Monday, June 9, 2014

TEXAS MAD COW COVER UP (human BSE) AGAIN IN TEXAS, Mr. President Sir, we need your help please

Governor Rick Perry has done everything he can to cover up mad cow disease and human TSE prion disease there from in Texas over the last 15 years or so. We have another nvCJD case here in Texas i.e. human BSE, still no information there from, another lame excuse, typical though, and more junk science, we need help Mr. President...

 

 
Sent: Monday, June 09, 2014 12:25 PM
Subject: MAD COW COVER UP AGAIN IN TEXAS Mr. President Sir, I need your help please
 

Mr. President Sir, I need your help please. USDA inc is covering up more mad cow disease and human TSE there from in Texas. this cover up of this recent case is raising much suspicion. why the secret of this man's age, and other information of travel and how long in the USA, diet, medical, while here in the USA. I lost my mother to hvCJD 'confirmed', and in the past 16 years have proven beyond a shadow of any doubt that the USDA inc is covering up mad cow disease. why can't you help me Sir? please read my evidence. I do NOT advertise, this is for education use only. please help us...

 
nvcjd human bse aka mad cow disease TEXAS, WHAT'S THE BIG SECRET ???
 
You all do know this is making you all look very, very suspicious, not that it matters much anymore. but really?
 
for your files cjdsupport, please take it with how ever many grains of salt you wish. ...kindest regards, terry
 
 
Monday, June 02, 2014
 
Confirmed Human BSE aka mad cow Variant CJD vCJD or nvCJD Case in Texas
 
 
what’s the big secret about the age and history of this poor gentleman ???
 
MAD COW COVER UP USA, THE EVIDENCE MOUNTS $$$ 
 
Monday, June 02, 2014
 
Confirmed Human BSE aka mad cow Variant CJD vCJD or nvCJD Case in Texas
 
 
 
just saying...kind regards, terry
 

Thank You!

Thank you for contacting the White House.
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Thank you again for your message.
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================================
 
Sent: Wednesday, June 04, 2014 3:50 PM
Subject: RE: nvCJD case confirmed Texas question please
 
Thank you for your interest. 
 
As this is an ongoing investigation, the information stated on our website is all that we can provide at this time.
Please see:  http://www.dshs.state.tx.us/default.shtm
 
Sincerely,
 
Michael P. Fischer, MD, MPH & TM
Emerging and Acute Infectious Disease Branch
Infectious Disease Control Unit
Telephone: 512-776-6338 ~ Fax: 512-776-7616
E-mail: michael.fischer@dshs.state.tx.us
 
Mailing Address:
MC 1960
P.O. Box 149347
Austin, Texas 78714-9347
 
From: Cantu,Rita M (DSHS) On Behalf Of DSHS IDCU, Feedback
Sent: Wednesday, June 04, 2014 3:26 PM
To: Fischer,Michael (DSHS)
Subject: FW: nvCJD case confirmed Texas question please
 
Please forward to correct person or respond with a cc to DSHS IDCU, Feedback, thanks!
 
Rita Cantu
Infectious Disease Control Unit
Texas Department of State Health Services  
P.O. Box 149347 Austin, Texas 78714-9347
Phone (512) 776-6281  
rita.cantu@dshs.state.tx.us
 
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Wednesday, June 04, 2014 11:59 AM
To: DSHS IDCU, Feedback
Subject: nvCJD case confirmed Texas question please
 
Greetings Texas IDCU et al,
 
I have followed closely the cjd bse saga since December 14, 1997, when I lost my mom to the hvCJD.
 
can you please at least tell us the age of this vCJD or nvCJD victim ???
 
kind regards, terry
 
=============================================
 
Sent: Thursday, June 05, 2014 1:49 PM
Subject: RE: re-human bse nvcjd TEXAS USA
 
Dear Mr Singeltary,
You will have to make this inquiry to the Texas Department of Health.  The contact person there is:
 
Michael Fischer, MD
Emerging and Acute Infectious Disease Branch
Infectious Disease Control Unit
Telephone: 512-776-6338 
E-mail: michael.fischer@dshs.state.tx.us
 
From: Terry S. Singeltary Sr.
Sent: Tuesday, June 03, 2014 9:40:19 PM (UTC-05:00) Eastern Time (US & Canada)
To: PRION (CDC)
Subject: re-human bse nvcjd TEXAS USA
NO AGE ??? any help here ??? kind regards, terry
 
Monday, June 02, 2014
 
Confirmed Variant CJD Case in Texas
 
http://vcjd.blogspot.com/2014/06/confirmed-variant-cjd-case-in-texas.html
 
 
===========================================================
 
Sent: Wednesday, June 04, 2014 11:52 AM
Subject: RE: nvCJD Texas ???
 
Adult male from Texas with extensive travel history. That’s the extent of the information I can provide at this time.
 
......................................................
Carrie Williams
Director of Media Relations
512-776-7119
 
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]
Sent: Wednesday, June 04, 2014 11:51 AM
To: Williams,Carrie C (DSHS)
Subject: Re: nvCJD Texas ???
 
Thank you for your kind reply. can you please tell me anything else? age? sex? length of stay here in USA, diet, surgeries, blood, etc., anything???
 
kind regards, terry
 
Sent: Tuesday, June 03, 2014 9:08 AM
Subject: Re: nvCJD Texas ???
 
Yes, we have some info and links on our home page - www.dshs.state.tx.us

Sent from my iPhone

On Jun 2, 2014, at 8:12 PM, "Terry S. Singeltary Sr." <flounder9@verizon.net> wrote:
Greetings Carrie,
 
I am wondering if there is any validity to this news report, and if so, is there a statement from DSHS or anyone else in Texas ?
 
Published On: Mon, Jun 2nd, 2014
 
Outbreak News / US News | By Robert Herriman
 
Texas: Variant Creutzfeldt-Jakob Disease death confirmed, infection likely occurred overseas
 
 
 
kind regards,
terry
 
================================================
 

Rick Perry, Texas, and Mad Cow Disease--12 Years of Lies
For related articles and more information, please visit OCA's Mad Cow Disease page.
 
I am sure that most of you are aware of the Texas mad cow cases that were covered up. the 1st documented cover-up was successful, the second documented case of mad cow in Texas would have been successful, but after literally, an act of Congress to override Austin, Texas officials (rick perry), only after the Honorable Fong of the OIG, and scientist all over the world, and a few others, including myself wrote to the OIG about said cover-up, and 7 months later, did they finally retest that covered-up highly suspect mad cow, and said covered up mad cow was finally _confirmed_ by Weybridge as a confirmed Texas BSE mad cow case. this 7 months after the fact on a Government BSE REDBOOK regulations of a 48 turn around on said test. over course this was all done for a reason, the BSE MRR policy was being put into place while all this was going on, and Heaven forbid if rick perry would have had a confirmed BSE mad cow case while those regulations were over riding the BSE GBR risk assessments. however, during all this political science on mad cow disease, it was nothing more than a crap shoot, and 15 years later, we now know that some of the sporadic CJD cases are indeed tied to the atypical BSE cases here in North America. How many people during the Bush/Perry era, how many did they needlessly expose to mad cow disease? how many will go clinical and die in the decades to come? Whether or not you dare care, during the Bush/Perry era, they exposed our kids to mad cow disease, by feeding them dead stock downer cows via the NSLP, for over 4 years. DEAD STOCK DOWNER COWS ARE THE MOST HIGH RISK COW FOR MAD COW DISEASE. WHO will watch the children for the next 5 decades for CJD ???
 
http://www.organicconsumers.org/articles/article_23850.cfm
 
 
Sunday, August 28, 2011
 
Rick Perry, Texas, BSE aka mad cow disease, CJD, and 12 years of lies there from
 
 
From: Terry S. Singeltary Sr.
 
Sent: Monday, June 09, 2014 9:56 AM
 
 
Subject: nvcjd human bse aka mad cow disease TEXAS, WHAT'S THE BIG SECRET ???
 
nvcjd human bse aka mad cow disease TEXAS, WHAT'S THE BIG SECRET ???
 
You all do know this is making you all look very, very suspicious, not that it matters much anymore. but really?
 
for your files cjdsupport, please take it with how ever many grains of salt you wish. ...kindest regards, terry
 
Monday, June 02, 2014
 
Confirmed Human BSE aka mad cow Variant CJD vCJD or nvCJD Case in Texas
 
 
what’s the big secret about the age and history of this poor gentleman ???
 
MAD COW COVER UP USA, THE EVIDENCE MOUNTS $$$
 
TEXAS MAD COW
 
THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE THE BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i confirmed this case 7 months earlier to the TAHC, and then, only after i contacted the Honorable Phyllis Fong and after an act of Congress, this animal was finally confirmed ;
 
During the course of the investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE. 200 adult animals of interest were determined to have left the index farm. Of these 200, APHIS officials determined that 143 had gone to slaughter, two were found alive (one was determined not to be of interest because of its age and the other tested negative), 34 are presumed dead, one is known dead and 20 have been classified as untraceable. In addition to the adult animals, APHIS was looking for two calves born to the index animal. Due to record keeping and identification issues, APHIS had to trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter channels, four are presumed to have entered feeding and slaughter channels and one calf was untraceable.
 
 
USDA regulations, any cow that exhibits signs of central nervous system (CNS)
 
According to a 1997 Animal and Plant Health Inspection Service (NHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "it is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."
 
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
 
May 13,2004
 
Page 2
 
snip...
 
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
 
This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:
 
 
2004, highly suspect stumbling and staggering mad cow reported, however, NO TESTING DONE, ON ORDERS FROM AUSTIN $
 
May 4, 2004
 
Statement on Texas Cow With Central Nervous System Symptoms
 
On Friday, April 30th, the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
 
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
 
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
 
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison)...
 
 
FDA MAD COW FEED BAN NOTHING BUT INK ON PAPER
 
Note:
 
On Dec. 23, 2003, the U.S. Department of Agriculture reported that a cow in Washington state had tested positive for bovine spongiform encephalopathy (BSE, or mad cow disease). As a result, information on this Web page stating that no BSE cases had been found in the United States is now incorrect. However, because other information on this page continues to have value, the page will remain available for viewing.
 
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
 
Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle. FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds. It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated. According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE." Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual. FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities. This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely. FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.
 
 
NEWS RELEASE Texas Animal Health Commission Box l2966 •Austin, Texas 78711 •(800) 550-8242• FAX (512) 719-0719 Linda Logan, DVM, PhD• Executive Director For info, contact Carla Everett, information officer, at 1-800-550-8242, ext. 710, or ceverett@tahc.state.tx.us
 
For Immediate Release-- Feed Contamination Issue Resolved by FDA
 
Although many of you may have heard the latest regarding the resolution of the cattle feed contamination situation in Texas, I wanted to ensure that you received this statement issued by the Food and Drug Administration (FDA), the agency in charge of regulating feed components. The FDA has said the cattle involved are to be rendered and the material will not enter ruminant or human food channels. The Texas Animal Health Commission (TAHC) will provided assistance to the FDA as requested and needed. FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT Today (Tuesday, Jan. the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle. FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds. It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated. According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE." Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual. FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities. This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely. FDA will continue working with USDA as well as state and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply. ---30--
 
 
resolved ??? HA, HA, HA, were still feeding cows to cows in 2013, see OAI’s in link below, December 13, 2013...tss
 
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.
 
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
 
Risk of oral infection with bovine spongiform encephalopathy agent in primates
 
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
 
snip...
 
BSE bovine brain inoculum
 
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
 
Primate (oral route)* 1/2 (50%)
 
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
 
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
 
PrPres biochemical detection
 
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
 
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
 
Published online January 27, 2005
 
 
It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.
 
 
it is clear that the designing scientists must have also shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.
 
 
P04.27
 
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
 
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
 
Background:
 
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
 
Aims:
 
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
 
Methods:
 
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
 
Results:
 
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
 
Conclusions:
 
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.
 
The work referenced was performed in partial fulfillment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
 
 
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
 
 
P.9.21 Molecular characterization of BSE in Canada
 
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
 
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
 
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.
 
Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
 
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
 
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *** It also suggests a similar cause or source for atypical BSE in these countries.
 
 
Saturday, August 14, 2010
 
***BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY ***
 
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
 
 
*** What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”
 
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”
 
 
 
*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS
 
THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$
 
 
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
 
Date: March 21, 2007 at 2:27 pm PST
 
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
 
___________________________________
 
PRODUCT
 
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
 
CODE
 
Cattle feed delivered between 01/12/2007 and 01/26/2007
 
RECALLING FIRM/MANUFACTURER
 
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
 
Firm initiated recall is ongoing.
 
REASON
 
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
 
VOLUME OF PRODUCT IN COMMERCE
 
42,090 lbs.
 
DISTRIBUTION
 
WI
 
___________________________________
 
PRODUCT
 
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
 
CODE
 
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
 
RECALLING FIRM/MANUFACTURER
 
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
 
REASON
 
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
 
VOLUME OF PRODUCT IN COMMERCE
 
9,997,976 lbs.
 
DISTRIBUTION
 
ID and NV
 
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
 
 
 
Saturday, August 14, 2010
 
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
 
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)
 
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
 
Date: September 6, 2006 at 7:58 am PST PRODUCT
 
a) EVSRC Custom dairy feed, Recall # V-130-6;
 
b) Performance Chick Starter, Recall # V-131-6;
 
c) Performance Quail Grower, Recall # V-132-6;
 
d) Performance Pheasant Finisher, Recall # V-133-6.
 
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
 
REASON
 
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
 
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
 
DISTRIBUTION AL
______________________________
 
 
PRODUCT Bulk custom dairy pre-mixes,
 
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
 
VOLUME OF PRODUCT IN COMMERCE 350 tons
 
DISTRIBUTION AL and MS
 
______________________________
 
PRODUCT
 
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
 
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
 
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
 
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
 
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
 
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
 
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
 
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
 
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
 
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
 
DISTRIBUTION AL, GA, MS, and TN
 
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
 
###
 
 
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
 
Date: August 6, 2006 at 6:16 pm PST PRODUCT
 
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
 
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
 
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
 
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
 
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
 
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
 
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
 
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
 
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
 
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
 
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
 
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
 
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
 
Product manufactured from 02/01/2005 until 06/06/2006
 
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
 
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
 
VOLUME OF PRODUCT IN COMMERCE 125 tons
 
DISTRIBUTION AL and FL
 
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
 
###
 
 
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
 
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
 
______________________________
 
PRODUCT
 
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
 
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
 
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
 
d) Feather Meal, Recall # V-082-6 CODE
 
a) Bulk
 
b) None
 
c) Bulk
 
d) Bulk
 
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
 
REASON
 
Possible contamination of animal feeds with ruminent derived meat and bone meal.
 
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
 
DISTRIBUTION Nationwide
 
END OF ENFORCEMENT REPORT FOR July 12, 2006
 
###
 
 
please see full text ;
 
 
THIS IS WHEN THE MAD COW FEED BAN WARNING LETTERS WERE WEEKLY, AND INFORMATIVE FOR THE PUBLIC ;
 
DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND DRUG ADMINISTRATION
 
April 9, 2001 WARNING LETTER
 
01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED
 
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145 PHILADELPHIA DISTRICT
 
Tel: 215-597-4390
 
Dear Mr. Raymond:
 
Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23, 2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).
 
Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.
 
In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal. Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.
 
The above is not intended to be an all-inclusive list of deviations from the regulations. As a manufacturer of materials intended for animal feed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. We have enclosed a copy of FDA's Small Entity Compliance Guide to assist you with complying with the regulation... blah, blah, blah...
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
LAST MAD COW IN USA, IN CALIFORNIA, WAS ATYPICAL L-TYPE BASE BSE TSE PRION DISEASE
 
Thursday, February 20, 2014
 
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model
 
 
***Infectivity in skeletal muscle of BASE-infected cattle
 
 
***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries. ***
 
 
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.
 
 
full text ;
 
atypical L-type BASE BSE
 
 
However, a BSE expert said that consumption of infected material is the only known way that cattle get the disease under natural conditons.
 
*** “In view of what we know about BSE after almost 20 years experience, contaminated feed has been the source of the epidemic,” said Paul Brown, a scientist retired from the National Institute of Neurological Diseases and Stroke. BSE is not caused by a microbe. It is caused by the misfolding of the so-called “prion protein” that is a normal constituent of brain and other tissues. If a diseased version of the protein enters the brain somehow, it can slowly cause all the normal versions to become misfolded. It is possible the disease could arise spontaneously, though such an event has never been recorded, Brown said.
 
 
*** What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.” The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”
 
 
ATYPICAL BSE CASES AND FEED THERE FROM ;
 
***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries. ***
 
 
2012 ATYPICAL L-TYPE BSE BASE CALIFORNIA ‘confirmed’ Saturday, August 4, 2012
 
*** Final Feed Investigation Summary - California BSE Case - July 2012 (atypical L-type BASE BSE)
 
 
Saturday, August 14, 2010
 
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
 
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
 
 
Wednesday, October 30, 2013
 
SPECIFIED RISK MATERIAL (SRM) CONTROL VERIFICATION TASK FSIS NOTICE 70-13 10/30/13
 
 
 
*** Singeltary Submission
 
Owens, Julie
 
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
 
Sent: Monday, July 24, 2006 1:09 PM
 
To: FSIS RegulationsComments
 
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98
 
 
*** FSIS, USDA, REPLY TO SINGELTARY ***
 
 
*** Sunday, December 15, 2013 ***
 
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE ***
 
 
Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013
 
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***
 
 
Sunday, October 13, 2013
 
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
 
 
Tuesday, April 01, 2014
 
*** Questions linger in U.S. CJD cases 2005, and still do in 2014
 
 
Monday, March 29, 2010
 
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
 
URGENT, PLEASE NOTE ;
 
>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
 
 
 
CJD NE TEXAS CLUSTER
 
Creutzfeldt-Jakob Disease in Northeast Texas
 
J.A. Rawlings,*1 K.A. Hendricks1, O.M. Nuno1, D.A. Brown1, D.A. Evans2, Texas Department of Health, 1Austin and 2Tyler, Texas Creutzfeldt-Jacob Disease (CJD), a transmissible spongiform encephalopathy, is caused by prions composed of proteinaceous material devoid of nucleic acid. CJD occurs sporadically (generally 1 case/1,000,000 population per year) in older patients (average age of 65) and is characterized by rapidly progressive dementia, accompanied by severe muscle spasms and incoordination. Death usually occurs within 3 to 12 months (average 7 months). CJD activity in Texas, which has a population of nearly 19 million, appeared to be typical. The statewide death rate for 1995 and 1996 was just under 1/1,000,000. In April of 1997, the Texas Department of Health became aware of an increased number of possible CJD cases in a 23-county area of NE Texas with a population of just over one million. After review of medical and pathology records, four patients were identified with definite classic CJD and three were identified with probable CJD. Dates of death for the eight patients were from April, 1996 through mid-July 1997. The patients were from 46 through 65 years of age; four were male and three were female. A case-control study to identify risks for CJD in NE Texas has been initiated. http://www.jifsan.umd.edu/tse/Rawlings.htm
 
we get them young cases of tse prion disease in Texas, that is not related to anything $$$ money and politics will buy anything, especially junk science... sporadic ffi and sporadic gss ;
 
NOT THIS CASE !!! but another one a while back in Texas...see ;
 
We report a case of a 33-year-old female who died of a prion disease for whom the diagnosis of sFI or FFI was not considered clinically. Following death of this patient, an interview with a close family member indicated the patient's illness included a major change in her sleep pattern, corroborating the reported autopsy diagnosis of sFI.
 
 
sporadic FFI or nvCJD Texas style ???
 
 
Creutzfeldt-Jakob Disease Surveillance in Texas
 
 
Sunday, July 11, 2010
 
CJD or prion disease 2 CASES McLennan County Texas population 230,213 both cases in their 40s
 
 
 
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
 
 
Thursday, August 12, 2010
 
Seven main threats for the future linked to prions
 
***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...
 
 
Monday, October 10, 2011
 
EFSA Journal 2011 The European Response to BSE: A Success Story
 
snip...
 
*** 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...
 
 
 
***In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
 
 
Monday, May 19, 2014
 
Variant CJD: 18 years of research and surveillance
 
 
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis
 
 
 
 
full text with source references ;
 
 
re-Human Prion Diseases in the United States
 
Posted by flounder on 01 Jan 2010 at 18:11 GMT
 
 
Views & Reviews
 
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
 
Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and Lawrence B. Schonberger, MD
 
+ Author Affiliations
 
From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.
 
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.
 
 
26 March 2003
 
Terry S. Singeltary, retired (medically) CJD WATCH
 
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?
 
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
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.
 
Terry S. Singeltary, Sr Bacliff, Tex
 
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
 
 
 
2 January 2000
 
British Medical Journal
 
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
 
 
15 November 1999
 
British Medical Journal
 
vCJD in the USA * BSE in U.S.
 
 
Saturday, January 2, 2010
 
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
 
 
14th ICID International Scientific Exchange Brochure -
 
Final Abstract Number: ISE.114
 
Session: International Scientific Exchange
 
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
 
T. Singeltary
 
Bacliff, TX, USA
 
Background:
 
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
 
Methods:
 
12 years independent research of available data
 
Results:
 
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
 
Conclusion:
 
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
2001-2002ish
 
greetings TSE PRION WORLD,
 
i am reminded of a few things deep throat told me years ago;
 
*** 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 at least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the wood work 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 agreat 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.)
 
================================================
 
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 SINGELTARY HACKS IN (DEEP THROAT ABOVE HELPED ME GET IN)
 
 
 
NOW, remember, the federal government lied to us for 100 years about other long incubating disease i.e. tobacco and asbestos, just to protect the industry. ...
 
just saying...
 
kind regards, terry
 
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
 
Monday, June 02, 2014
 
Confirmed Human BSE aka mad cow Variant CJD vCJD or nvCJD Case in Texas
 
 fact is, BSE cases in Europe of the past years have dropped dramatically due to feed ban that was enforced, and extensive BSE testing, in large numbers. just the opposite has happened in the USA. it’s all been documented. there is ample evidence that there is as much of a chance (if not more), that this victim contracted human mad cow disease from sources right here in the USA. this PR push to alienate a USA source factor for human BSE in the USA is a PR stunt by the USDA inc., and not justified now, in my opinion. compare BSE testing figures in the EU compared to the USA, compare mad cow feed ban breaches, and you will see. hell, the 2004 enhanced BSE surveillance program was flawed so bad, the top Prion God at the NIH TSE prion expert Paul Brown, says he does not trust anything from the USDA since Texas covered up a mad cow for 7 months, on a 48 hour confirmation turn around. it’s all documented below in link. USDA inc shut down the mad cow testing after so many atypical BSE cases started showing up.
 
 yes, another foreigner comes to the USA, or another USA citizens does some traveling, and all of a sudden, it’s a foreign disease. evidently, these folks never eat anything in the USA, and contracts nvcjd. right. just like the last one in 2005. really? here are the facts of the TEXAS MAD COW, MAD COW FEED in Texas, CJD CLUSTER in Texas, CJD CASE IN 38 YEAR OLD WOMAN THAT APPARENTLY WORKED ON THE SLAUGHTER LINE FOR TYSON in Texas, AND OTHER STRANGE TSE PRION DISEASE IN VERY YOUNG VICTIMS HERE IN TEXAS with long duration of illness from onset of clinical symptoms to death, CALLED SPORADIC FFI (except it is not linked to any genetic make up of that family), another nvcjd victim back in 2005 in Texas, apparently another UK victim that had moved to Texas, and never ate anything. these are the facts as I have come to know them (official documents), since hvcjd took my mom in December of 1997. just made a promise to mom, never forget, and never let them forget, the rest of the story, the truth you don’t hear about. ...our fine federal friends and the USDA inc, has lied to all of us...
 
 
 
Monday, June 02, 2014
 
Confirmed Human BSE aka mad cow Variant CJD vCJD or nvCJD Case in Texas
 
 
 
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Thursday, May 15, 2014

Distribution of Peripheral PrPSc in Sheep with Naturally Acquired Scrapie

Research Article

 

Distribution of Peripheral PrPSc in Sheep with Naturally Acquired Scrapie

 

María Carmen Garza, Marta Monzón, Belén Marín, Juan José Badiola, Eva Monleón mail

 

Published: May 14, 2014 •DOI: 10.1371/journal.pone.0097768

 

Abstract

 

Accumulation of prion protein (PrPSc) in the central nervous system is the hallmark of transmissible spongiform encephalopathies. However, in some of these diseases such as scrapie or chronic wasting disease, the PrPSc can also accumulate in other tissues, particularly in the lymphoreticular system. In recent years, PrPSc in organs other than nervous and lymphoid have been described, suggesting that distribution of this protein in affected individuals may be much larger than previously thought. In the present study, 11 non-nervous/non-lymphoid organs from 16 naturally scrapie infected sheep in advanced stages of the disease were examined for the presence of PrPSc. Fourteen infected sheep were of the ARQ/ARQ PRNP genotype and 2 of the VRQ/VRQ, where the letters A, R, Q, and V represent the codes for amino-acids alanine, arginine, glutamine and valine, respectively. Adrenal gland, pancreas, heart, skin, urinary bladder and mammary gland were positive for PrPSc by immunohistochemistry and IDEXX HerdChek scrapie/BSE Antigen EIA Test in at least one animal. Lung, liver, kidney and skeletal muscle exhibited PrPSc deposits by immunohistochemistry only. To our knowledge, this is the first report regarding the presence of PrPSc in the heart, pancreas and urinary bladder in naturally acquired scrapie infections. In some other organs examined, in which PrPSc had been previously detected, PrPSc immunolabeling was observed to be associated with new structures within those organs. The results of the present study illustrate a wide dissemination of PrPSc in both ARQ/ARQ and VRQ/VRQ infected sheep, even when the involvement of the lymphoreticular system is scarce or absent, thus highlighting the role of the peripheral nervous system in the spread of PrPSc.

 

Citation: Garza MC, Monzón M, Marín B, Badiola JJ, Monleón E (2014) Distribution of Peripheral PrPSc in Sheep with Naturally Acquired Scrapie. PLoS ONE 9(5): e97768. doi:10.1371/journal.pone.0097768

 

Editor: Anthony E. Kincaid, Creighton University, United States of America

 

Received: January 30, 2014; Accepted: April 22, 2014; Published: May 14, 2014

 

Copyright: © 2014 Garza et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Funding: This study was supported by the Gobierno de Aragón (grant 218-315/3) and FEDER (CONCOTSA EFA205/11). Dr. Garza was supported by a FPU doctoral grant from the Spanish Ministry of Education (grant AP2007-03842). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 

snip...

 

Overall, the results from the present study showed large variation in peripheral spread of PrPSc among sheep. Although all of the infected animals included in the study presented a widespread PrPSc accumulation in the CNS, they did not show a similar PrPSc dissemination through the PNS. The heterogeneous distribution of PrPSc-containing nerve fibres within the peripheral organs in conjunction with the small amounts observed could explain the variation between animals. This variation has also been observed in the skeletal muscle [6], kidney [7], liver [10] and skin [9] of sheep infected with scrapie. It should be highlighted that only 2 pieces of tissue were collected from fairly big organs, one for IHC and one for EIA test. Sampling multiple sites within organs and using more sensitive techniques would most likely result in a higher number of peripheral positive organs in each animal, but the study is not intended to be representative in nature. In addition, the results from the IHC and IDEXX EIA analyses showed a poor correlation between both techniques, with a higher number of positive samples observed via IHC in comparison with the IDEXX EIA. This IDEXX EIA is a commercial immunoassay for PrPSc detection in nervous or lymphoid tissues. In the present study, all samples were analysed and interpreted according to the manufacturer’s cut-off criterion. In some previous studies that have used commercial ELISA tests for PrPSc detection in non-nervous or non-lymphoid tissues, the cut-off value has been recalculated as a function of the type of tissue analysed (as 3 standard deviations above the mean of the negative controls [10], [41]). The cut off values determined in these cases were lower than those set by the manufacturers (i.e., 0.059 for liver samples [10]). Equally, we calculated the cut off for liver, pancreas and urinary bladder from 10 negative sheep (as 4 standard deviations above the mean) and obtained values of 0.069, 0.040 and 0.063, respectively. If these cut off values were used, all of the samples that were positive by IHC only, would be confirmed by IDEXX EIA; however, we would also have 1 positive sample only by IDEXX EIA in the case of liver tissue, 7 in the pancreas and 2 in the urinary bladder. Therefore, although it is possible that by applying the manufacturer’s cut-off criterion we would obtain a lower IDEXX EIA sensitivity, a more in-depth study is needed to adapt the cut off value for each individual tissue.

 

Together with previous reports, the present study indicates that scrapie infection may spread through the PNS to most, if not all, parts of the body. The PrPSc presence in non-nervous organs does not appear to have any additional pathological role but demonstrates that some of these organs are potentially infectious (which has not been considered thus far [21]) and generates new insights into horizontal transmission. In addition, our observations regarding naturally acquired scrapie may provide indirect information about the spread of the agent in related TSEs such as vCJD and CWD.

 

Supporting Information

 

snip...see full text ;

 


 

 

ONCE again, many many thanks to PLOS et al AND especially the authors, scientist et al that participate in open access, thank you kindly for OPEN ACCESS for dummies like me. ...tss

 

 

why do we not want to do TSE transmission studies on chimpanzees $

 

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

 

snip...

 

R. BRADLEY

 


 

1: J Infect Dis 1980 Aug;142(2):205-8

 

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

 

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

 

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

 

snip...

 

The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

 

PMID: 6997404

 


 

Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"

 

Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.

 

snip...

 

76/10.12/4.6

 


 

Nature. 1972 Mar 10;236(5341):73-4.

 

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

 

Gibbs CJ Jr, Gajdusek DC.

 

Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

 

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

 

C. J. GIBBS jun. & D. C. GAJDUSEK

 

National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

 

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

 


 


 

Wednesday, February 16, 2011

 

IN CONFIDENCE

 

SCRAPIE TRANSMISSION TO CHIMPANZEES

 

IN CONFIDENCE

 


 

Sunday, December 12, 2010

 

EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010

 


 

Sunday, April 18, 2010

 

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

 


 

Thursday, December 23, 2010

 

Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009

 

Volume 17, Number 1 January 2011

 


 

Thursday, November 18, 2010

 

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

 


 

Monday, April 25, 2011

 

Experimental Oral Transmission of Atypical Scrapie to Sheep

 

Volume 17, Number 5-May 2011

 


 

Friday, February 11, 2011

 

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

 


 

Thursday, March 29, 2012

 

atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

 

NIAA Annual Conference April 11-14, 2011San Antonio, Texas

 


 

Increased Atypical Scrapie Detections

 

Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.

 


 

Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits, see also ; All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.

 


 

Tuesday, July 29, 2008

 

Heidenhain Variant Creutzfeldt Jakob Disease Case Report

 

snip...

 

Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'

 

DIVISION OF NEUROPATHOLOGY

 

University of Texas Medical Branch 114 McCullough Bldg. Galveston, Texas 77555-0785

 

FAX COVER SHEET DATE: 4-23-98

 

TO: Mr. Terry Singeltary @ -------

 

FROM: Gerald Campbell FAX: (409) 772-5315 PHONE: (409) 772-2881 Number of Pages (including cover sheet):

 

Message: *CONFIDENTIALITY NOTICE*

 

This document accompanying this transmission contains confidential information belonging to the sender that is legally privileged. This information is intended only for the use of the individual or entry names above. If you are not the intended recipient, you are hereby notified that any disclosure, copying distribution, or the taking of any action in reliances on the contents of this telefaxed information is strictly prohibited. If you received this telefax in error, please notify us by telephone immediately to arrange for return of the original documents.

 

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

 

Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Admitting Race: C Attending Dr.: Date / Time Admitted : 12/14/97 1228 Copies to: UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858 Autopsy NO.: AU-97-00435 AUTOPSY INFORMATION: Occupation: Unknown Birthplace: Unknown Residence: Crystal Beach Date/Time of Death: 12/14/97 13:30 Date/Time of Autopsy: 12/15/97 15:00 Pathologist/Resident: Pencil/Fernandez Service: Private Restriction: Brain only FINAL AUTOPSY DIAGNOSIS I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.

 

snip...see full text ;

 


 

P.5.21 Parallels between different forms of sheep scrapie and types of Creutzfeldt-Jakob disease (CJD)

 

Wiebke M. Wemheuer1, Sylvie L. Benestad2, Arne Wrede1, Wilhelm E. Wemheuer3, Tatjana Pfander1, Bjørn Bratberg2, Bertram Brenig3,Walter J. Schulz-Schaeffer1 1University Medical Center Goettingen, Germany; 2Institute of Veterinary Medicine Oslo, Norway; 3Institute of Veterinary Medicine Goettingen, Germany

 

Background: Scrapie in sheep and goats is often regarded as the archetype of prion diseases. In 1998, a new form of scrapie - atypical/Nor98 scrapie - was described that differed from classical scrapie in terms of epidemiology, Western blot profile, the distribution of pathological prion protein (PrPSc) in the body and its stability against proteinase K. In a similar way, distinct disease types exist in sporadic Creutzfeldt-Jakob disease (CJD). They differ with regard to their clinical outcome, Western blot profile and PrPSc deposition pattern in the central nervous system (CNS). Objectives: The comparison of PrPSc deposits in sheep scrapie and human sporadic CJD.

 

Methods: Tissues of the CNS of sheep with classical scrapie, sheep with atypical/Nor98 scrapie and 20 patients with sporadic CJD were examined using the sensitive Paraffin Embedded Tissue (PET) blot method. The results were compared with those obtained by immunohistochemistry. With the objective of gaining information on the protein conformation, the PrPSc of classical and atypical/Nor98 sheep scrapie and sporadic CJD was tested for its stability against denaturation with guanidine hydrochloride (GdnHCl) using a Membrane Adsorption Assay.

 

Results: The PrPSc of atypical/Nor98 scrapie cases and of CJD prion type 1 patients exhibits a mainly reticular/synaptic deposition pattern in the brain and is relatively sensitive to denaturation with GdnHCl. In contrast classical scrapie cases and CJD prion type 2 patients have a more complex PrPSc deposition pattern in common that consists of larger PrPSc aggregates and the PrPSc itself is comparatively stable against denaturation.

 

Discussion: The similarity between CJD types and scrapie types indicates that at least two comparable forms of the misfolded prion protein exist beyond species barriers and can elicit prion diseases. It seems therefore reasonable to classify classical and atypical/Nor98 scrapie - in analogy to the existing CJD types - as different scrapie types.

 


 

What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?

 

28 Mar 01

 

Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.

 

Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.

 

Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.

 

"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.

 

Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.

 

Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.

 

As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.

 

"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.

 

But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.

 

People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.

 

But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."

 

There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.

 

Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.

 


 

Monday, December 1, 2008

 

When Atypical Scrapie cross species barriers

 


 

Thursday, December 20, 2012

 

OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED, WISHES TO CONTINUE SPREADING IT AROUND THE GLOBE

 


 

Monday, November 30, 2009

 

USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE, DOES NOT SURPRISE ME $

 


 

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 ;

 


 

AND ATYPICAL NOR-98 SCRAPIE IS EVEN MORE OF A CONCERN FOR TRANSMISSION TO HUMANS, AND THE ATYPICAL NOR-98 HAS SPREAD FROM COAST TO COAST HERE IN THE USA ;

 

Thursday, March 29, 2012

 

atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

 

NIAA Annual Conference April 11-14, 2011San Antonio, Texas

 


 

AND WHAT HAVE THE PRION GODS SAID OF THE ATYPICAL NOR-98, AND IT'S POTENTIAL FOR TRANSMISSION TO HUMANS ;

 

A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes

 

Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations

 

*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway

 

***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)

 

Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice.

 

*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

 


 

OR

 

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

 


 

OR

 

*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.

 


 

 *** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

 

VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $

 

OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles

 

Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA

 

Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.

 

Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.

 

Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.

 

In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.

 

Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.

 

The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

 


 

IN A NUT SHELL ;

 

(Adopted by the International Committee of the OIE on 23 May 2006) 11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,

 


 

Thursday, May 30, 2013

 

World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease U.S. gets top mad-cow rating from international group and risk further exposing the globe to the TSE prion mad cow type disease

 


 


 

Saturday, April 19, 2014

 

Exploring the zoonotic potential of animal prion diseases: In vivo and in vitro approaches

 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).

 


 


 

*** also see ;

 

REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS COMMISSION Paris, 19–28 February 2013

 

In response to a Member Country’s detailed justification for listing of chronic wasting disease of cervids (CWD) against the criteria of Article 1.2.2., the Code Commission recommended this disease be reconsidered for listing.

 


 

REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS COMMISSION Paris, 17–26 September 2013

 

Item 5 Criteria for listing diseases (Chapter 1.2.)

 

Comments were received from Australia, EU, Japan, New Zealand, Switzerland, Thailand and AU-IBAR The Code Commission noted a Member Country’s comment suggesting that greater clarity was needed for the term ‘significant morbidity and mortality’. As noted in the February 2013 report, the Code Commission considered that the structured process of listing diseases, first by an expert group whose conclusions are documented and circulated for Member Countries’ review and comment, then consideration by the World Assembly of Delegates before final adoption, is sufficiently rigorous and transparent.

 


 

link updated ;

 

Monday, May 05, 2014

 

*** Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing

 


 

Wednesday, February 26, 2014

 

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION 2004 THROUGHT PRION 2013 CONFERENCE ABSTRACT BOOKS

 


 

Friday, April 25, 2014

 

Accuracy of administrative diagnostic data for pathologically confirmed cases of Creutzfeldt-Jakob disease

 

Article in Press

 


 

WHAT about the sporadic CJD TSE proteins ?

 

WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$

 

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

 

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

 


 

Sunday, October 13, 2013

 

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

 


 

Sunday, March 09, 2014

 

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

 

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES

 


 

Sunday, April 06, 2014

 

SPORADIC CJD and the potential for zoonotic transmission there from, either directly or indirectly via friendly fire iatrogenic mode, evidence to date

 


 

***Singeltary reply to Plos ;

 

Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

***Singeltary submission to PLOS ;

 

No competing interests declared.

 

see full text ;

 


 

Re: vCJD in the USA * BSE in U.S. 15 November 1999 Terry S Singeltary, NA

 

CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997. So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie.

 

It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses.

 


 

 U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...

 

2 January 2000 Terry S Singeltary

 

The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;

 

"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."

 

Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.

 

Something else I find odd, page 16;

 

"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."

 

A few more factors to consider, page 15;

 

"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."

 

"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."

 

"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."

 

Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.

 

To be continued...

 

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

 

Competing interests: None declared

 


 

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.

 


 

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

 


 

14th ICID International Scientific Exchange Brochure - Final Abstract Number: ISE.114

 

Session: International Scientific Exchange

 

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

 

T. Singeltary Bacliff, TX, USA

 

Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

 

Methods: 12 years independent research of available data

 

Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

 

Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

 


 

The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI

 

Tracking spongiform encephalopathies in North America

 

Original

 

Xavier Bosch

 

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...

 


 


 

SEE FULL TEXT ;

 

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

 

Subject: Tracking spongiform encephalopathies in North America LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003

 

Date: Tue, 29 Jul 2003 17:35:30 –0500

 

From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy

 

To: BSE-L@uni-karlsruhe.de

 

Volume 3, Number 8 01 August 2003

 

Previous

 

Next

 

Newsdesk

 

Tracking spongiform encephalopathies in North America

 

Xavier Bosch

 

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.

 

49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.

 

Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.

 

Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.

 

To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.

 

Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.

 

Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.

 

Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.

 

Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.

 

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.

 

CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.

 


 

Owens, Julie

 

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

 

Sent: Monday, July 24, 2006 1:09 PM

 

To: FSIS RegulationsComments

 

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98

 


 

FSIS, USDA, REPLY TO SINGELTARY

 


 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

Saturday, December 21, 2013

 

Complementary studies detecting classical bovine spongiform encephalopathy infectivity in jejunum, ileum and ileocaecal junction in incubating cattle

 


 

Sunday, December 22, 2013

 

10 years after mad cow cover up started, and 16 years after Moms demise to hvCJD, were still feeding cows to cows

 


 

 

layperson

 

mom dod 12/14/97 confirmed hvCJD...just made a promise to mom, never forget, and never let them forget...tss

 

 

Terry S. Singeltary Sr.

Bacliff, Texas USA 77518


 
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