutzfeldt jakob disease, as with what Mr. Belknap was diagnosed with, was not documented as you put ‘HUMAN form of CWD’.
what the obituary stated was simply creutzfeldt jakob disease, meaning here in the USA and by NPDPS and the CJD Foundation, the diagnosis was sporadic CJD.

with that said, it very well could be from Chronic Wasting Disease CWD transmitting to humans in the case of Mr. Belknap, either directly or indirectly via the medical, surgical, dental, i.e. friendly fire mode i.e. iatrogenic CJD. all iatrogenic CJD is, is sporadic CJD, before the route and source of the iatrogenic event which took place, confirmed, documented, and then put into the academic domain as such, which very rarely happens. please be advised, the prion gods have stated, that cwd in cervids, transmitted to humans, would not necessarily look like nvCJD or vCJD (the same) in humans from bovine spongiform encephalopathy, and it might very well look like sporadic CJD. there are many sub-types of the sporadic CJD, with atypical sub-types mounting, the victims are becoming much younger, their symptoms now match that of nvCJD, with duration of illness, from first onset of symptoms to death, being much longer than the typical sporadic CJD. have I confused you yet, well, that’s what they want. this all really is not rocket science. I cannot stress enough the risk factors from iatrogenic CJD, from humans consuming CWD positive, sub-clinical cervids, and products there from, that are then exposed, but yet never go clinical in their lifetime and die do to something else, BUT YET, during that lifespan, these same CWD exposed people go on to have many medical, surgical, dental procedures that go on to expose many, many, more people for years, decades to come. you must remember, this is not just science, this is a big game of political science, in which the political part is winning. $$$ USDA INC, CFIA, MAFF/DEFRA, OIE, WTO $$$


snip...



HUMAN FORM OF CWD, what might that look like ? continued part 2




PRION2013 CONGRESSIONAL ABSTRACTS CWD



Sunday, August 25, 2013



HD.13: CWD infection in the spleen of humanized transgenic mice



Liuting Qing and Qingzhong Kong



Case Western Reserve University; Cleveland, OH USA



Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals. ***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.



Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system



Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1



1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK



Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.



Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.



Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.



Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay. ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.





PRION2013 CONGRESSIONAL ABSTRACTS CWD





Sunday, August 25, 2013



***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission



http://chronic-wasting-disease.blogspot.com/2013/08/prion2013-chronic-wasting-disease-cwd.html






Sunday, July 21, 2013



*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?



http://chronic-wasting-disease.blogspot.com/2013/07/as-chronic-wasting-disease-cwd-rises-in.html






Envt.07:



Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease



Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2 Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany †Presenting author; Email: dausm@rki.de



Chronic wasting disease (CWD) is a contagious, rapidly spreading transmissible spongiform encephalopathy (TSE) occurring in cervids in North America. Despite efficient horizontal transmission of CWD among cervids natural transmission of the disease to other species has not yet been observed. Here, we report a direct biochemical demonstration of pathological prion protein PrPTSE and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected cervids. The presence of PrPTSE was detected by Western- and postfixed frozen tissue blotting, while the seeding activity of PrPTSE was revealed by protein misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal muscles of CWD-infected WTD was estimated to be approximately 2000- to 10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE was located in muscle- associated nerve fascicles but not, in detectable amounts, in myocytes.

***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.



http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975






PPo3-7:



Prion Transmission from Cervids to Humans is Strain-dependent



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



Key words: CWD, strain, human transmission



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



Acknowledgement Supported by NINDS NS052319 and NIA AG14359.




PPo2-27:



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



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



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



PPo2-7:



Biochemical and Biophysical Characterization of Different CWD Isolates



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



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



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



http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099






2012



Envt.06:



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



Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2 Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6 and Jean-Philippe Deslys1



1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa, ON Canada



†Presenting author; Email: emmanuel.comoy@cea.fr



The constant increase of chronic wasting disease (CWD) incidence in North America raises a question about their zoonotic potential. A recent publication showed their transmissibility to new-world monkeys, but no transmission to old-world monkeys, which are phylogenetically closer to humans, has so far been reported. Moreover, several studies have failed to transmit CWD to transgenic mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the only animal prion disease for which a zoonotic potential has been proven. We described the transmission of the atypical BSE-L strain of BSE to cynomolgus monkeys, suggesting a weak cattle-to-primate species barrier. We observed the same phenomenon with a cattleadapted strain of TME (Transmissible Mink Encephalopathy). Since cattle experimentally exposed to CWD strains have also developed spongiform encephalopathies, we inoculated brain tissue from CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice overexpressing bovine or human PrP. Since CWD prion strains are highly lymphotropic, suggesting an adaptation of these agents after peripheral exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid brains using the oral route. Nearly four years post-exposure, monkeys exposed to CWD-related prion strains remain asymptomatic. In contrast, bovinized and humanized transgenic mice showed signs of infection, suggesting that CWD-related prion strains may be capable of crossing the cattle-to-primate species barrier. Comparisons with transmission results and incubation periods obtained after exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted TME) will also be presented, in order to evaluate the respective risks of each strain.



Envt.07:



Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease



Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2 Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany †Presenting author; Email: dausm@rki.de



Chronic wasting disease (CWD) is a contagious, rapidly spreading transmissible spongiform encephalopathy (TSE) occurring in cervids in North America. Despite efficient horizontal transmission of CWD among cervids natural transmission of the disease to other species has not yet been observed. Here, we report a direct biochemical demonstration of pathological prion protein PrPTSE and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected cervids. The presence of PrPTSE was detected by Western- and postfixed frozen tissue blotting, while the seeding activity of PrPTSE was revealed by protein misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal muscles of CWD-infected WTD was estimated to be approximately 2000- to 10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE was located in muscle- associated nerve fascicles but not, in detectable amounts, in myocytes. The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.



http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975




Wednesday, December 4, 2013

Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products; Final Rule Federal Register / Vol. 78 , No. 233 / Wednesday, December 4, 2013

TO ALL IMPORTING COUNTRIES THAT IMPORTS FROM THE USA, BE WARNED, NEW MAD COW BSE REGULATIONS USDA, AND OIE, not worth the paper the regulations were wrote on, kind of like the mad cow feed ban of August 1997, nothing but ink on paper $$$

full text ;

http://madcowusda.blogspot.com/2013/12/bovine-spongiform-encephalopathy.html



Sunday, August 11, 2013

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010

http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html


Sunday, October 13, 2013

*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012

http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-tse-prion-disease-cases-in-texas-by.html




[COLOR= ] [SIZE=+0]From:[/SIZE][SIZE=+0]noreply@parliament.uk[/SIZE]
[SIZE=+0]Sent:[/SIZE][SIZE=+0] Tuesday, December 03, 2013 4:49 AM[/SIZE]
[SIZE=+0]To:[/SIZE][SIZE=+0]Terry Singeltary Sr[/SIZE]
[SIZE=+0]Subject:[/SIZE][SIZE=+0] Written submission to House of Commons Science and Technology Committee inquiry[/SIZE]



[/COLOR]
[COLOR= ]
parliament-uk-logo.gif

[SIZE=+0]Thank you for your written submission to the House of Commons Science and Technology Committee inquiry on Blood, tissue and organ screening. [/SIZE]
[SIZE=+0]We will be in touch if we have any further questions. [/SIZE]


[COLOR= ][/COLOR]

[SIZE=+0]From:[/SIZE][SIZE=+0]Terry S. Singeltary Sr.[/SIZE]
[SIZE=+0]Sent:[/SIZE][SIZE=+0] Monday, December 02, 2013 9:18 PM[/SIZE]
[SIZE=+0]To:[/SIZE][SIZE=+0]CJDVOICE CJDVOICE[/SIZE]
[SIZE=+0]Cc:[/SIZE][SIZE=+0]bloodcjd bloodcjd[/SIZE]
[SIZE=+0]Subject:[/SIZE][SIZE=+0] [BLOODCJD] A parliamentary inquiry has been launched today into the safety of blood, tissue and organ screening following fears that vCJD – the human form of ‘mad cow’ disease – may be being spread by medical procedures [/SIZE]



[/COLOR]
[COLOR= ]
[COLOR= ] [SIZE=+0]Monday, December 02, 2013 [/SIZE]

[SIZE=+0]A parliamentary inquiry has been launched today into the safety of blood, tissue and organ screening following fears that vCJD – the human form of ‘mad cow’ disease – may be being spread by medical procedures [/SIZE]

[SIZE=+0]http://creutzfeldt-jakob-disease.blogspot.com/2013/12/a-parliamentary-inquiry-has-been.html[/SIZE]



Wednesday, November 27, 2013

NHS failed to sterilise surgical instruments contaminated with 'mad cow' disease

http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/nhs-failed-to-sterilise-surgical.html



IATROGENIC

all iatrogenic cjd is, is sporadic CJD, until route and source of the iatrogenic event that took place, is detected, documented, placed in the academic domain as fact, and recorded, which happens very seldom due to a lot of factors, besides the incubation period, and that be mainly industry. kind of like asbestos and tobacco and the industry there from, they knew in the early 1900’s that they both were killing, and they both had long incubation, and somebody chose not to do anything about if for decades and decades. kind of like what we have here with the TSE prion disease. $$$

> In 12 of 15 hospitals with neurosurgical incidents, a decision was made to notify patients of their potential exposure.

SO, X number of patients, from 3 hospitals, where

''exposure to potentially CJD-contaminated instruments ''

took place on these patients, the final decision NOT to tell those folks about the potential exposure to the CJD TSE prion

insane, thus, the TSE prion agent continues to spread. ...please see further comments here ;


http://creutzfeldt-jakob-disease.blogspot.com/2013/11/management-of-neurosurgical-instruments.html


Saturday, November 16, 2013

Management of neurosurgical instruments and patients exposed to creutzfeldt-jakob disease 2013 December

Infect Control Hosp Epidemiol.

http://creutzfeldt-jakob-disease.blogspot.com/2013/11/management-of-neurosurgical-instruments.html



Thursday, November 14, 2013

Prion diseases in humans: Oral and dental implications

http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/prion-diseases-in-humans-oral-and.html


Saturday, November 2, 2013

Recommendation of the Swiss Expert Committee for Biosafety on the classification of activities using prion genes and prion protein January 2013

http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/recommendation-of-swiss-expert.html


[SIZE=+0]Friday, November 29, 2013

Identification of Misfolded Proteins in Body Fluids for the Diagnosis of Prion Diseases

International Journal of Cell Biology

[/SIZE][SIZE=+0]http://transmissiblespongiformencephalopathy.blogspot.com/2013/11/identification-of-misfolded-proteins-in.html[/SIZE]




U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001


http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html


http://madcowusda.blogspot.com/2012/02/eight-former-secretaries-of-agriculture.html



Alzheimer’s, Parkinson, ALS, Prion ???


Romans 12:19 ESV

Beloved, never avenge yourselves, but leave it to the wrath of God, for it is written, “Vengeance is mine, I will repay, says the Lord.”

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Tuesday, November 26, 2013

Transmission of multiple system atrophy prions to transgenic mice

http://proteinopathies.blogspot.com/2013/11/transmission-of-multiple-system-atrophy.html




kind regards,
terry
 
Sir,

Can you shed ANY light on how Mr. Belknap got the disease? And please list other recent cases of Crutzfeldt-Jacobs in Iowa.
 
Sir,

Can you shed ANY light on how Mr. Belknap got the disease? And please list other recent cases of Crutzfeldt-Jacobs in Iowa.


sporadic cjd simply means 'UNKOWN', it does not mean spontaneous, as many officials and some scientist claim, without proof. there is NO scientific evidence that proves 85%+ of all human TSE prion disease i.e. sporadic CJD, happens _spontaneously_, without cause, just a happenstance of bad luck. if that was the case, then cwd would be everywhere. sporadic cjd consists of 85%+ of all human TSE prion disease. you will here 1 in a million floated around a lot with sporadic CJD, but in reality, in the age group of 55 years and greater, that figure drastically changes to 1 in 9,000 (CJD Foundation figures).


also, there is science now that shows ;



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...

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1

http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf


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 ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html


Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

Second threat

snip...

http://www.neuroprion.org/en/np-neuroprion.html

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/variably-protease-sensitive-prionopathy.html

http://prionopathy.blogspot.com/2010/11/variably-protease-sensitive-prionopathy.html



>>> And please list other recent cases of Crutzfeldt-Jacobs in Iowa


IMPOSSIBLE SIR!

they have no clue of how many cases of CJD/TSE in humans, apparently, CJD/TSE/PRION disease in humans is not reportable in the state of IOWA or Nationally here in the USA, however many states HAS made CJD reportable on their own, sadly, it appears IOWA is not one of them ;



Iowa Department of Public Health Table of Reportable Communicable and Infectious Diseases

To report diseases immediately, use the 24/7 disease reporting telephone hotline: 1-800-362-2736


http://www.idph.state.ia.us/hcci/common/pdf/naeyc/ia_reportable_diseases.pdf


http://www.idph.state.ia.us/cade/ReportableDiseases.aspx


Notice to Readers: Final 2012 Reports of Nationally Notifiable Infectious Diseases


http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6233a6.htm


http://www.cdc.gov/mmwr/pdf/wk/mm5953.pdf


now, government officials will claim they don't need to report CJD, because they scan death certificates.

this has already been proven not to work.

that's what I been screaming for almost 16 years, daily. due to the friendly fire, pass if forward mode of transmission i.e. iatrogenic, all human TSE prion disease should be made to mandatory reportable in EVERY STATE, and INTERNATIONALLY, with a CJD questionnaire, asking realy questions pertaining to route and source of the TSE prion agent, not just a questionnaire asking whom diagnosed, and how, and where the victim is from. ...



Published March 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States

Terry S. Singeltary, retired (medically)

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

Published March 26, 2003

http://www.neurology.org/content/60/2/176/reply#neurology_el_535


Letters

JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Terry S. Singeltary, Sr Bacliff, Tex

Since this article does not have an abstract, we have provided the first 150 words of the full text.

KEYWORDS: creutzfeldt-jakob disease, diagnosis. To the Editor:

In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.

http://jama.ama-assn.org/content/285/6/733.extract



CJD SURVEILLANCE IOWA, only scanning death certificates, and NOT REPORTABLE ???



routine passive mortality CJD surveillance USA ?


THIS has been proven not to be very useful in the U.K.;


THE EPIDEMIOLOGY OF CJD RG WILL 1984 (182 PAGES)

snip...

One reason for this was the _inaccuracy_ in coding of cases correctly certified as CJD Coding is carried out by staff who are not medically qualified and it is not surprising that coding errors occur in the processing of large numbers of certificates. In 1982, 12,000 certificates per week were processed at the office of population censuses and surveys by 15 coders and 6 checkers (Alderson et al., 1983). The occurrence of both inter- and intra-observer coding errors has been described (Curb et al., 1983) and the _inaccuracies_ of BOTH certification and coding discovered in this study _support_ the introduction of a more accurate system of death certificates and a more detailed and specific coding system...

snip...


http://web.archive.org/web/20040521215716/http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf




Draft Proposal For The Monitoring of Creutzfeldt-Kakob Disease 1989 Dr. R. Will

snip...

IDENTIFICATION OF CASES

Cases of CJD may be identified from death certificates, but this alone is unlikely to provide adequate monitoring. ERRORS are made in certification and diagnosis; in the Oxford study death certificates were obtained on a series of known confirmed cases and CJD was mentioned in only 66% of certificates. In another series of 175 certified cases, 42 patients were judged not to have suffered from CJD after examination of case notes (7)...

full text;


http://web.archive.org/web/20050526035006/http://www.bseinquiry.gov.uk/files/yb/1989/05/00005001.pdf


see my full text submission here ;



http://www.plosone.org/article/fetchArticleComments.action?annotationId=363&articleURI=info%3Adoi%2F10.1371%2Fjournal.pone.0008521



http://www.plosone.org/annotation/listThread.action;jsessionid=3A07F5D8F6488DF25386CCFDD619ACE9?root=363



CJD QUESTIONNAIRE USA


http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html


http://cjdquestionnaire.blogspot.com/



Alzheimer's, _fast_ Alzhiemer's disease in the young ???


misdiagnosis there from, or ???




AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.

snip...



AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.

snip...


http://web.archive.org/web/20060307063542/http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf




Tuesday, November 26, 2013

Transmission of multiple system atrophy prions to transgenic mice

http://proteinopathies.blogspot.com/2013/11/transmission-of-multiple-system-atrophy.html



kind regards,
terry



 
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