Saturday, December 29, 2012

MAD COW USA HUMAN TSE PRION DISEASE DECEMBER 29 2012 CJD CASE LAB REPORT

MAD COW USA HUMAN TSE PRION DISEASE DECEMBER 29 2012 CJD CASE LAB REPORT





A tribute to Anna Henderson



November 30, 2012
From: DH
Sent: Saturday, December 29, 2012 5:23 PM
To: Terry S. Singeltary Sr. Subject:
Re: Mad Cow Disease
Thanks for the nice comments. She worked in surgery as a house keeper. Her primary Doctor, Dr. Dooley signed her death certificate and knew she was going to be cremated. Kind of makes me wonder now that I think about it. That would be nice to add her to the blog. There’s a news company here in Spokane who has her story and I did a on camera interview with me early last week. I thought they wanted to do the story ASAP! I think they are dragging their feet on this. If you want to beat them to the media, go for it. When you get done with your blog, would you send me a link?
 
Thanks, Dwight (My story about Anna and all other information related to Anna Henderson is my opinion).
==========END...TSS==========
The National Prion Disease Pathology Surveillance Center
November 16, 2012
LAB REPORT
snip...
 
With reference to the patient Anna Henderson...snip..., we found that the patient has a positive tau amount of 8602 pg/ml in CSF (decision point; 1150 pg/ml). The 14-3-3 was also positive, Thus, in the context of dementia, the finding is consistent with prion disease, probably CJD...snip...Since the tau test was positive and therefore the diagnosis of CJD likely, you will be contacted about this patient in approximately 10 days to follow up...snip...end
===========END...TSS=======
 
 
 
CERTIFICATE OF DEATH
 
 
CAUSE OF DEATH
 
 
A. ENCEPHALOPATHY DUE TO PRION DISEASE
 
 
 
END...TSS
 
 
 
Greetings again Dwight et al,
a few comments and then followed up with some information that may be of interest to you.
THE USA has had more documented TSE prion disease documented in livestock, and in the wild, (not including zoo TSE prion disease), than any other Country in the world, most all of it at one time rendered into feed for livestock for human and animal consumption, iatrogenic CJD there from any one of those species ??? but yet, not one documented case of human TSE there from any one of these species that carry a TSE prion disease here in the USA $$$
really?
My deepest condolences to Dwight and the family and friends of Anna, may she rest in peace, and thanks for sharing this information. Thanks to Gary Chandler for also bringing this to my attention and helping this family out.
but we have seen this time and time and time again.
I will post the latest statistics on CJD here in the USA, you do know we have a new strain of CJD in young and old that rising here in the USA, besides the typical sporadic CJD and the 6 sub-types of CJD there from. they call it ‘cases pending sporadic CJD’. the USA prion unit hasn’t a clue as to route and source, or even what it is, other than a new prion disease in young and old, with some of long duration from onset of clinical symptoms to death. but they will insist it’s another sporadic spontaneous event, not tied to anything. and the cover-up continues $$$
with saddest regards,
terry
====================================
DECEMBER 29, 2012
 
 
From:
 
Sent: Friday, December 28, 2012 10:23 PM
To: DH
Cc: Terry Singeltary
Subject:
Re: Mad Cow Disease
 
 
snip...
 
 
 
Thanks for the response and the information. You do not have to protect my privacy, I don’t care about that. The city here is Spokane WA. There is a local news channel here that seems interested, they have had the story now for more than two weeks. They haven’t run it yet, and I don’t know why. I have a lab report from the The National Prion Disease Pathology Surveillance Center. It reads she tested positive. I will try to scan a copy later tonight and e-mail it to you. I have been contacted by the local Spokane Regional Health, and a Dr. from WA. State. Below is a copy of both of our conversations. Let me know if they come through OK? If it’s all jumbled up I will send you two e-mails with separate conversations.



 I would like this story told because I believe this is MUCH BIGGER than we know.


Dwight


My wife just passed away on 11/25/12 with Mad Cow Disease (C J D) or better known as Prion Disease. She got it from eating meat products in our food supply. It’s a terrible way to die. It attacks and destroys the brain, travels down the spinal cord, attacks the nerves, and then starts shutting down the vital organs. The Doctors told me there is no treatment or cure for it. Spokane Regional Health contacted me because I have been telling people what happened to Anna. Spokane Regional Health who is responsible for keeping our food safe is brushing it off as no big deal, and that it never happened. They want me to shut up. Thanks for reading this. Below is a conversation I had with an employee there.
12/18/12
Spokane Regional Health-Dorothy Macakeran, (Epidemiologist) left a message saying she wanted to talk to me about Anna's death. To call phone: xxx-xxxxor her cell number: xxx-xxxx.
12/19/12 12:45 pm.
I called Dorothy back.
Dorothy said: "Dwight, I would like to ask you some questions about Anna and how she died".
I said: "That's fine".
Dorothy said: "Do you have any idea how or where she got this disease. Did she or any of her family members have mental or CJD history? Do you know anyone who has had it in the past?".
I said: "No"
I said: "Dorothy, where do you think it came from?".
Dorothy said: "Well, we are not sure" She continued talking about how Prion disease is a mystery.
I said: "let me stop you right there. First of all, she had Mad Cow Disease, and it came from the food supply".
Dorothy said: "We don't know that for sure, and Prion can't be pinned down".
I said: "Anna had two Spinal Taps and tested positive both times for CJD, Mad Cow Disease. This report is from The National Prion Disease Pathology Surveillance Center. I have the lab report right here in front of me. I also have three statements from three different doctors.
1. 11/9/12 Doctor's Statement: Late evening. Sacred Heart Center. "Anna has Mad Cow Disease" I asked: "Where did it come from?". He said: "From eating food".
2. 11/10/12 Doctor's Statement: Sacred Heart Medical Center. "Anna has Mad Cow Disease and it is fatal. She will not make it through the Holidays. He said, it come from the food supply".
3. 11/21/12 Doctors Statement: Sacred Heart Doctors Building. "Anna has less than thirty days left. It came from the food supply".
Dorothy said: "I don't know where the doctors got that from".
I said: "Dorothy, are you a doctor?".
Dorothy said: "No".
I said: "Dorothy, what is your title there at work, and what is your degree?"
Dorothy said: "I am a Epidemiologist, I do investigations, and I have a BS degree".
I said: "Dorothy, I totally disagree with your position on Anna's death. I accept all three Doctor's Diagnosis as fact".
Dorothy said: "I don't know how those doctors came up with that!".
I said: "Are you over ruling all three Doctors and their diagnosis"?
Dorothy: No answer.
I said: "If I were you, I would focus your investigation on the Food Supply".
Dorothy asked: "Where did she eat at?"
I said: "Restaurants, here in Spokane, mostly around the local area, such as the Broadway Truck Stop, Sherries, Jack In The Box ".
Dorothy asked: "Did Anna ever have cataract surgery with cornea donations from donors?". My answer: "No, she had a lens replacement from a manufacturer, not a human donor".
Dorothy asked: " Did Anna ever eat any brains from animals?" My answer: "No".
Dorothy asked: "Did Anna ever eat any wild game such as deer?" My answer: "No, never".
Dorothy asked: "How long has Anna lived in Spokane?" My answer: "Since 1975, and before that when she was a young girl. We lived for a little while in Seattle, Tacoma".
Dorothy asked: "Where was she born?". I said: "She was born in Linz, Austria, and came over here when she was five years old".
Dorothy asked: "Did she ever go out of the country?" My answer: "Never".
Dorothy asked: "Cook at home" My answer: "Hardly ever".
I said: "Awhile back it was in the news here in WA. State. that there was a Mad Cow outbreak".
Dorothy said: "It was just a minor, Isolated, incident, and nothing to worry about!".
I said: "Dorothy, it's easy for you to say, it was a Minor, Isolated Incident!. I think it was a VERY SERIOUS incident!. My wife lost her life, and it came from the food supply here in Spokane!. How many other people have Mad Cow from the food we eat!".
I said: "Dorothy, I'm REALLY PISSED OFF that this happened to Anna. I thought our food supply was suppose to be safe!".
We bid each other farewell.
During our conversation, I had this over whelming feeling that Dorothy was trying to trip me up. It seems, she's trying to brush it off as if it didn't happen. Seems like a cover-up! I know I, can't bring Anna back, but I'm concerned about the food safety and if it's being monitored like it should. Kind of scary, wondering how many other people might be sick from mad cow (C J D) Disease.
12/22/12 at 11:30 am. Saturday.
Washington State: Dr. Kathy Lofy called me.
Her phone number: 1-206-xxx-xxxx
Dr. Lofy asked: "Dwight, could I ask you some questions about Anna's death".
I said: "yes".
Dr. Lofy said: "Going over Anna's records here we can't really determine which type of C J D that she had for sure".
I said: "What do you mean by that?"
Dr. Lofy said: "Well, there are three different types of Prion Disease. One type is Sparatic. The second type is Genetic. The third type is Variant. She said I believe that Anna might of had the Sparatic kind, and we do not know that much about it at the present time".
I said: "How do you know Anna had that type if you don't know that much about it?".
Dr. Lofy said: "Our tests indicate that could be the type".
I said: "Then Dr., if you don't know that much about the Sparatic type. Then, that means you cannot rule that one out of the food supply either, Is that correct".
Dr. Lofy: Had no answer.
Dr. Lofy said: "With the Varient type, the patient symptoms start about twelve to fourteen months before the symptoms worsen".
I said: "Anna's symptoms were starting about two years before. She was having trouble walking, falling, she said she felt lopsided while she walked. When she went grocery shopping she would hang on to a grocery cart to help her walk".
I said: "I have the Lab Report right here in front of me and it says she was tested positive for C J D, Mad Cow Disease. In fact, she was tested twice. Both times positive for C J D Mad Cow Disease".
Dr. Lofy said: "Do you know Dr. Pugh, Anna's Neurologist?"
I said: "Yes"
Dr. Lofy said: "I spoke to Dr. Pugh, and he said in his notes he did tell you Anna had Mad Cow Disease and he said it did come from the food supply. After I spoke to Dr. Pugh he decided to change his statement to say it could be the Sparatic type of Prion."
I said: "Dr. Lofy, I was there with Dr. Pugh during Anna's appointment. While talking to Dr. Pugh, his Nurse opened the door and handed him the Lab Report which stated beyond a shadow of a doubt that Anna has tested positive for C J D, Mad Cow. Dr. Pugh read the Lab findings to me and sat it down in his lap and said. "Dwight she has C J D which is the human version of Mad Cow Disease" "I said, Dr. could this be the tip of the Iceberg for the spread of this kind of disease"?. Dr. Pugh "said yes". Dr. Pugh said: "this comes from our food supply". Dr. Pugh said, when an infected cow is butchered, reprocessed, and is put back into more cow feed, then this infects the cows that feed from that source".
I said: "I, was told by three Doctors on separate dates and times that Anna had Mad Cow Disease"
Dr. Lofy: No answer.
Dr. Lofy said: "There are safeguards and tests in place for C J D.
I asked: "I need the name of the test you use" And what safeguards are you talking about?".
Dr. Lofy said: "Ah, I don't know, and I don't know exactly how to answer that".
I said: "Then How do you know, and how can you say that our food supply is safe?".
Dr. Lofy: Did not have any answers.
I said: "Dr. Lofy, I'm not a Doctor, but, If I were you, I would focus your investigation on our food supply here in WA.".
I said: Dr. Lofy, this is Saturday. Why are you calling me today. Is it because the Media called you".
Dr' Lofy said: "Yes, they called."
I said: "Dr. I'm thinking that you people doing damage control and are trying to cover your asses and point this Mad Cow in a different direction. Dr. this is no time to worry about covering your butts. This is too serious of a matter for that. There could be a lot more people out there coming down with this disease if action isn't taken".
I said: "Back some years ago in the news papers it was reported that a Mad Cow Disease outbreak happened here in WA. State. It was also reported that you, the WA. State Government was going to protect us from this disease, and that we had nothing to worry about. Is that correct?".
Dr. Lofy said: "Yes, and that it did in fact happen".
I said: "How do you go about keeping our food safe from Mad Cow?"
Dr. Lofy said: "The cattlemen are suppose to test their cattle for Bovine"
I said: "How do you know for sure that they are in fact testing their cattle? Do you check them out or what?".
Dr. Lofty said: "No, not that I know of ".
I said: "Dr. Lofy, Do you check out slaughter houses, and meat departments in grocery stores for Mad Cow Disease?". "And what kind of tests do you do to detect Mad Cow?". "If you do test, what is the name of the test?".
Dr. Lofy said: "We don't do that."
I said: "Then Dr., how can you say our food is safe and that Mad Cow does not come from the food?".
I said: "Doctor, I lost my wife and I know I can't bring her back. If I didn't bring this up and you don't act to stop it, and people started coming down with this disease it would be a crime."
Dr. Lofy: Then asked me some of the same questions that Dorothy from Spokane Regional Health asked me such as, did Anna ever eat Deer or wild game. Did she ever travel out of the country. My answer was "NO"
I said: "Dr. Lofy, I know as a fact that Mad Cow Disease is found in the spinal cords of animals. When the Mad Cow outbreak happened here in WA. The order was put out to Meat Cutters and Slaughter House employees, Do Not Cut through the spinal cords of animals while processing meat items. Because, if the animal is infected, the disease will spill into and infect the rest of the meat.
I said: "The spinal cord of a cow runs from the Neck which is the chuck area all the way down the center of the back bone to the upper part of the rump area just behind the top sirloin. This is about six feet long. When ever I go past a meat department, the meat cutters are usually working fast to keep up with their work load. How do you check to see if the cutters are doing this properly?". Do you do this?".
Dr. Lofy said: "No, we do not"
I said: "I am worried about our food supply, aren't you?".
Dr. Lofty said: "Yes, we are worried about it too".
I said: "Dr., I want to leave on good terms with you, have a good x-mas.
The Dr. gave me her phone number and said goodbye.
snip...
 
 
 
 
 
Anna's Story 12/21/12
 
 
My wife just passed away on 11/25/12 with Mad Cow Disease (C J D) or better known as Prion Disease. She got it from eating meat products in our food supply. It’s a terrible way to die. It attacks and destroys the brain, travels down the spinal cord, attacks the nerves, and then starts shutting down the vital organs. The Doctors told me there is no treatment or cure for it.
 
 
The end of September Anna started having trouble walking and standing. She started getting confused and had trouble seeing. She could not hold still. While trying to sleep she threw herself out of bed at least three times onto the floor. I moved a mattress to the living room floor so she could sleep there and not hurt herself. I started dressing her, putting on her makeup because she couldn't see well enough to do it her self. I fed her, and had to hold her drinks because she could not hold them level and would spill them on herself. I had to help her walk by holding her up. She only weighed 98 Lbs. and we have stairs in our house and at one point I gave her piggy-back rides up and down the stairs.
 
 
This went on until we went to Group Health to get her checked out. Her Doctor seen her on 10/12/12. He sent Anna to Sacred Heart Emergency to get her blood sugar and fast beating heart stabilized. Anna was discharged that night to home.
 
 
Anna went to see her doctor at Group Health for a follow-up appointment on 11/2/12. Her doctor couldn't get Anna to respond to him. Her doctor then sent her back to Sacred Heart Emergency for testing. She was admitted in to the hospital. She was sleeping too much, having nightmares, throwing herself around in bed. The nurses liked her and nick named her wiggle worm. I stayed there as much as possible learning from the nurses how to feed her, change her briefs, how to move her. Anna was tested for everything the doctors could think of. She had at least three MRI tests, Two CAT Scans, Two Spinal Taps and so on. Anna stayed there being tested until her discharge to home on 11/8/12.
 
 
While at home on 11/9/12 in the evening Anna became unresponsive. I washed her face with cold towels and tried to get her to wake up. After about thirty minutes I called 911, and they sent an ambulance, two fire trucks, and crew to check her out. They couldn't get her to wake up. They sent her back to Sacred Heart Emergency. I asked the Doctor there what is wrong with her. He said she had Mad Cow Disease. This is the first time I herd this. I asked the doctor how could she get Mad Cow. He said "from eating food". He admitted her into the hospital from the emergency room. I spent most of the night with her there.
 
 
On/11/10/12 A doctor from Group Health walked into Anna's room and asked me if I would talk to him in private. He told me that Anna had Mad Cow Disease and there is no treatment or cure for her. He said she would not make it through the holidays. He said it is a VERY NASTY Disease. He said it will attack her brain, travel down the spinal cord and destroy her nervous system and then shut down her vital organs. He said prepare for the worst, it is going to get REAL UGLY. He said to make her funeral plans. I asked him how do you think she got it. His answer was "from the food supply". The Doctor and I signed a Physician Order for Life-Sustaining Treatment (POLST) form, for comfort measures only. After a stay in the hospital on or about 11/13/12 Anna was discharged.
 
 
She was moved to the Gardens on University, a Nursing Home. While there I stayed by her side almost all the time. I wanted to be with her as much as possible. I would wake her, dress her, put her in her wheelchair, comb her hair, brush her teeth, take her to the dinning room for her meals. She was put on a soft food diet because she was not able to chew her food. When I put a spoonful of food in her mouth I had to tell her to swallow. Toward the end she was only eating about one spoonful of food each meal. The same went for water, coffee and such. The Hospice Manual said when people reach the end of life they eat and drink less, sleep a lot because they are shutting down. Her first few days there she slept a lot in her wheelchair. She was starting to scream out loud, thrash about, and have seizures. I noticed that she was losing the fight more each day. The nurses gave her sedatives to help her calm down.
 
 
On 11/21/12 Anna had a Doctors appointment with her Neurologist. While we were sitting there the Doctor's nurse handed him a lab report. He read it and said she tested positive and confirmed the earlier diagnosis of the other Doctors. He said she has Mad Cow and its from eating infected food. He explained how infected cows were slaughtered and fed back to other cows who became infected . He said she has about thirty days left and recommends immediate Hospice care. I asked him for a copy of that lab report that he read to me. He made a copy for me and we left.
 
 
We went back to the nursing home, and after a couple of days I, noticed Anna was getting worse. On 11/23/12 I talked to the admin office about getting Anna discharged to home because she wanted to be at home when she passed. The young lady there in the office said "Oh, there is no way we can discharge her before next Wednesday 11/28/12 too much paper work". I new this was total BS because Group Health was paying them for her stay. I went down the hall and called Anna's doctor. Within an hour Hospice walked in with doctors orders to have Anna discharged. The lady in the admin office had Anna's discharge papers done in less than an hour. As soon as Anna's hospital bed and wheelchair was delivered to my house. On 11/24/12 an ambulance brought her home because her condition was dire. I told Anna she was at home now. I put her puppies in her lap. Anna had a real peaceful look on her face. All the time she was in the hospital and nursing home she had a look of distress on her face. I fed her about a spoonful of baby food and some water that night. The next morning, I woke her up, just before Seven am. I dressed her in her favorite blouse, her favorite Pink Panther pants and shoes, sat her in her wheelchair, combed her hair. It was now 7:20 am, I was ready to feed her breakfast when she took a deep breath and died in my arms. I ran and called the Hospice Nurse to come over quick, "I think Anna just died" She came and checked her vitals and confirmed she passed. The nurse called the funeral home for me. They came and got her at 10:30 am.
 
 
12/06/12 at 5:50 pm. Anna's Neurologist called and wanted to know how Anna was doing. I told him Anna died on 11/25/12. He said an autopsy was not necessary in this case because of her positive tests. He said the State was tracking these conditions and may contact me later on. We talked a little more and said goodbye.
 
 
snip...
 
 
 
================end...tss=================
 
 
 
 
NOW, let’s go back in time and work our way up until today on the infamous UKBSEnvCJD only theory, the theory that just keeps on helping spread and spread the human TSE prion agent. $$$
 
 
 
IN CONFIDENCE
 
 
Perceptions of unconventional slow virus in the USA
 
 
GAH WELLS Report of a visit to the U.S.A. April-May 1989
 
 
snip...
 
 
3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed.
 
 
 
Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the USA AT ALL COSTS.
 
 
 
 
 
 
and they meant it. in today’s terms, it’s called the SSS policy of shoot, shovel, and shut the hell up, don’t test, at all cost, don’t test. ...tss
 


 
 
 
Texas SSS Policy


 
ceverett@tahc.state.tx.us For Immediate Release-- Anthrax Confirmed in Sutton County, Texas
 
 
 
 
Anthrax Confirmed in Sutton County, Texas

 
snip...
 
 
 
 
Two ranches in Sutton County, Texas have laboratory-confirmed cases of anthrax in horses, deer and cattle, and laboratory results are pending for several other sites in the county, where livestock and deer losses have been reported. Although this bacterial disease occurs almost yearly in this region of the state, cases have not been confirmed within Sutton County for more than 20 years. Typically, outbreaks are in Val Verde, Edwards, Kinney and Uvalde counties, but on rare occasions, cases have been confirmed as far south as Starr County, reports Dr. Thurman Fancher, director of Area 6 (West Texas) for the Texas Animal Health Commission (TAHC).
 
 
 
 
 
“Anthrax is under-reported, because many ranchers in this area automatically dispose of carcasses and vaccinate livestock when they find dead animals that are bloated or bloody--common signs of the disease,” said Dr. Fancher. “Anthrax is a reportable disease, however, and it’s important to know when an outbreak occurs, so other ranchers can be notified to vaccinate.........
 
 
snip...end
 

 
 
TSS REPORT ON 2ND TEJAS MAD COW


 
Mon, 22 Nov 2004 17:12:15 -0600 (the one that did NOT get away, thanks to the Honorable Phyllis Fong)
 
 
-------- Original Message --------


 
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 
 
Date: Mon, 22 Nov 2004 17:12:15 –0600
 

 
From: "Terry S. Singeltary Sr."

 
 
To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>

 
 
Greetings Carla,
 

 
still hear a rumor;

 
 
Texas single beef cow not born in Canada no beef entered the food chain?

 
 
and i see the TEXAS department of animal health is ramping up for something, but they forgot a url for update?

 
 
I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
 
 
terry

 
 
 
==============================
 
 
 
-------- Original Message --------
 

 
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 
 
Date: Fri, 19 Nov 2004 11:38:21 –0600

 
 
From: Carla Everett

 
 
To: "Terry S. Singeltary Sr." References: <[log in to unmask]>

 
 
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no informationabout the animal being in Texas.
 

 
Carla
 
 
 
At 09:44 AM 11/19/2004,
 

 
you wrote:>Greetings Carla,

 
 
>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from
 
 
>TEXAS. can you comment on this either way please?
 
 
>>thank you,
 
 
>Terry S. Singeltary Sr.>>
 


 
===================
===================


 
 
-------- Original Message --------
 
 
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
 
 
Date: Mon, 22 Nov 2004 18:33:20 –0600
 
 
From: Carla Everett
 
 
To: "Terry S. Singeltary Sr." References: <[log in to unmask]> <[log in to unmask] us> <[log in to unmask]> <[log in to unmask] us> <[log in to unmask]>
 
 
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.
 
 
At 06:05 PM 11/22/2004,


 
 
you wrote:
 
 
>why was the announcement on your TAHC site removed?
 
 
>>Bovine Spongiform Encephalopathy:
 
 
>November 22: Press Release title here
 
 
>>star image More BSE information
 
 
>>>>terry
 
 
>>Carla Everett wrote:
 
>>>no confirmation on the U.S.' inconclusive test...
 
 
>>no confirmation on location of animal.
 
 
>>>>>>
 
 
 
 
 
==========================
==========================
 
 
ONE YEAR LATER, AFTER CONGRESS OIG DOING THE END AROUND JOHANNS, DEHAVEN ET AL, and getting the above Tejas mad cow tissue sample to Weybridge, that cow was CONFIRMED. IT would have never been confirmed if not for the Honorable Phyllis Fong, and a few others.
FULL 130 LASHINGS TO USDA BY OIG again


 
 
HOW ABOUT THAT TEXAS MAD COW THAT WAS COVERED UP FOR 7 MONTHS...
BIO-RAD BSE TEST POLITICAL REPLY TO TSS
Subject: FSIS NOTICE SAMPLE COLLECTION FROM CATTLE UNDER THE BOVINE SPONGIFORM ENCEPHALOPATHY (BSE ONGOING SURVEILLANCE PROGRAM
 
 
From: "Terry S. Singeltary Sr."
 
Reply-To: Sustainable Agriculture Network Discussion Group
 
 
Date: Fri, 2 Feb 2007 17:32:58 –0600
 
 
Subject: Re: USDA/APHIS JUNE 2004 'ENHANCED' BSE/TSE COVER UP UPDATE DECEMBER 19, 2004 USA
 
 
Date: Thu, 30 Dec 2004 12:27:06 –0600
 
 
From: "Terry S. Singeltary Sr.
BSE-L
snip...
>
> OH, i did ask Bio-Rad about this with NO reply to date;
>
>
> -------- Original Message --------
> Subject: USA BIO-RADs INCONCLUSIVEs
> Date: Fri, 17 Dec 2004 15:37:28 -0600
> From: "Terry S. Singeltary Sr."
> To: susan_berg@bio-rad.com
>
>
>
> Hello Susan and Bio-Rad,
>
> Happy Holidays!
>
> I wish to ask a question about Bio-Rad and USDA BSE/TSE testing
> and there inconclusive. IS the Bio-Rad test for BSE/TSE that complicated,
> or is there most likely some human error we are seeing here?
>
> HOW can Japan have 2 positive cows with
> No clinical signs WB+, IHC-, HP- ,
> BUT in the USA, these cows are considered 'negative'?
>
> IS there more politics working here than science in the USA?
>
> What am I missing?
>
>
>
> -------- Original Message --------
> Subject: Re: USDA: More mad cow testing will demonstrate beef's safety
> Date: Fri, 17 Dec 2004 09:26:19 -0600
> From: "Terry S. Singeltary Sr."
> snip...end
>
>
> Experts doubt USDA's mad cow results
 
 
snip...END
 
 
 
WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;



 
Bio-Rad, TSS phone conversation 12/28/04 Finally spoke with ;


 
 
 
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX



 
at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.
 
 
 
 
 
my question;


 
 
 
Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???

 
 
 
 
ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.

 

 
again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there.



 
"very difficult to answer"

 

 
"very political"


 
 
 
"very loaded question"



 
outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing.


 
 
 
said something about Dr. Houston stating; any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives?



 
said something about ''just look at the sheep that tested IHC- but were positive''. ...
 


 
 
TSS
 


 
-------- Original Message --------


 
Subject: Your questions
 

 
Date: Mon, 27 Dec 2004 15:58:11 –0800
 
 
 
From: To: flounder@wt.net

 
Hi Terry:
 

 
............................................
 
 
 
snip

 
 
Let me know your phone number so I can talk to you about the Bio-Rad BSE test.

 
 
 
Thank you Regards
 
 
 
 
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630
 
 
 
Email:
 

 
=================================

 
 
 
snip...end...TSS


 
Tuesday, November 02, 2010
 
 
 
IN CONFIDENCE

 
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".


 
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992



 
 
 
 
 
 
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
 
 
 
 
 


 
Comments on technical aspects of the risk assessment were then submitted to FSIS.

 
Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.
 
 
 
This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:

 
 


 
 
 
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
 
 
 
 

 
 
FACTS are facts, the Triple SSS policy of shoot, shovel and shut the hell up, is and has been alive and well in TEXAS. hate to disappoint some of you folks that are saying Canada has a greater problem of mad cow disease than the USA. That's a real hoot. IT just aint so though. why in the hell do you think they shut the 2004 Enhanced BSE cover-up down? AFTER those two atypical BSE cows in Texas and Alabama, the ones that the pathology DID NOT resemble nvCJD or vCJD of the ukbse strain, but the pathology of some of the sporadic CJDs in the USA, that changed everything, and they simply were not going to document anymore cases. YOU would have thought after that they would have enhanced the surveillance even more. BUT NOW we cannot even get USDA to document a TOKEN SO CALLED spontaneous case of mad cow disease, which most of us know is just wishful thinking anyway. ...TSS
 
 
 
DEEP THROAT TO TSS 2000-2001
 
 
(take these old snips of emails with how ever many grains of salt you wish. ...tss)
 

 
The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why????than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!! Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....
 


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


 
 
 
And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...
 
 
 
 
 
 
Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"
 
 


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


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


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

 
 
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
 
 
 
 
 
 

 
Questions linger in U.S. CJD cases
 
 
Published: Oct. 21, 2005 at 9:49 PM
 
 
 
 
By STEVE MITCHELL, Senior Medical Correspondent
 

 
WASHINGTON, Oct. 21 (UPI) -- French researchers have ruled out the human form of mad cow disease in a deceased California man, even though they did not conduct the critical test widely regarded as the only way to determine precisely the nature of his disease, United Press International has learned.

 
The case of Patrick Hicks, who died last November from his condition, has remained murky from the beginning. Dr. Ron Bailey, of Riverside, Calif., the man's neurologist, had suspected the 49-year-old Hicks of having contracted variant Creutzfeldt Jakob disease -- a fatal, brain-wasting illness humans can contract from eating beef products contaminated with the mad cow pathogen -- and both he and the family wanted an autopsy conducted to determine if Hicks had succumbed to the disorder.

 
 
Bailey became concerned that Hicks might have contracted vCJD because he initially had exhibited psychiatric symptoms, his illness appears to have lasted for more than one year and he showed normal brain-wave patterns via EEGs until the late stages -- all consistent with the disease. In addition, Hicks's relatively young age raised concerns, because nearly all of the more than 150 cases of vCJD detected worldwide have occurred in people under age 55.

 
 
The first hint of oddness began when, according to both Hicks's brother and mother, a team of six doctors, who they suspect were with the Centers for Disease Control and Prevention in Atlanta, visited Patrick last October while he was still alive and under care at Loma Linda University Medical Center in Loma Linda, Calif.
 

 
They said they were asked to leave when the doctors arrived to examine Patrick.

 
 
CDC officials would not confirm to UPI whether they had investigated the case, but the agency's policy does require examining all suspected cases of vCJD in anyone under 55.

 
 
The family also said Loma Linda refused to released Hicks's medical records to them.
 
 
The oddities continued after Hicks's death. Bailey found it almost impossible to get an autopsy conducted on Hicks, the only way to determine conclusively whether he had variant or sporadic CJD -- a version of the disease not related to mad cow. One county coroner's office referred him to another and both refused to conduct the procedure, he said.
 

 
Then, the National Prion Disease Pathology Surveillance Center in Cleveland, Ohio -- which was established by the CDC to investigate potential vCJD cases in the United States -- dispatched a mobile autopsy company called 1-800-Autopsy, but the company failed to follow the center's protocol and did not collect frozen sections of brain, which are required for tests to determine whether the disease is vCJD or sCJD. Instead, the autopsy company fixed the entire brain in formalin.
 

 
The NPDPSC, however, considers the collection of frozen brain tissue essential to distinguishing vCJD from other forms of CJD.
 

 
"Only frozen brain tissue examination definitely confirms or excludes the diagnosis of prion disease and provides the information to identify the type of prion disease," the center's Web site says. Prions are abnormal proteins thought to play a role in causing vCJD and sCJD.
 

 
The problem raised enough concern that both Bailey and Hicks's family sought a second opinion.

 
 
Experts had told them that animal-injection studies could be done with formalin-fixed tissue, so the family arranged to have a sample of Patrick's brain sent to Dr. Jean Jacques Hauw at the Laboratoire De Neuropathologie at the Groupe Hospitalier Pitie-Salpetriere in Paris, who they thought had agreed to do the studies.
 

 
The NPDPSC, however, delayed sending the sample to France for two months after the family's request last March. During the delay, Pierluigi Gambetti, the NPDPSC's director, sent a letter to Hicks's wife.

 
 
"We can definitely rule out the diagnosis of variant CJD," the letter stated.

 
 
Gambetti's strong conclusion sounded strange to Bailey, because the NPDPSC had not conducted further tests since January, when they had said vCJD was unlikely but that they were unable to rule it out entirely.
 

 
After examining the brain tissue, Hauw's team told the family the disease was consistent with sCJD, but to date they have not explained why they did not conduct the animal-injection studies -- the family's reason for sending samples of his brain to France.
 

 
Asked the reasons for not following the family's wishes and conducting the animal studies, Hauw told UPI, "I cannot answer your question," citing French regulations that prohibited him from providing information about a specific patient.
 
He did say, however, that "animal injection is not needed for the routine diagnosis of Creutzfeldt-Jakob disease and its various variants, at least in France and in the United Kingdom."

 
 
That may be true, but it remains unclear why he accepted the case in the first place, knowing that is what the family wanted.
 
 
 
Moreover, this was not a "routine diagnosis." If Hicks suffered from vCJD, he potentially would have been the first person in the United States to have acquired the disease domestically, a development with significant domestic and international ramifications.
 

 
In addition, other experts, such as Dr. Laura Manuelidis, section chief of surgery in the neuropathology department at Yale University, have said the only way to know conclusively whether the disease is due to sCJD or vCJD is through animal-injection studies.
 
 
"From what I gather, the result was merely rubber stamped," Bailey told UPI. "I guess we will never really know for sure."

 
 
The handling of the case is noteworthy, because the NPDPSC currently is investigating nine potential sCJD cases in Idaho. Experts suspect some of those cases could be vCJD.

 
 
Bailey and some patient advocates said they are now skeptical of the NPDPSC's behavior.
 

 
"How could my experience with the Hicks case ... and the interaction with NPDPSC not lessen my confidence?" Bailey asked. "I anticipate that all of the Idaho cluster of CJD patients will turn out to have sCJD. I cannot for a minute see their results indicating anything but this. After all, if any patient were to have vCJD, it would have been Patrick Hicks. The results of NPDPSC are not definitive in excluding Hicks as not having vCJD. There certainly will always be that question in my mind."
 

 
Terry Singletary, a patient advocate whose mother died of a form of the disease called Heidenhain variant, told UPI he likewise had lost confidence in the NPDPSC.

 
 
"I do not trust them," Singletary said. "It's all going to be sporadic. This is the way they want it. They do not want to find out all the routes and sources of this agent."

 
 
Both vCJD and mad cow disease are politically sensitive issues because they can impact international trade. Dozens of nations closed their borders to American beef after a lone U.S. cow tested positive for the disease in 2003, resulting in more than $4.7 billion in losses for the industry, and the U.S. Department of Agriculture delayed doing confirmatory tests for seven months on what turned out to be a second case of mad cow.

 
The NPDPSC did not respond to UPI's phone call requesting comment about the Idaho cases. The CDC referred UPI to Idaho officials.

 
 
Of the nine Idaho cases, three people have tested positive for a CJD-like illness, but officials are conducting further tests to determine whether the disease is sCJD. Two others tested negative and four were buried without autopsies.
 

 
The cases could just be a statistical fluke, but the state averages about 1.2 sCJD cases per year and has never had more than three in a single year. The disease is rare and generally is thought to occur at the rate of one case per million people.
 
 
 
 
Several CJD clusters in other states have far exceeded that rate, however. These included:
 

 
--southern New Jersey (2000-2003),
 

 
--Lehigh, Pa. (1986-90),
 
 
 
 
--Allentown, Pa. (1989-92),

 
 
--Tampa, Fla. (1996-97),
 

 
--Oregon (2001-02), and
 

 
--Nassau County, N.Y. (1999-2000).

 
 
Some of the clusters involved as many as 18 deaths, and ranged from a rate of four to eight cases per million people.

 
 
A group of J.P. Morgan analysts issued an advisory last year on the impact the clusters could have on the beef industry, and said that some of the cases could be due to vCJD.
 
 
 
 
"The existence of clusters raises the question of 'contamination' or 'infection,' and also raises the hypothesis that rather than cases of sCJD, these might have been cases of vCJD," the advisory said. "Given that sCJD occurs randomly in one out of 1 million cases, it is a statistical rarity to find an sCJD cluster -- let alone six."
 
 
 
If that assessment is accurate, another cluster in Idaho would be even more unlikely.
 
 
 
 
Another possibility is some of the Idaho cases could be due to chronic wasting disease, which is similar to mad cow disease and currently is epidemic among deer and elk in several states, including Idaho's neighbors Wyoming and Utah.
 

 
No human cases of CWD have ever been confirmed, but the disease has been shown to infect human cells in a lab dish. Also, a team of researchers led by Jason Bartz of Creighton University in Omaha, Neb., report in the November issue of the Journal of Virology they had experimentally transmitted CWD to squirrel monkeys --the first reported transmission of CWD to primates.
 

 
If CWD is capable of infecting humans, it is unknown whether the resulting disease would resemble sCJD, vCJD or a novel disorder. If the disease looks like sCJD, cases could be going undetected or misdiagnosed.
 

 
--

 
 
 
 
 
 
 


 
 
 
NIH may destroy human brain collection
 
 
 
 
By Steve Mitchell Medical Correspondent
 
 
 
Washington, DC, Mar. 24 (UPI) -- The National Institutes of Health may discard part or all of a rare collection that includes hundreds of human brain samples from patients that suffered from a disorder similar to mad cow disease -- unless another researcher or institution takes them on, United Press International has learned.
 
 
see full history of the day they almost destroyed all donated brains samples from CJD victims ;
 

 
 

 
see follow up on that here ;
 
 
 
 

 
 
Monday, October 10, 2011
 
 
EFSA Journal 2011 The European Response to BSE: A Success Story
 
 
snip...
 
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
 
 
 
snip...
 
 
 
 
 
 
 
Thursday, August 12, 2010
 
 
Seven main threats for the future linked to prions
 
 
First threat
 
 
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
 
 
 
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
 
 
 
Second threat

 
snip...
 
 
 
 
 
 
Rural and Regional Affairs and Transport References Committee
 
 
The possible impacts and consequences for public health, trade and agriculture of the Government's decision to relax import restrictions on beef Final report June 2010
 
 
2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49
 
 
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
 
 
 
 
 
 
 
Atypical BSE in Cattle
 
 
 
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.
 
 
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.
 
 
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
 
 
 
 
 

 
P.4.23
Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA
 
Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.
 
Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.
 
Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time.*** The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.
 
Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
 
 
P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS
 
Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA
 
Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C.
 
 
*** The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.
 
III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)
 
 
 
I ask Professor Kong ;
 
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
 
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
 
Professor Kong reply ;
.....snip
 
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
 
Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
 
END...TSS
 
Thursday, December 04, 2008 2:37 PM
 
"we have found that H-BSE can infect humans."
 
personal communication with Professor Kong. ...TSS
 
BSE-H is also transmissible in our humanized Tg mice.
 
The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
 
 
 
 
 
 

 
 
 
 
Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate
 
Emmanuel E. Comoy1*, Cristina Casalone2, Nathalie Lescoutra-Etchegaray1, Gianluigi Zanusso3, Sophie Freire1, Dominique Marcé1, Frédéric Auvré1, Marie-Magdeleine Ruchoux1, Sergio Ferrari3, Salvatore Monaco3, Nicole Salès4, Maria Caramelli2, Philippe Leboulch1,5, Paul Brown1, Corinne I. Lasmézas4, Jean-Philippe Deslys1
 
1 Institute of Emerging Diseases and Innovative Therapies, CEA, Fontenay-aux-Roses, France, 2 Istituto Zooprofilattico Sperimentale del Piemonte, Turin, Italy, 3 Policlinico G.B. Rossi, Verona, Italy, 4 Scripps Florida, Jupiter, Florida, United States of America, 5 Genetics Division, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
 
Abstract
 
Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne transmission of prions from slaughtered cattle with classical Bovine Spongiform Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic in aging cattle, were recently identified at slaughterhouses throughout Europe and North America, raising a question about human susceptibility to these new prion strains.
 
Methodology/Principal Findings Brain homogenates from cattle with classical BSE and atypical (BASE) infections were inoculated intracerebrally into cynomolgus monkeys (Macacca fascicularis), a non-human primate model previously demonstrated to be susceptible to the original strain of cBSE. The resulting diseases were compared in terms of clinical signs, histology and biochemistry of the abnormal prion protein (PrPres). The single monkey infected with BASE had a shorter survival, and a different clinical evolution, histopathology, and prion protein (PrPres) pattern than was observed for either classical BSE or vCJD-inoculated animals. Also, the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine.
 
Conclusion/Significance Our results point to a possibly higher degree of pathogenicity of BASE than classical BSE in primates and also raise a question about a possible link to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning epidemic of classical BSE, the occurrence of atypical strains should temper the urge to relax measures currently in place to protect public health from accidental contamination by BSE-contaminated products.
 
Citation: Comoy EE, Casalone C, Lescoutra-Etchegaray N, Zanusso G, Freire S, et al. (2008) Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate. PLoS ONE 3(8): e3017. doi:10.1371/journal.pone.0003017
Editor: Neil Mabbott, University of Edinburgh, United Kingdom
 
Received: April 24, 2008; Accepted: August 1, 2008; Published: August 20, 2008
 
Copyright: © 2008 Comoy 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 work has been supported by the Network of Excellence NeuroPrion.
 
Competing interests: CEA owns a patent covering the BSE diagnostic tests commercialized by the company Bio-Rad.
 
snip...
In summary, we have transmitted one atypical form of BSE (BASE) to a cynomolgus macaque monkey that had a shorter incubation period than monkeys infected with classical BSE, with distinctive clinical, neuropathological, and biochemical features; and have shown that the molecular biological signature resembled that seen in a comparatively uncommon subtype of sporadic CJD. We cannot yet say whether BASE is more pathogenic for primates (including humans) than cBSE, nor can we predict whether its molecular biological features represent a clue to one cause of apparently sporadic human CJD. However, the evidence presented here and by others justifies concern about a potential human health hazard from undetected atypical forms of BSE, and despite the waning epizoonosis of classical BSE, it would be premature to abandon the precautionary measures that have been so successful in reversing the impact of cBSE. We would instead urge a gradual, staged reduction that takes into account the evolving knowledge about atypical ruminant diseases, and both a permanent ban on the use of bovine central nervous system tissue for either animal or human use, and its destruction so as to eliminate any risk of environmental contamination.
 
 
Proc Natl Acad Sci U S A. 2004 March 2; 101(9): 3065–3070. Published online 2004 February 17. doi: 10.1073/pnas.0305777101 PMCID: PMC365745 Medical Sciences
Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease
Cristina Casalone,*† Gianluigi Zanusso,†‡ Pierluigi Acutis,* Sergio Ferrari,‡ Lorenzo Capucci,§ Fabrizio Tagliavini,¶ Salvatore Monaco,‡ and Maria Caramelli*
Abstract
Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called ”species barrier” between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.
 
 
snip...
 
 
Phenotypic Similarities Between BASE and sCJD. The transmissibility of CJD brains was initially demonstrated in primates (27), and classification of atypical cases as CJD was based on this property (28). To date, no systematic studies of strain typing in sCJD have been provided, and classification of different subtypes is based on clinical, neuropathological, and molecular features (the polymorphic PRNP codon 129 and the PrPSc glycotype) (8, 9, 15, 19). The importance of molecular PrPSc characterization in assessing the identity of TSE strains is underscored by several studies, showing that the stability of given disease-specific PrPSc types is maintained upon experimental propagation of sCJD, familial CJD, and vCJD isolates in transgenic PrP-humanized mice (8, 29). Similarly, biochemical properties of BSE- and vCJD-associated PrPSc molecules remain stable after passage to mice expressing bovine PrP (30). Recently, however, it has been reported that PrP-humanized mice inoculated with BSE tissues may also propagate a distinctive PrPSc type, with a ”monoglycosylated-dominant” pattern and electrophoretic mobility of the unglycosylated fragment slower than that of vCJD and BSE (31). Strikingly, this PrPSc type shares its molecular properties with the a PrPSc molecule found in classical sCJD. This observation is at variance with the PrPSc type found in M/V2 sCJD cases and in cattle BASE, showing a monoglycosylated-dominant pattern but faster electrophoretic mobility of the protease-resistant fragment as compared with BSE. In addition to molecular properties of PrPSc, BASE and M/V2 sCJD share a distinctive pattern of intracerebral PrP deposition, which occurs as plaque-like and amyloid-kuru plaques. Differences were, however, observed in the regional distribution of PrPSc. While in M/V2 sCJD cases the largest amounts of PrPSc were detected in the cerebellum, brainstem, and striatum, in cattle BASE these areas were less involved and the highest levels of PrPSc were recovered from the thalamus and olfactory regions.
 
 
In conclusion, decoding the biochemical PrPSc signature of individual human and animal TSE strains may allow the identification of potential risk factors for human disorders with unknown etiology, such as sCJD. However, although BASE and sCJD share several characteristics, caution is dictated in assessing a link between conditions affecting two different mammalian species, based on convergent biochemical properties of disease-associated PrPSc types. Strains of TSE agents may be better characterized upon passage to transgenic mice. In the interim until this is accomplished, our present findings suggest a strict epidemiological surveillance of cattle TSE and sCJD based on molecular criteria.
 
 
 
 
 
Thursday, June 21, 2012
 
Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy Associated with E211K Prion Protein Polymorphism
 
Atypical cases presumably of spontaneous or, in the case of E211K BSE-H, genetic origins highlight that it may not be possible to eradicate BSE entirely and that it would be hazardous to remove disease control measures such as prohibiting the feeding of meat and bone meal to ruminants.
 
 
 
 
 
bbbut ???
Thursday, June 21, 2012
 
Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy Associated with E211K Prion Protein Polymorphism
 
 
 
 
Friday, May 11, 2012
 
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
 
 
 
 
***+++***
 
Thursday, July 10, 2008
 
 
A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008 Friday, June 20, 2008

 
 
 
 
Here we go folks. AS predicted. THIS JUST OUT !
 
 
Tuesday, August 03, 2010

 
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein

 
 
 
 
 
 
Monday, August 9, 2010
 
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?
 
snip...see full text ;

 
 
 
 
 
 
 
O.K. let's compare some recent cases of this prionpathy in other countries besides Gambetti's first 10 recently, that he claims is a spontaneous event, from a genetic disorder, that is not genetic, but sporadic, that is related to no animal TSE in North America, or the world. ...
 

 
Wednesday, October 27, 2010

 
A novel variant of human disease with a protease-sensitive prion protein and heterozygosity methionine/valine at codon 129: Case report

 
 
Sunday, August 09, 2009
 
 
 
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009

 
 
 
Tuesday, August 18, 2009
 
 
 
BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009

 
 
 
====================================
 
The familial mutations, Gajdusek proposed, lowered the barrier to such accidental conversion. "Thus," he wrote in 1996, "with these mutations, this ordinarily rare event becomes a ... dominant inherited trait." But Weissmann's qualification still remained to be refuted: the mutations might simply allow easier entry to a lurking virus. ...page 202 Deadly Feast
 
===================================
 
 
 
something to think about for sure.
 
 
 
but i interpret this as (1st not the gold standard, just my opinion;-), as because of certain gene mutations, one or a family, would be more susceptible to the many different strains of TSE, and the many different proven routes and sources, (which will cause different symptoms, different incubation periods from onset of clinical symptoms to death, different parts of the brain infected, etc.). in other words, it's NOT the gene mutation that CAUSES the disease, but the fact that it makes you more SUSCEPTIBLE, to the TSEs from the surrounding environment, and PLUS accumulation, i think this plays a critical role. maybe there is a one dose scenario, but i think there is more of the 'accumulators' that go clinical, than the 'one dose'. and what is the threshold to sub-clinical to clinical ?
 
 
anyway, just pondering out loud here.
 
also, for anyone interested, there are some studies with links to follow here ;
 
 
 
 
 
 
Thursday, June 21, 2012
 
 
 
Clinical and Pathologic Features of H-Type Bovine Spongiform Encephalopathy Associated with E211K Prion Protein Polymorphism

 
 
 
 
let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.
 
 
 
This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$

 
ALABAMA MAD COW g-h-BSEalabama

 
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
 
 
 

 

 
her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
 
 
This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine–human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.
 
 
 
Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA

 
NATURE|Vol 457|26 February 2009
 
 
 
 
 
 
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)
 
 
 

 
 
 
Tuesday, November 6, 2012

 
***Transmission of New Bovine Prion to Mice, Atypical Scrapie, BSE, and Sporadic CJD, November-December 2012 update

 
 
 
 
 
 
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012
Summary Report BSE 2012
 
Executive Summary
 
 
 
 
Saturday, August 4, 2012
 
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation
 
 
 
 
Saturday, August 4, 2012

 
*** Final Feed Investigation Summary - California BSE Case - July 2012
 
 
 
 
 
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012
 
 
 
Saturday, October 6, 2012
 
TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2011 Annual Report
 
 
 
 
Tuesday, November 02, 2010
 
*** BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
 
 
 
 
Sunday, November 13, 2011
*** California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock
snip...
QFC's Delayed Mad Cow Response Draws Lawsuit
 
 
... subsidiary of Kroger , claiming the grocery store chain should
 
 
... beef potentially tainted with "mad cow disease
 
 
... beef at approximately 40 stores across Washington.
 
 
 
snip...
 
 
SUPERIOR COURT OF THE STATE OF WASHINGTON FOR KING COUNTY
 
 
JILL CROWSON, ET AL., PLAINTIFFS

 
VS

 
QUALITY FOOD CENTERS, INC., an Ohio corporation Defendent
 
 
 
NO. 04-2-05608-0 SEA
 
 
 
snip...

 
The Court hereby GRANTS the defendant's motion to dismiss the plaintiff's claims based on a manufacturer's strict liability (Counts I and II) and DENIES the defendant's motion to dismiss the plaintiff's claim of negligence by a product seller (Count III).
 
 
 
DATED this 14th day of June, 2004
snip...
 
 
 
 
 
 
Date Filed: March 5, 2004 Court: King County Superior Court (Washington) Location: Seattle Ticker Symbol: NYSE:KR
 
 
 
Join This Suit Tell a Friend

 
Consumers filed a proposed class-action lawsuit against Quality Food Centers (QFC), a subsidiary of Kroger (NYSE: KR), claiming the grocery store chain should have used information gathered through its customer loyalty program to warn those who purchased beef potentially tainted with ?mad cow disease.? The USDA issued a recall notice for the meat on December 23, 2003. QFC sold the meat through its approximately 40 stores across Washington.

 
The suit claims that even though QFC had the ability to quickly warn every customer who purchased the potentially deadly meat if they used the QFC Advantage Card at the time of purchase, the grocery store neglected to do so.

 
The suit seeks to represent every consumer in Washington state who purchased the recalled meat from QFC.

 
Recent Updates

 
June 14, 2004 - the King County Superior Court gave the green light to a suit claiming QFC didn't do enough to warn customers about beef potentially tainted with 'mad cow disease,' finding enough questions about the beef and QFC's responsibility to explore in the courtroom.
 
 
 
Read the court order.
 
 
 
 
 
QFC - 'Mad Cow' Frequently Asked Questions
The Suit
What is the key issue in this suit?
On December 23, 2003, the United States Department of Agriculture (USDA) recalled more than 10,000 pounds of raw beef that could have been exposed to bovine spongiform encephalopathy (BSE). Humans consuming BSE-tainted meat can contract Creutzfeldt-Jakob Disease (vCJD), an always-fatal condition.
QFC sold this meat throughout its stores in Washington. Even though QFC had the ability to quickly warn every customer who purchased the potentially deadly meat if they used the QFC advantage card at the time of purchase, the grocery store neglected to do so, the suit alleges.
Who does the suit seek to represent?
The suit seeks to represent all persons who purchased recalled meat from any QFC store in the state of Washington.
Who are the defendants?
Quality Food Centers, or QFC. Once a local, Northwest company, QFC is now a wholly owned subsidiary of the grocery chain giant, Kroger.
What does the suit seek?
The suit asks the court to order QFC to establish a medical monitoring fund which would allow those who purchased and consumed the meat to seek medical care, checking for, and if necessary, treating --- the infection of vCJD. The suit also seeks the creation of a medical notification system, allowing those who may have been exposed to the disease to receive periodic updates on research and treatment of vCJD. The suit also seeks unspecified damages for the plaintiffs.
Does the suit claim QFC violated specific laws?
Yes. The lawsuit claims QFC violated the Washington Product Liability Act. In addition, the suit claims QFC was negligent by not warning consumers of the dangers associated with the affected meat.
Where was the lawsuit filed?
The suit was filed in King County Superior Court on March 4, 2004.
How do I determine if I qualify to join the lawsuit?
If you have a QFC Advantage card and believe that you bought recalled meat from a QFC store, you may be eligible to join the lawsuit. Click here to fill out the sign-up request form, or you can contact Hagens Berman attorneys.
QFC
What is the QFC Advantage Card?
 
 
The Advantage Card is known in the grocery industry as a Customer Loyalty Card. Customers who sign up for QFC's Advantage Card receive special discounts on selected items, but gives the grocery store chain the ability to track consumers purchases in order to enhance their marketing efforts. In addition, grocery chains which offer affinity card programs often use the database and shopping pattern data to send users coupons and other marketing material. According to the complaint, QFC tracks every purchase made by consumers presenting the Advantage Card, including product description, date of purchase, store of purchase and the price, and saves that data with customer contact information.
What was QFC's response to the meat recall?
On Dec. 23, 2003, QFC received notice from the U.S. Department of Agriculture (USDA) of a recall of approximately 10,410 lbs. of raw meat that may have been contaminated with the infectious agent that causes mad cow disease. QFC did not act immediately on the recall notice but initially responded by denying that it had any of the tainted meat. On December 24 QFC pulled the meat from its shelves, but the company took no steps to directly warn consumers. It was not until Dec. 27 that QFC posted small signs in its stores recalling the tainted beef, according to the complaint. During that four day period when QFC was silent hundreds of consumers may have eaten the meat.
Can QFC determine if an Advantage Card holder purchased the potentially dangerous meat?
Yes. In fact, consumers can now contact QFC directly and the company will provide information about meat purchases ? but only if you ask. Hundreds of other consumers who purchased the meat and are unaware of the situation have not heard from QFC, the complaint states.
Why was QFC sued even though they pulled the meat? Under Washington law since QFC ground the meat it is deemed a manufacturer and is strictly liable for any unsafe product. In addition QFC possessed specific and easily obtainable information on which customers purchased the recalled meat, but did not act to inform customers, the suit states. Considering the potential danger and risk of worry for consumers, and the ease of contacting consumers using database information, simply pulling the meat from the shelves and belatedly posting small signs was not an adequate response, according to the complaint.
What information on customer purchases does QFC track with the Advantage Card? QFC tracks every purchase that a customer with an Advantage Card makes, regardless of whether discounts are offered or not, according to the complaint.
Does the recently announced larger-than-expected recall of beef affect the lawsuit? No. Regardless of the size of the beef recall, attorneys believe the facts in the case remain the same.
How can I find out if I bought recalled meat from QFC? If you believe that you may have purchased recalled meat from a QFC store, and you have an Advantage Card, you can contact QFC and ask if your record shows you purchased recalled beef. You can contact QFC at 866-221-4141.
Isn't QFC prohibited by privacy laws from contacting consumers with warnings like this? No ? the suit notes that the company will return car keys returned to the store if the keys have an Advantage Card attached. According the complaint, If QFC can return car keys by mail, why can't they send a notice saying the meat a customer purchased in their store could cause an incurable, fatal disease? Further privacy laws would prevent QFC from disclosing information to third parties, disclosing the information to the customer whose card it is does not violate privacy laws. For example, if a trade group wanted to know the names of consumers who purchased a given drug sold at QFC, disclosure of that private information might be a privacy concern. However, disclosure to a consumer of his own records is not.
Mad Cow Disease
What is Mad Cow disease? In cows, mad cow disease is defined as bovine spongiform encephalopathy (BSE), and is a progressive neurological disease. The human disease variant is know as Creutzfeldt-Jakob Disease (vCJD), which is a rare brain disorder that causes a rapid, progressive dementia and is always fatal, according to the complaint.
Where can I get more information on Mad Cow disease? The USDA provides information on the disease at www.usda.gov/.
What should I do if I believe that I've eaten recalled meat? According to the complaint, no screening tests or treatments have been found for Creutzfeldt-Jakob disease. Those who suspect they've eaten recalled meat should contact their physician for more information.
 
 
 
Do Stores That Offer Loyalty Cards Have a Duty to Notify Customers of Product Safety Recalls? A Recent Suit Raises This Novel Question By ANITA RAMASASTRY ----
Thursday, Aug. 05, 2004
An interesting new Washington state court suit raises an important question: If a retailer benefits from collecting personally identifiable information about its customers, does it have a corresponding duty to use such data to alert its customers that products they've bought have been recalled for health or safety reasons? And if so, could turning over private data to companies actually create benefits, as well as privacy risks, for the consumer?
In the suit, consumer Jill Crowson is suing her grocery store -- Quality Food Center (QFC), a subsidiary of Kroger -- for negligent infliction of emotional distress and disregard of a "duty to warn" under the Washington Product Liability Act. Crowson alleges in her complaint that QFC failed to alert her family that ground beef it had sold them had been recalled in December's mad-cow scare.
Yet, Crowson says, QFC easily could have done so through information it maintained connected with her Advantage card - a "loyalty card" that meant QFC had Crowson's name, address and purchasing information. According to her complaint, QFC tracks every purchase made by consumers presenting the Advantage Card, including product description, date of purchase, store of purchase and the price, and saves that data alongside customer contact information.
Now, Crowson says, her family members "feel like walking time bombs" knowing they may be infected with the human form of mad-cow disease which the complaint states may have an up-to-30-year incubation period. And they are not the only ones: Crowson is seeking class action status for herself and what she believes are "hundreds" of similarly-situated Washington customers at QFC's approximately 40 stores in the state.
Some lawyers think Crowson's suit is a stretch. Federal law does not impose on companies a specific duty to notify consumers when tainted meat is recalled under the direction of the U.S. Department of Agriculture (USDA), as was the case here. Also, Crowson and her family, and the class she seeks to represent, are suing based on fear (and possible future harm), not current illness. Moreover, the chance they will actually get Mad Cow Disease some time in the future are apparently remote.
Nevertheless, the lawsuit has strong intuitive appeal: QFC could have saved the Crowsons and others like them a lot of worry, and perhaps sleepless nights, with what appears would have been minimal effort, using information at its digital fingertips. And the court has already once refused to dismiss it - finding that there were sufficient factual questions about the beef and about QFC's responsibility to the Crowsons, to merit further exploration of the evidence, through discovery and in the courtroom.
Regardless of the outcome of Crowson's suit, it underscores the need for retailers and policymakers to examine what sort of responsibilities come with private data gathering under loyalty card schemes.
The Lawsuit: The Chronology of Facts Alleged, and the Loyalty Card at Issue
On December 22 and 23, 2003, Crowson bought ground beef from a QFC store. Also on December 23, 2003, the USDA recalled Washington beef after it confirmed that a cow slaughtered in Washington had been infected with Mad Cow Disease. But Crowson says QFC did not pull the affected meat from its shelves until December 24, and did not post signs in its stores announcing the recall until December 27. By then, the Crowson family had eaten the meat.
Crowson states that she only learned of the recall by reading an article in her local newspaper. She said she subsequently called the supermarket chain, then faxed QFC a letter asking that her purchase be traced through her QFC Advantage card. On January 10, she was notified that her ground beef purchase was indeed from the recalled batch.
Crowson says that what QFC allegedly did in response to the recall - pulling the beef from shelves the next day, and posting signs three days after that -- was far from enough. She says it should have immediately warned customers who had bought possibly tainted meat through newspaper, radio and television advertising -- and by contacting individually those who, like her, had Advantage cards. Its failure to do so, she says, is what makes the company liable to her and other shoppers.
The Advantage Card is known in the retail industry as a customer "loyalty card" - providing discounts on specific items, in exchange for consumer information that will aid in better tailoring the company's marketing efforts. Combining the data from one's loyalty card application with data from other commercial databases or public records (for examples, mortgage records, or court filings) can often allow a very specific profile of each consumer.
Some states limit the types of information that a grocery store can collect from you when you register for a loyalty card. For example, California state law prohibits a grocery store from requiring that you turn over your social security or your driver's license number.
Companies, of course, stress the potential savings that might result from use of a loyalty card. Consider, for instance, the sales pitch on the QFC website it reads: "If you don't have a QFC Advantage Card, you're missing out! The Advantage Card is a powerful new way to save on the groceries you buy every day. It gives you the best of all possible worlds: premium quality, superb service and lower prices. That's something no other grocery store can match. So make sure you take advantage of the big savings."
Privacy advocates complain that loyalty cards result in the improper use - and, often, sale to third parties - of customers' private information. QFC apparently doesn't sell customers' data to third parties, however. Its website promises that "QFC will not release your name to any list service or manufacturer, and that such information will be held in the strictest of confidence-even within our company."
Privacy advocates also warn, however, that even if third-party sales of data are not allowed, the data compiled can always be accessed with a subpoena or warrant and used against the customer in court proceedings. Meanwhile, consumer advocates claim that certain loyalty cards don't really offer the savings they promise. Nevertheless, numerous stores employ loyalty cards.
Turning the Privacy Debate on Its Head: With Great Information, Comes Great Responsibility?
The Crowson lawsuit turns the privacy debate on its head. Typically, privacy advocates ask retailers to safeguard the personal information they collect about their shoppers. In this case, in contrast, plaintiff is asking that QFC delve into its database to notify her about a meat recall.
QFC does this very thing if a consumer loses his or her keys with an Advantage Card attached to them - returning the keys free of charge. So Crowson's attorney, Steve Berman, asks: "If they can contact you over a lost set of car keys, why couldn't they contact you and tell you that the beef you purchased could kill you?"
According to some news reports, QFC was reluctant to call customers regarding the recall based on privacy concerns. But in this case, the concerns seem misplaced. No privacy law is violated when a consumer communicates with the customer herself regarding private information - indeed, every offer the customer receives is, in a sense, this kind of communication. When the customer is receiving personalized discounts based on her purchase history, why can't she receive personalized health and safety warnings based on that history, too?
Was There a Duty to Warn Here?
From the law's perspective, the question will be not whether QFC ideally should have warned the Crowsons - of course it should have. The question will be if it had a legal duty to do so. Such a duty would come from either the common law of torts, which allows claims where there is a duty to behave reasonably to prevent foreseeable harm to others. . Or it might come from the Washington product liability statute - which, as noted above, creates a "duty to warn" in certain situations.
And of course, if there is no current duty, the legislature may see fit to pass a statute creating such a duty. :It may seem more prudent, however, for retailers to voluntarily assume such a responsibility. When companies benefit from collecting customer information, shouldn't they also assume a duty to protect customers from known risks associated with that very information? Some risks, of course, may be a matter of opinion. But this one was not: The fact of the risk was acknowledged by the USDA recall of the meat. With this kind of clear notice of the risk, it seems that QFC either does - or ought to - have a duty to protect customers from this risk.
Of course, should a retailer not wish to take on this responsibility, it can also change its loyalty program. QFC and other retailers could still track consumer purchases without asking them for personally identifiable information.
 
 
 
FindLaw's Writ - Ramasastry: Mad Cow in the USA
 
 
 
Family to sue grocery chain
A Seattle family that ate beef linked to the US's only known case of BSE has filed a classaction lawsuit against the grocery chain QFC, claiming the company negligently exposed them and others to "highly hazardous" meat and did not properly notify them that they had bought it.34 The suit contends that Jill Crowson and her family bought and later ate ground beef from their local QFC that was part of a batch processed at Vern's Moses Lake Meats on 9 December 2003 and included meat from the diseased Holstein. The beef was later shipped to wholesalers and retailers in Washington, Oregon, California, Idaho, Montana and Nevada.
After government scientists confirmed on 23 December that the Holstein was infected with BSE, businesses began pulling potentially affected beef from store shelves under a voluntary recall. But, the family's suit claims, although QFC was aware of the recall, the store did not begin pulling the beef from about 40 of its stores until 24 December. The company also did not try to warn customers about the recalled beef until 27 December – and only then with small, inconspicuous signs inside the stores, the suit claims. The family only learned QFC had
9
sold any of the beef in question after reading a news story on 10 January about a man who discovered his family had eaten affected beef that he bought at a local QFC store, Crowson said. She later called QFC and faxed the company a signed letter asking that it track purchases made on her QFC Advantage Card, and on 12 January the company notified Crowson that the beef she bought and served to her family was, in fact, part of the recalled batch, she said.
The family seeks unspecified damages for emotional distress and medical monitoring costs. Crowson said her reason for bringing the lawsuit is not about money. "The more I've thought about this, the angrier I've gotten," she said. Neither the company nor its parent corporation, Kroger, have commented.
 
 
 
snip...see full text and more here on this litigation ;
 
 
 
 
 
===============================================================
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,
Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
 
 
PR-26
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS
R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway
Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.
*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
119
 
 
 
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.
 
 
 
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
Authors
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.
Content
Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.
The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.
Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross species barriers
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.
 
 
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
Wiebke M. Wemheuer,* Sylvie L. Benestad,† Arne Wrede,* Ulf Schulze-Sturm,* Wilhelm E. Wemheuer,‡ Uwe Hahmann,* Joanna Gawinecka,§ Ekkehard Schu¨ tz,‡ Inga Zerr,§ Bertram Brenig,‡ Bjørn Bratberg,† Olivier Andre´ oletti,¶ and Walter J. Schulz-Schaeffer*
From the Prion and Dementia Research Unit,* Department of Neuropathology, and the National Transmissible Spongiform Encephalopathies Reference Center,§ Department of Neurology, University Medical Center Goettingen, Goettingen, Germany; the Department of Pathology,† National Veterinary Institute, Oslo, Norway; the Institute of Veterinary Medicine,‡ Faculty for Agricultural Sciences, University of Goettingen, Goettingen, Germany; and Animal Health,¶ Interactions Hôte Agent Pathogène, Ecole Nationale Ve´te´rinaire de Toulouse, Toulouse, France
Transmissible spongiform encephalopathies such as scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and bovine sporadic encephalopathy in cattle are characterized by the accumulation of a misfolded protein: the pathological prion protein. Ever since bovine sporadic encephalopathy was discovered as the likely cause of the new variant of CJD in humans, parallels between human and animal transmissible spongiform encephalopathies must be viewed under the aspect of a disease risk for humans. In our study we have compared prion characteristics of different forms of sheep scrapie with those of different phenotypes of sporadic CJD. The disease characteristics of sporadic CJD depend considerably on the prion type 1 or 2. Our results show that there are obvious parallels between sporadic CJD type 1 and the so-called atypical/Nor98 scrapie. These parelleles apply to the deposition form of pathological prion protein in the brain, detected by the paraffin-embedded- tissue blot and the prion aggregate stability with regard to denaturation by the chaotropic salt guanidine hydrochloride. The same applies to sporadic CJD type 2 and classical scrapie. The observed parallels between types of sporadic CJD and types of sheep scrapie demonstrate that distinct groups of prion disease exist in different species. This should be taken into consideration when discussing interspecies transmission. (Am J Pathol 2009, 175:2566–2573; DOI: 10.2353/ajpath.2009.090623)
snip...
Discussion
In humans, different prion types are linked with clinically and neuropathologically distinct prion diseases.8 The present work emphasizes that the differences in deposition characteristics and stability with regard to denaturation between atypical/Nor98 and classical scrapie also account for different prion types. Moreover, the two scrapie types that have been characterized show a number of striking similarities with human PrPSc types in sporadic CJD. Hence, we propose that the existence of different PrPSc types might be a common denominator of prion diseases in humans and animals. Since these two prion types show an across-the-species comparability with similar biochemical and pathological characteristics, it is most likely that they exist due to a different conformational pattern of the disease-related prion protein.
snip...
Conclusion
As the prion protein is a highly conserved protein in terms of evolution, parallels between characteristics of prion types in TSEs of different species are of interest. In the present study, we report previously unknown similarities between sheep scrapie forms and human sporadic CJD types. We propose that the observed similarities between sheep scrapie and sporadic CJD in humans justify new interspecies groups of prion diseases in which prion types, not prion strains, are the major determinant for prion disease forms. While epidemiology implies that classical scrapie is not related to human TSEs,47 the atypical/Nor98 scrapie risk for human transmission has not yet been elucidated. Currently there is no compelling evidence that sCJD has a different origin than sporadic genesis. However, the finding of prion types with an across-the-species comparability might provide further understanding of the pathogenesis in prion diseases.
Prion Types Encode Interspecies TSEs 2571 AJP December 2009, Vol. 175, No. 6
 
 
 
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
 
 
 
 
 
BSE: TIME TO TAKE H.B. PARRY SERIOUSLY
If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...
 
 
 
 
 
Wednesday, February 16, 2011
 
 
IN CONFIDENCE
 
SCRAPIE TRANSMISSION TO CHIMPANZEES
 
IN CONFIDENCE
 
Sunday, April 18, 2010
 
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
 
 
 
Monday, April 25, 2011
 
 
Experimental Oral Transmission of Atypical Scrapie to Sheep
 
Volume 17, Number 5-May 2011
 
 
 
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
 
 
 
 
12/10/76
 
 
AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE
 
 
Office Note CHAIRMAN: PROFESSOR PETER WILDY
 
snip...
 
 
A The Present Position with respect to Scrapie A] The Problem Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries. The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep. It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible. 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).
 
 
 
 
 
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
 
 
 
 
 
 
 
 
Sunday, January 22, 2012
 
Chronic Wasting Disease CWD cervids interspecies transmission
 
 
 
 
Friday, October 26, 2012
 
***CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT PRODUCTS, BAITING, AND MINERAL LICKS
 
Friday, November 09, 2012

 
*** Chronic Wasting Disease CWD in cervidae and transmission to other species

 
 
 
 
Friday, December 14, 2012

 
Susceptibility of domestic cats to chronic wasting disease

 
 
 
 
Tuesday, December 25, 2012
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
 
 
 
Thursday, August 4, 2011
 
 
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011 (SEE VIDEO)
 
 
 
 
Sunday, August 21, 2011
 
 
The British disease, or a disease gone global, The TSE Prion Disease (SEE VIDEO)
 
 
 
 
Sunday, September 6, 2009
 
MAD COW USA 1997 (SEE SECRET VIDEO)
 
 
 
 
 
Saturday, March 5, 2011
 
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
 
 
 
POLITICAL BSe and CJD and THE WOW FACTOR $$$
 
 
 
Monday, September 26, 2011
 
 
 
Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS, gCJD, hvCJD, sCJD, TSE, PRION, update 2011

 
Wednesday, March 28, 2012
 
 
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion poker goes up again $
 
 
Tuesday, December 25, 2012
 
 
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25, 2012
snip...
USA PRION UNIT LATEST HUMAN TSE PRION DISEASE UPDATE AUGUST 14, 2012
National Prion Disease Pathology Surveillance Center Cases Examined1 (August 14, 2012)
1996 & earlier 28 cases of sporadic CJD.
see steady increase to ;
2010 cases of sporadic CJD 216.
2011 cases of sporadic CJD 214.
snip...
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 8 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 10 (9 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded.
The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2224 cases of sporadic Creutzfeldt-Jakob disease (sCJD).
snip...see full case reports here ;
 
 
 
please see full text for Texas and USA with more updated data on the TSE BSE CWD Scrapie CJD prion disease outbreak in the USA here ;
Tuesday, December 25, 2012
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25, 2012
 
 
 
Friday, August 10, 2012
 
Incidents of Potential iatrogenic Creutzfeldt-Jakob disease (CJD) biannual update (July 2012)
 
 
 
 
 
Tuesday, December 18, 2012

 
Bioassay Studies Support the Potential for Iatrogenic Transmission of Variant Creutzfeldt Jakob Disease through Dental Procedures

 
Sunday, December 9, 2012

 
Prions, prionoids and pathogenic proteins in Alzheimer disease

 
Wednesday, May 16, 2012
 
 
 
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
 
 
 
Proposal ID: 29403
 
 
 
Monday, August 20, 2012
 
CASE REPORTS CREUTZFELDT-JAKOB DISEASE: AN UNDER-RECOGNIZED CAUSE OF DEMENTIA
 
 
 
Friday, October 05, 2012
 
 
Differential Diagnosis of Jakob-Creutzfeldt Disease
 
 
 
 
 
see the Duke, Pa, Yale, and Mexican study here, showing the misdiagnosis of CJD TSE prion disease as Alzheimers ;
 
Monday, July 23, 2012
 
 
The National Prion Disease Pathology Surveillance Center July 2012
 
 
IT is of my opinion, that the OIE and the USDA et al, are the soul reason, and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion diseases, including typical and atypical BSE, typical and atypical Scrapie, and all strains of CWD, and human TSE there from, spreading around the globe.
 
 
 
I have lost all confidence of this organization as a regulatory authority on animal disease, and consider it nothing more than a National Trading Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.
 
 
 
JUST because of low documented human body count with nvCJD and the long incubation periods, the lack of sound science being replaced by political and corporate science in relations with the fact that science has now linked some sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call for this organization to be dissolved. ...
 
 
 
Tuesday, July 17, 2012
 
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th General Session, 20 - 25 May 2012
 
 
 
Thursday, December 20, 2012
 
 
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe WITH BOVINE MAD COW DISEASE
 
 
 
 
 
 
 
as a layperson, these are my opinions, from the sound science to date documented here from, through daily investigation of the TSE prion science over the last 15 years. ...
 
 
 
 
TSS

posted by Terry S. Singeltary Sr. at 10:10 PM