Monday, July 27, 2009

U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ?

(strange, this would have been my mothers birthday, but she had been dead for 8 years hvCJD confirmed here in the U.S.A....TSS)




video







CBC’s The National

October 17, 2005

Safe To Eat?

PETER MANSBRIDGE (HOST):

Safe To Eat? She thought her son died of a random illness, one with no known cause, no cure. Now some scientists are questioning whether there's a new link to mad cow disease. Kelly Crowe reports. -

For years, scientists have known that B.S.E. causes variant Creutzfeldt-Jakob disease. What some people call the human form of Mad Cow Disease. But another form of C.J.D., Sporadic C.J.D., has always confounded them. The most common theory has been that the deadly illness occurs spontaneously with no known cause. Now some of the world's leading scientists in the field are having another look at sporadic C.J.D. and the possibility that it too is linked to mad cow. Here's Kelly Crowe with a feature report.

KELLY CROWE (REPORTER):

It starts out slowly. At first, the victims don't know what's wrong with them. They can't put their finger on it. They keep making little mistakes. The spelling mistakes that just look sloppy... numbers become easily confused... the words on the page become blurry. It's the beginning of a terrifying slide in to dementia and death. That's what happened to Jeff Schwan. Little by little, his brain was ravaged by a disease so rare, his mother had never even heard of it.

UNIDENTIFIED WOMAN (MOTHER OF JEFF SCHWAN):

And finally on August 11th, we received words you'll never want to hear. He has a disease that has no treatment and no cure, and we just tried to take that in.

NORMAN FOSTER (DOCTOR):

Check eye movements, look right here at my finger.

KELLY CROWE (REPORTER):

It was Dr. Norman Foster who discovered the terrible truth. He specializes in diseases of the brain, and he's the one who finally figured out what was wrong with Jeff Schwan.

NORMAN FOSTER (DOCTOR):

The major problem was a seizure disorder, and that was investigated and treated, but despite treatment, he became progressively worse. And it was unclear at the time what was causing these seizures, and it was suspected that this was due to an encephalitis or meningitis or some other problem, and I strongly advocated that everything be done to identify what the cause of this is, and that led to a brain biopsy. When we examined the tissue under the microscope, we were somewhat surprised to find evidence of Creutzfeldt-Jakob disease.

KELLY CROWE (REPORTER):

Jeff Schwan died from a mysterious illness called Sporadic Creutzfeldt-Jakob disease or Sporadic C.J.D. It's a rare and fatal brain-wasting disease that seems to strike out of nowhere. But was it really just bad luck that killed this healthy 26-year-old man, or is there another explanation? Sporadic Creutzfeldt-Jakob disease is a type of prion disease. Prions are proteins found in humans and other mammals, but when an altered form of the prion appears, it somehow starts a critical chain reaction turning healthy prions in to deadly ones that ultimately destroy the brain. Prion diseases are always fatal. There is no cure, no treatment. And science now knows that prion diseases can be spread by eating meat. It was first realized here in Papua New Guinea back in 1957 where a brain-wasting disease called Curu was sweeping through a tribe of cannibals.

Scientists realized these people were developing Curu after feasting on the remains of their dead who were already infected. It was the first evidence that prion diseases could be spread through eating infected material. 30 years later, British cattle began developing a prion disease. It was called B.S.E. or Mad Cow Disease. It was spread when the animals ate feed made from diseased cattle. Then young Britons began dying, and scientists realized humans could catch a prion disease from eating infected beef. That disease is called Variant C.J.D. So far, it has claimed 170 victims. But none of that seems to explain what happened to Jeff Schwan. He had the other prion disease, the one that is thought to strike at random, so-called Sporadic C.J.D. Like the other prion diseases, the brain fills with sponge-like holes, but scientists don't know what causes sporadic C.J.D., and some are asking, could it also be caused by eating meat? Here's one possible clue: The disease sometimes shows up in clusters in people who live near each other. It happens too often to be explained only by chance. British epidemiologist Simon Cousins worked on two scientific studies that documented clusters of the disease in both England and France. The studies concluded that it must be caused by something on the outside, that it can't be just a spontaneous disease.

SIMON COUSINS (EPIDEMIOLOGIST):

The spontaneous event would be, doesn't really explain why they might be clustering. So the clustering is pointing one in the direction of thinking from time to time people are exposed to a common external source.

KELLY CROWE (REPORTER):

One common external source, infected meat. It's a frightening possibility that is being actively investigated by some European scientists. Here in Switzerland, there was an epidemic of Mad Cow Disease in the 1990s, and now they're seeing a more than doubling in the rate of Sporadic C.J.D. Swiss scientists think there might be a connection.

ADRIANO AGUTZY (SCIENTIST):

What we need to find out is whether the whole problem of the enhanced Creutzfeldt-Jakob does, indeed, have something to do with mad cow's disease, but we certainly did have our definite window of exposure, and so if we now, if we had B.S.E. ten years ago and now we have enhanced Creutzfeldt-Jakob disease, it's unavoidable to ask the question whether the two phenomena are related.

KELLY CROWE (REPORTER):

DR. Adriano Agutzy is one of the world's experts on prion diseases. He says he has ruled out most of the other explanations, and now his main working hypothesis is that at least some Sporadic C.J.D. in Switzerland could be another form of human Mad Cow Disease.

ADRIANO AGUTZY (SCIENTIST):

But this by no means excludes that B.S.E. may manifest itself in humans with different characteristics, and maybe B.S.E. in Switzerland is also different from B.S.E. in the U.K., and then variant C.J.D. will also be different. So I think from the U.K. experience, it's impossible to draw the conclusion that B.S.E. will only give rise to what we know as variant C.J.D.

KELLY CROWE (REPORTER):

What it means is cattle infected with prion disease might be causing Sporadic C.J.D. To find out, the scientists are trying to match the tissue from infected Swiss cattle with the tissue from Swiss victims. If the tissue looks the same on the lab tests, then it will be strong evidence the two are connected. Right next door in Italy, they might have already made that connection. This doctor was studying the brains from B.S.E. infected cattle when he noticed a form of the disease he'd never seen before. He realized it was a new form of Mad Cow Disease. It was the first time scientists realized there could be more than one kind of prion disease in cattle.

UNIDENTIFIED MAN:

So our assumption is that since there is this biochemical similarities together with this, we think there might be a connection between the two.

KELLY CROWE (REPORTER):

He got a second shock when he ran the new cattle prion through the lab tests. It looked exactly like Sporadic C.J.D. He could hardly believe his eyes. He was looking at possible proof that humans could catch a second prion disease from cattle.

UNIDENTIFIED MAN:

Yes, this is only a biochemical evidence because at the beginning when B.S.E. has been discovered and the Variant C.J.D. had been discovered in the U.K., They found the single cell. I mean, the biochemical part of both B.S.E. and variant were similar. We found the same biochemical. There are pathological similarities and ecological similarities.

KELLY CROWE (REPORTER):

There is still one more step to prove the link. This new strain of B.S.E. will be injected into mice that have human genes. It will take two years, but the results will bring scientists a little bit closer to the answer of whether Sporadic C.J.D. is caused by meat. ADRIANO AGUTZY (SCIENTIST):

I think that that is a possibility. Personally, I would say that it's possible that some of the cases are caused, I mean, maybe what would cause Sporadic C.J.D. is a collection of different diseases, and some of it could actually be transmission of B.S.E.

UNIDENTIFIED MAN:

It might be a possibility because it is an infectious disease. I mean, if you get a piece of brain of this with classic C.J.D. and you inoculate the animal, you transmit the disease, but on the other side, it's not clear whether the animal transmit the disease to man.

KELLY CROWE (REPORTER):

Scientists agree that cattle prion disease must be kept out of the human food supply. The problem is finding it before the animal is slaughtered. Bitter experience has already proven that the disease can be lurking even as officials boast that their herd is B.S.E.-free. After years of making those claims, the U.S. has had to admit to a homegrown case of B.S.E. in a Texas cow this past June. And that case was discovered only after testing was dramatically increased. And yet the U.S. and Canada are still only testing cattle that look sick. And with that kind of testing and millions of animals slaughtered every year, the disease is easy to miss. A lesson the Italians already learned. In Italy, they didn't know for sure that they had Mad Cow Disease until they started testing, not just the animals that looked sick, but every single animal over 24 months that goes into the food chain. Now four years later, they've only had one animal that looks sick, but they've found more than 130 cases of Mad Cow Disease in healthy looking animals. In other words, if they hadn't been testing those 130 animals would have gone into the food chain. In North America, they're only looking at symptomatic cases, zero so they could be missing a lot of disease.

UNIDENTIFIED MAN:

Sure, they take only neurological cattle, cattle with neurological symptoms or downer cattle. So this is the so-called passive surveillance. When you have neurological, you make the potential diagnosis of C.J.D. And the only way to get rid of this is that all the animals should be tested, and people at least buy a piece of meat to say this is B.S.E.-free.

KELLY CROWE (REPORTER):

Dr. Agutzy says the United States isn't trying hard enough to find prion disease in its cattle.

ADRIANO AGUTZY (SCIENTIST):

I think that in North America, there is a huge problem because North America has refused for many years to put in place any kind of serious surveillance of cattle, and I think this is a disgrace, and it really cries to Heaven about the fact that particularly the U.S. has just refused to even take into consideration the possibility that B.S.E. may be prevalent. It's a huge problem.

KELLY CROWE (REPORTER):

It's also not clear how widespread Sporadic C.J.D. is. The final diagnosis can only be made after death by examining the brain in an autopsy, but today autopsies are rarely done. And although Sporadic C.J.D. is a rare condition, estimated at one in a million, Dr. Norman Foster suspects the rate is higher.

NORMAN FOSTER (DOCTOR):

In many states in the United States, if a physician suspects a case, they can report it as a public health problem, but there's no mechanism to investigate or no way to pursue this in a systematic way.

KELLY CROWE (REPORTER):

So you could be missing lots of cases?

NORMAN FOSTER (DOCTOR):

So we are missing lots of cases.

KELLY CROWE (REPORTER):

Jeff Schwan is on the official record as just another unfortunate victim of a rare disease that seems to strike for no reason. And for his mother, it is the unanswered questions that weigh most heavily on her shoulders.

UNIDENTIFIED WOMAN (MOTHER OF JEFF SCHWAN):

So all of these people who are dying of Sporadic C.J.D., they don't have an answer for. It's very, very frustrating because we want answers.

KELLY CROWE (REPORTER):

To get those answers, she must wait for the slow deliberate pace of science. Kelly Crowe, CBC News, Sterling Heights, Michigan.



http://www.healthcoalition.ca/cbccjd.pdf




P.S.S. (July 31, 2009)



PLEASE REMEMBER, (and i had to wrote to terry schwann to make sure my mind was not decieving me, and she did confirm it was NOT), that there was another young man, 28 years old, in the same hospital, the same week as jeff schwann 26 was, that he too had cjd.



>>>There was another young man, 28, diagnosed with CJD as well. Same floor, same week. He died in Feb. 2002 I think. This young man's aunt contacted me some time later and confirmed CJD, but the young man's wife really did not want any contact or discussion--SNIP...TSS...He was in the military and had been stationed in Europe...and I never heard the final diagnosis...but I can guess...sCJD. They lived in the Port Huron area (Michigan). Dr. Norman Foster (in the video) diagnosed him as well. I believe he's now practicing in Utah.<<<


TSS



WHY DID THIS VIDEO NOT SHOW ON EVERY NEWS CHANNEL IN THE U.S.A. $$$


IT IS A DAMNING VIDEO !!!


I WATCHED THIS RECENTLY, and had never seen it. i was so mad, i was spitting nails out faster than a framing gun.


WHY DID THE CANADIAN MEDIA ONLY PRESENT THIS TO THE U.S.A. PUBLIC (thank you very much though), and why has the U.S.A. MEDIA FAILED US ???


WHY DID R-CALF NOT SHOW THIS ??? where was r-calf when you needed them back then $$$


Thursday, April 9, 2009

Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed



http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html



http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html#comments



Sunday, April 12, 2009 r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada



http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html



http://prionunitusaupdate2008.blogspot.com/2009/04/cjd-foundation-sides-with-r-calfers-no.html#comments



Tuesday, July 14, 2009

U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST



WHERE did we go wrong $$$



http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html



Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]



http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html



Transmissible mink encephalopathy - review of the etiology



http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.html



Wednesday, July 1, 2009

Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)



http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html



Monday, June 01, 2009 Biochemical typing of pathological prion protein in aging cattle with BSE

SOMETHING TO PONDER ???

O.K. confusious asks, IF all these new atypical BSEs i.e. new strains of mad cow disease is just an 'OLD COW PRION DISEASE', why then can not the 'old human prion disease' such as the sporadic CJD, be from an 'old cow prion disease', same as the nvCJD 'young people mad cow disease' (which also happens in 74 year old), but why cannot the 'old cow prion diseases', i.e. l-BSE, h-BSE, and ibncBSE, cause the 'old people prion disease', which looks like sporadic CJD. seems that is what some of the pathology is showing ???

OH, that probably makes too much sense, and that the only answer could be that it's all just a happenstance of bad luck and or a spontaneous event, that just happens out of the clear blue sky $$$

IF this is the case, then where are all the SPONTANEOUS BSE CASES OF MAD COW DISEASE IN THE U.S.A., AND WHERE HAVE THEY BEEN BURIED IN THE USA OVER THE LAST 25 YEARS ???



http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html



USDA FDA CERTIFIED MAD COW FEED BAN of August 4, 1997, i.e. BSE FIREWALLS, never existed, it was nothing more than ink on paper ;

10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

___________________________________

PRODUCT

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.

REASON

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI

___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html

NEW URL



http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm



Thursday, March 19, 2009 MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$



http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html



Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009



http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html



U.S.A. PLAYING A SERIOUS GAME OF 'PASS IT FORWARD' WITH T.S.E.'s ...TSS



Friday, July 24, 2009

UW Hospital and Clinics Addresses Creutzfeldt-Jakob Disease Risk



http://creutzfeldt-jakob-disease.blogspot.com/2009/07/uw-hospital-and-clinics-addresses.html




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




video

Labels: , , , , , , , , , ,

Friday, July 24, 2009

UW Hospital and Clinics Addresses Creutzfeldt-Jakob Disease Risk

UW Hospital and Clinics Addresses Creutzfeldt-Jakob Disease Risk

Media Inquiries

mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000601/!x-usc:mailto:news@uwhealth.org

MADISON - On Monday, July 20, UW Hospital and Clinics received a confirmed diagnosis of likely-sporadic Creutzfeldt-Jakob Disease (CJD) in a patient who underwent brain surgery at our hospital on June 11.

During a press conference held by UW Hospital and Clinics following the confirmed diagnosis, Senior Vice President for Medical Affairs and Associate Dean for Hospital Affairs Carl Getto explained, "Our primary concern is to ensure our patients are fully aware and informed about this extremely rare occurrence."

CJD is an extremely rare and progressive neurological disease that affects approximately one person per million per year worldwide. It can be transmitted by direct contact of brain tissue or spinal cord fluid from an infected person with brain tissue or spinal cord fluid of another individual.

CJD was not suspected at the time of the June 11 surgery to remove a brain tumor. When the patient's condition deteriorated rapidly in the weeks following surgery, additional tests were performed, and CJD was confirmed.

"In this case, the individual had a space occupying lesion, which provided the diagnosis for why the symptoms might have been occurring. That is why CJD was not considered a possibility at the time of the surgery," explained UW Health infectious disease physician Nasia Safdar, MD.

Because the means of CJD transmission are specific and limited, staff are not at risk. From the patient perspective, there has not been a single reported case worldwide of CJD transmission by surgical instruments since 1976, when current sterilization and processing techniques were adopted. Nevertheless, the infectious agents in CJD – called prions – are considered more resistant than other organisms to standard disinfectants and sterilization procedures

"Although the likelihood of CJD transmission is virtually non-existent," said Getto, "we have taken immediate and extraordinary aggressive measures to ensure that all surgical instruments used during this procedure are re-sterilized according to CJD-specific sterilization processes as recommended by the Centers for Disease Control."

In addition, UW Hospital and Clinics leaders are taking the following steps: •Notifying through a letter and personal phone call from medical staff a subset of 53 neurosurgery patients who underwent within-brain and spinal cord procedures between June 11 and July 20 •Conducting surgery with instruments that were definitely not affected by the June 11 procedure •Resterilizing and reprocessing all other instruments using enhanced sterilizing techniques and disinfecting agents, per Centers for Disease Control recommendations "We have notified 53 neurosurgery patients and offered them our assistance, information and reassurance. These surgical patients were only those who were undergoing surgery within the brain," explained Getto.

The 53 patients will have a follow up appointment with their neurosurgeon and be offered an appointment with a neurologist. If further neurologic or psychologic care is necessary, UW Hospital and Clinics will provide the necessary resources to the patients.

Other hospitals in the U.S. have experienced similar situations, including Tulane Medical Center, Emory Healthcare and Froedtert.

"We are confident that we have followed standard procedures and followed the best procedures recommended to us," concluded Getto. "Our processes are exactly what you should expect from a quality hospital."

Common Concerns Related to Creutzfeldt-Jakob Disease

In addition, Dr. Safdar addresses common concerns in the video FAQs below.

What is the risk of patient exposure to Creutzfeldt-Jakob Disease? Why is exposure risk so low?

Why is UW Hospital notifying patients of the risk? What are the symptoms of Creutzfeldt-Jakob Disease?

Are current patients at risk for Creutzfeldt-Jakob Disease? What should patients who may have been exposed do?

Has possible Creutzfeldt-Jakob Disease exposure occurred at other hospitals? How many people in other hospitals have developed Creutzfeldt-Jakob Disease?

Whom should I contact at UW Hospital if I have concerns?



http://www.uwhealth.org/news/cjdrisk/20673



a simple auto-claving just will not kill this agent, considering the fact this agent can survive ashing to 600 degrees celsius;

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication Paul Brown*,dagger , Edward H. RauDagger , Bruce K. Johnson*, Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§

* Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, and Dagger Environmental Protection Branch, Division of Safety, Office of Research Services, National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France

Contributed by D. Carleton Gajdusek, December 22, 1999

Abstract

One-gram samples from a pool of crude brain tissue from hamsters infected with the 263K strain of hamster-adapted scrapie agent were placed in covered quartz-glass crucibles and exposed for either 5 or 15 min to dry heat at temperatures ranging from 150°C to 1,000°C. Residual infectivity in the treated samples was assayed by the intracerebral inoculation of dilution series into healthy weanling hamsters, which were observed for 10 months; disease transmissions were verified by Western blot testing for proteinase-resistant protein in brains from clinically positive hamsters. Unheated control tissue contained 9.9 log10LD50/g tissue; after exposure to 150°C, titers equaled or exceeded 6 log10LD50/g, and after exposure to 300°C, titers equaled or exceeded 4 log10LD50/g. Exposure to 600°C completely ashed the brain samples, which, when reconstituted with saline to their original weights, transmitted disease to 5 of 35 inoculated hamsters. No transmissions occurred after exposure to 1,000°C. These results suggest that an inorganic molecular template with a decomposition point near 600°C is capable of nucleating the biological replication of the scrapie agent.

transmissible spongiform encephalopathy scrapie prion medical waste incineration

Introduction

The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin. It also has been assumed that the replication of these agents is a strictly biological process (1), although the notion of a "virus" nucleant of an inorganic molecular cast of the infectious beta -pleated peptide also has been advanced (2). In this paper, we address these issues by means of dry heat inactivation studies.

see full text:



http://www.pnas.org/cgi/content/full/97/7/3418



Greetings again,

please believe me when i tell you this goes far far beyond the hamburger/deerburger/elkburger/sheepburger. Pandora's box of the demented has been opened for decades, closing it will be most impossible with current safeguards. until they can perfect a test, not only to confirm TSE agent, but also to differentiate between the many differnt strains (there are over 20 in sheep scrapie, and sheep scrapie is the sole model for CJD studies), they then will have to perfect a test that will differentiate between the many different routes. so, as you can see, this could very well take many more decades to answer these questions. but in the mean time, i will not now or ever accept the 'spontaneous/sporadic' theory without any source and route.

CJD/TSEs MUST BE MADE REPORTABLE NATIONALLY, SUPPORTED WITH A CJD QUESTIONNAIRE TO EVERY VICTIM/FAMILY THAT ASK REAL QUESTIONS PERTAINING TO ROUTE/SOURCE...TSS

Diagnosis and Reporting of Creutzfeldt-Jakob Disease T. S. Singeltary, Sr; D. E. Kraemer; R. V. Gibbons, R. C. Holman, E. D. Belay, L. B. Schonberger



http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=cjd+singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT



2 January 2000

British Medical Journal

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



http://www.bmj.com/cgi/eletters/320/7226/8/b#6117



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


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


http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(03)00715-1/fulltext



http://linkinghub.elsevier.com/retrieve/pii/S1473309903007151



15 November 1999

British Medical Journal

vCJD in the USA * BSE in U.S.



http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406



Thursday, July 23, 2009

UW Hospital warning 53 patients about possible exposure to rare brain disease



http://creutzfeldt-jakob-disease.blogspot.com/2009/07/uw-hospital-warning-53-patients-about.html



http://creutzfeldt-jakob-disease.blogspot.com/



see also ;

Friday, July 17, 2009

Revision to pre-surgical assessment of risk for vCJD in neurosurgery and eye surgery units Volume 3 No 28; 17 July 2009



http://creutzfeldt-jakob-disease.blogspot.com/2009/07/revision-to-pre-surgical-assessment-of.html



Tuesday, August 12, 2008

Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)



http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html



Thursday, January 29, 2009

Medical Procedures and Risk for Sporadic Creutzfeldt-Jakob Disease, Japan, 1999-2008 (WARNING TO Neurosurgeons and Ophthalmologists) Volume 15, Number 2-February 2009 Research



http://creutzfeldt-jakob-disease.blogspot.com/2009/01/medical-procedures-and-risk-for.html




Tuesday, April 21, 2009

Doctor Antonio Ruiz Villaespesa, pathologist and CJD researcher deceased because of Creutzfeldt-Jakob Disease SPAIN



http://cjdusa.blogspot.com/2009/04/doctor-antonio-ruiz-villaespesa.html



Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009

Greetings,

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena’s. North America seems to have the most species with documented Transmissible Spongiform Encephalopathies, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is not recourse, to date.

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, surgical, blood, medical, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub-clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE (one strain TSE in cows), and the nv/v CJD (one strain TSE humans) and that all the rest of human TSE are just one single strain i.e. sporadic CJD (when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al), and that no other animal TSE transmits to humans, to continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...

please see history, and the ever evolving TSE science to date ;

Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009



http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html



Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (TRANSCRIPT)



http://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/UCM171810.pdf



Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)



http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html



Tuesday, July 14, 2009

U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST

WHERE did we go wrong $$$



http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html



Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]



http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html



Transmissible mink encephalopathy - review of the etiology



http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.html



Wednesday, July 1, 2009

Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)



http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html



Monday, June 01, 2009 Biochemical typing of pathological prion protein in aging cattle with BSE

SOMETHING TO PONDER ???

O.K. confusious asks, IF all these new atypical BSEs i.e. new strains of mad cow disease is just an 'OLD COW PRION DISEASE', why then can not the 'old human prion disease' such as the sporadic CJD, be from an 'old cow prion disease', same as the nvCJD 'young people mad cow disease' (which also happens in 74 year old), but why cannot the 'old cow prion diseases', i.e. l-BSE, h-BSE, and ibncBSE, cause the 'old people prion disease', which looks like sporadic CJD. seems that is what some of the pathology is showing ???

OH, that probably makes too much sense, and that the only answer could be that it's all just a happenstance of bad luck and or a spontaneous event, that just happens out of the clear blue sky $$$

IF this is the case, then where are all the SPONTANEOUS BSE CASES OF MAD COW DISEASE IN THE U.S.A., AND WHERE HAVE THEY BEEN BURIED IN THE USA OVER THE LAST 25 YEARS ???



http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html



Sunday, April 12, 2009

CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains



http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html



Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease

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

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

snip...

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

snip...

full text ;



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



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

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

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

From: "Belay, Ermias"

To:

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

Ermias"

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

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

Dear Sir/Madam,

In the Archives of Neurology you quoted (the abstract of which was

attached to your email), we did not say CWD in humans will present like

variant CJD.

That assumption would be wrong. I encourage you to read the whole

article and call me if you have questions or need more clarification

(phone: 404-639-3091). Also, we do not claim that "no-one has ever been

infected with prion disease from eating venison." Our conclusion stating

that we found no strong evidence of CWD transmission to humans in the

article you quoted or in any other forum is limited to the patients we

investigated.

Ermias Belay, M.D.

Centers for Disease Control and Prevention

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

From:

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

To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000601/!x-usc:mailto:rr26k@nih.gov; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000601/!x-usc:mailto:rrace@niaid.nih.gov; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000601/!x-usc:mailto:ebb8@CDC.GOV

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

HUNTERS

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

also,

A. Aguzzi - Chronic Wasting Disease (CWD) also needs to be addressed. Most

serious because of rapid horizontal spread and higher prevalence than BSE in

UK, up to 15% in some populations. Also may be a risk to humans - evidence

that it is not dangerous to humans is thin.



http://www.tseandfoodsafety.org/activities/bse_conference_basel_april_02/2summar



SNIP...END...TSS

Chronic Wasting Disease and Potential Transmission to Humans

Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,? Michael W. Miller,? Pierluigi Gambetti,§ and Lawrence B. Schonberger*

*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; ?University of Wyoming, Laramie, Wyoming, USA; ?Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA

Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from:



http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm



Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWD-associated prions has been demonstrated in an in vitro cell-free experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.

snip...full text ;



http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm



Wednesday, July 1, 2009

Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454–463 (2009)



http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html



Tuesday, July 21, 2009

Transmissible mink encephalopathy - review of the etiology



http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.html



Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]


http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html




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

Labels: , , , ,

Thursday, July 23, 2009

UW Hospital warning 53 patients about possible exposure to rare brain disease

THU., JUL 23, 2009 - 7:13 PM STATE JOURNAL EXCLUSIVE:

UW Hospital warning 53 patients about possible exposure to rare brain disease

By DOUG ERICKSON and MARK PITSCH Wisconsin State Journal mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000260/!x-usc:mailto:wsjcity@madison.com UW

Hospital has told 53 patients they face an “extremely low” risk of contracting a rare brain disorder because they may have been operated on with contaminated surgical instruments.

Those instruments may have been used on a woman who died of the brain disorder Tuesday and had been operated on at the hospital.

Hospital officials say they immediately stopped using the surgical instruments once tests confirmed the woman’s diagnosis. However, the 53 patients all underwent a particular kind of neurosurgery during a 40-day window when the instruments were still in use, said Dr. Carl Getto, the hospital’s chief medical officer.

The hospital plans to continue using the surgical instruments once they go through a heightened sterilization process, an approach questioned by a national expert who said his hospital destroys the instruments in all such cases.

The situation poses no risk to the general public and an “infinitesimal” risk to the 53 patients, Getto said.

The female UW Hospital patient died of Creutzfeldt-Jakob Disease (CJD), an always-fatal neurological disorder that kills about 390 people per year in the U.S. It is characterized by rapidly progressing dementia, with death often coming within a year from the onset of symptoms.

“It’s a horrible situation, and I’m sure the university is as devastated by this as they possibly can be,” said Florence Kranitz, president of the CJD Foundation in Akron, Ohio.

The disease can set off alarm bells because it belongs to a family of human and animal diseases that includes a bovine version often referred to as “mad cow” disease. However, UW Hospital officials said the woman died from a category of the disease distinct from the bovine version.

“This is not mad cow disease,” said Dr. Nasia Safdar, a specialist in infectious diseases who oversees infection control at the hospital. “(People) need not be concerned about that relationship.”

Mad cow disease occurs only in cows, although eating infected beef is thought to be the cause of the variant form of CJD, which accounts for less than 1 percent of all human cases, according to the Creutzfeldt-Jakob Disease Foundation. No case of variant CJD has been documented as originating in the U.S., the foundation said.

UW Hospital officials said the female patient died from the sporadic form of CJD, which appears even though the person has no known risk factors. This is the prevalent form of the disease, accounting for about 85 percent of cases, so it also is referred to as the classic form.

Due to patient privacy, hospital officials would say only that the woman was in her 50s and had been transferred to UW Hospital June 8 from a regional hospital in Wisconsin. The woman suffered an upper-respiratory infection in March and April and saw her family doctor in May, Getto said.

Because she showed unsteadiness walking, vision problems and memory loss, doctors at the regional hospital determined she had viral encephalitis, a brain infection. Dr. Michael Geschwind, a CJD expert at the University of California Memory and Aging Center in San Francisco, said viral encephalitis is commonly mistaken for CJD.

Geschwind said there are no national protocols guiding doctors and hospitals to treat brain diseases that could be CJD. But he said any time a patient has rapid dementia or other symptoms of the disease, such as loss of motor function, CJD should be considered a possibility.

At the UCSF Medical Center, doctors destroy all instruments after operating on patients that possibly could have CJD, he said, which costs the hospital up to $20,000 per operation.

Getto said the woman also had a brain tumor, which doctors thought was causing her symptoms. There was no reason to suspect CJD, he said.

During surgery June 11 to remove the benign brain tumor, surgeons took samples of adjacent tissue, Getto said. The tissue was tested on site during the surgery, and there was no indication of CJD, he said.

However, over the next month, the woman’s condition declined unexpectedly and rapidly, so a sample of tissue from the earlier biopsy was sent to the National Prion Disease Pathology Survey Center Case Western, Getto said. Prions are deformed proteins that can cause brain disease.

Monday, UW Hospital officials received a preliminary report that the sample had tested positive for CJD. Immediately, staff pulled all instruments used in previous neurosurgical procedures and began re-sterilizing them according to Centers for Disease Control guidelines for confirmed cases of prion diseases, Getto said.

The next day, immediately following confirmation of the positive result, the hospital staff began identifying patients to be notified. All 53 patients have been notified by Fed-Ex letter and a phone call, Safdar said.

The letter reads in part: “First and foremost, we wish to reassure you that the risk of exposure to CJD as a result of surgical instruments is extremely low. In fact, there have been no cases of transmission from surgical instruments to patients since 1976, when the standardized sterilization processes now used throughout the country were put in place.”

The patients range in age from 3 to 83, although the great majority are between 30 and 60, said hospital spokeswoman Lisa Brunette. Most are from the Midwest, primarily Wisconsin and Illinois, she said.

UW Hospital will offer them free consultations with neurosurgeons in addition to visits they already have scheduled with their regular neurosurgeons. They also can receive free psychological counseling, Getto said. Because the disease is so rare and the risk of transmission so small, the letter is meant to be “informative and reassuring,” he said.

The patients will not be able to find out immediately if they contracted the disease because there is no test for pre-symptomatic CJD, Safdar said. Symptoms might not appear for years or decades, she said.

The patients will be under no restrictions imposed by UW Hospital, although individual organizations may decide not to accept blood or organ donations from them based on their exposure, Safdar said.

Kranitz, the president of the CJD Foundation, said that if the exposed patients need to have other medical procedures, they are required to say they have been exposed to CJD. Some medical centers may deny them care, she said.

“Considering how they were exposed, I would think that (UW Hospital) should be more than willing to provide the necessary care,” Kranitz said.

Brunette, the UW Hospital spokeswoman, said the patients should be able to get medical care in the future.

“These people don’t have a disease. They don’t have a diagnosis,” she said. “That wouldn’t be a factor for us. I don’t think it should be a factor for another institution.”

Transmission of the classic form of CJD occurs only through direct implantation of tissue into the brain, spinal cord or eye, Safdar said. That’s why health-care workers and others are not at risk. “You’d have to have an instrument with a patient’s tissue on it and then penetrate it into the brain, spinal cord or eye,” she said.

Oral transmission — for instance, from a doctor’s finger into his or her mouth — has not been reported as a route, she said.

If UW surgeons had suspected CJD prior to the woman’s brain tumor surgery, they would have instituted extra layers of precaution, Safdar said. They would have disposed of the instruments used for the tissue biopsy and sequestered all other instruments used in the surgery until a conclusive diagnosis, she said.

While incinerating the instruments is an option, Safdar said the hospital chose to follow the CDC guidelines for heightened sterilization because “they do work.” The instruments are being sterilized for at least 18 minutes at 134 degrees centigrade and bleached. The usual process at the hospital is sterilization for six minutes at 132-134 degrees and no bleaching, she said.

Brunette said hospital staff has not calculated the value of the instruments and did not consider cost in deciding whether to save or destroy the instruments.

Although no sterilization process is known to completely destroy all prions, the CDC guidelines — and additional cleaning and disinfecting — lower the tissue load “several fold,” which is adequate for preventing transmission, Safdar said. Asked what risk future patients have if operated on with the surgical instruments, Safdar said, “I would say none.”



http://www.madison.com/wsj/home/local/459435



PLEASE SEE ;

Pre-surgical risk assessment for variant Creutzfeldt-Jakob disease (vCJD) risk in neurosurgery and eye surgery units

Hospitals should already be using a questionnaire in Annex J of the ACDP TSE Working Group Infection Control guidance to find out whether any patients who are about to undergo any surgery or endoscopy may be at increased risk of being infected with CJD. If a patient is found to have an increased risk of CJD prior to their surgery or endoscopy then special infection control precautions may need to be taken.

Annex J of the TSE Infection Control guidance has recently been revised, and now advises that patients who are due to have high risk surgery [1] or neuro-endoscopy should be asked an additional question: whether they have received transfusions of blood or blood components from 80 or more donors since 1980. This is because these patients may have an increased risk of being infected with variant CJD (vCJD).

On 16 July 2009 the HPA wrote to the chief executives of NHS trusts asking them to ensure that the guidance is implemented. Detailed information and tools for implementing the guidance can be downloaded from the links below.

If you have any queries about the implementation of the guidance, please contact the HPA Centre for Infections CJD Section at mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000260/!x-usc:mailto:cjd@hpa.org.uk or on 020 8327 6074/6411.

Background information on this new pre-surgical assessment is contained in this Letter to chief executives - July 2009 (PDF, 73 KB) written to all hospitals in England.

The new version of Annex J of the TSE Infection Control Guidance contains new question for patients undergoing high risk surgery and neuro-endoscopy. These questions should be used to assess patients' CJD risk factors.

Clinicians carrying out the new pre-surgical assessment should read Pre-surgical assessment Information for healthcare staff - July 2009 (PDF, 163 KB) This vCJD Algorithm for per-surgical roles - July 2009 (PDF, 28 KB) shows suggested roles and responsibilities for infection control teams, surgical teams and blood transfusion specialists.

Information on patients' transfusion histories should be collected using the Highly transfused vCJD risk assessment form - July 2009 (Word Document, 328 KB) This form is also available as a vCJD risk assessment spreadsheet - July 2009 (Excel Spreadsheet, 2.7 MB). This may help calculate the number of blood donors to a patient. The form may be posted or emailed to the HPA Centre for Infections CJD Section mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000260/!x-usc:mailto:cjd@hpa.org.uk.

Blood transfusion laboratories may wish to use this draft Letter to other blood laboratories - July 2009 (Word Document, 31 KB) when collecting transfusion information from other hospitals.

Pre-surgical assessment teams and patients may wish to read this vCJD Information for presurgical patients - July 2009 (PDF, 29 KB) about this new pre-surgical assessment.

[1] High risk surgery is defined as surgery involving any of the following organs or tissues (high risk tissues): brain, spinal cord, cranial nerves (specifically the entire optic nerve and only the intercranial components of the other cranial nerves), cranial nerve ganglia, posterior eye (specifically the posterior hyaloid face, retina, retinal pigment epithelium, choroid, subretinal fluid, optic nerve) and pituitary gland.

Letter to chief executives - July 2009 (PDF, 73 KB) Added/updated: 16 July 2009



http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1247469060207



Pre-surgical assessment Information for healthcare staff - July 2009 (PDF, 163 KB) Added/updated: 16 July 2009



http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1247469061870



vCJD Algorithm for per-surgical roles - July 2009 (PDF, 28 KB) Added/updated: 16 July 2009



http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1247469062057



Highly transfused vCJD risk assessment form - July 2009 (Word Document, 328 KB) Added/updated: 16 July 2009



http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1247469062225



Letter to other blood laboratories - July 2009 (Word Document, 31 KB) Added/updated: 16 July 2009



http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1247469062420



vCJD Information for presurgical patients - July 2009 (PDF, 29 KB) Added/updated: 16 July 2009



http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1247469062586



vCJD risk assessment spreadsheet - July 2009 (Excel Spreadsheet, 2.7 MB) Added/updated: 16 July 2009



http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1247728926790



full text ;



http://www.hpa.org.uk/webw/HPAweb&Page&HPAwebAutoListName/Page/1247469069188



http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1247728926790



see also ;

Friday, July 17, 2009

Revision to pre-surgical assessment of risk for vCJD in neurosurgery and eye surgery units Volume 3 No 28; 17 July 2009



http://creutzfeldt-jakob-disease.blogspot.com/2009/07/revision-to-pre-surgical-assessment-of.html



Tuesday, August 12, 2008

Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)



http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html



Thursday, January 29, 2009

Medical Procedures and Risk for Sporadic Creutzfeldt-Jakob Disease, Japan, 1999-2008 (WARNING TO Neurosurgeons and Ophthalmologists) Volume 15, Number 2-February 2009 Research



http://creutzfeldt-jakob-disease.blogspot.com/2009/01/medical-procedures-and-risk-for.html



Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009

Greetings,

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena’s. North America seems to have the most species with documented Transmissible Spongiform Encephalopathies, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is not recourse, to date.

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, surgical, blood, medical, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub-clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE (one strain TSE in cows), and the nv/v CJD (one strain TSE humans) and that all the rest of human TSE are just one single strain i.e. sporadic CJD (when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al), and that no other animal TSE transmits to humans, to continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...

please see history, and the ever evolving TSE science to date ;

Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009



http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html



Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (TRANSCRIPT)



http://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/UCM171810.pdf



Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)



http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html



DEPARTMENT OF HEALTH AND HUMAN SERVICES UNITED STATES FOOD AND DRUG ADMINISTRATION CENTER FOR BIOLOGICS EVALUATION AND RESEARCH

This transcript has not been edited or corrected, but appears as received from the commercial transcribing service. Accordingly the Food and Drug Administration makes no representation as to its accuracy.

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE

21st Meeting Friday, June 12, 2009 8:00 a.m. Holiday Inn

DR. ROHWER: We first detected infectivity at that point, but that was part of several measurements over the incubation period and you could extrapolate that curve and it extrapolated to zero back around 30 percent of the incubation time.

DR. HOGAN: Dr. Manuelidis?

DR. MANUELIDIS: Yes, I think there are a couple of things that concern me. One is that using one model of animals may not always be the most effective one. In 1978 we wrote an article in Science showing that infectivity was present basically from about half way in the disease and went through the end and at the end it became highly infectious, much more infectious in the guinea pig for instance than in Bob's models. I would also like to point out that, for instance, vCJD is BSE and basically in a cow blood is not infectious and in primates it is. So, one must be very careful about this. The third thing which is a concern of mine is that in the report here it says we are talking about vCJD and my

PAPER MILL REPORTING 301 495-5831 163

concern is that we are limiting things to vCJD. It says because BSE has been detected in so few US cattleB-now, anybody who works with the USDA knows that the USDA has been impossible about letting anybody work with BSE and we actually had no surveillance. So, we have no idea about how many US cattle are really infected as compared to places like Japan that look at every single cow. The fourth thing is that there are recent reports that have been going back for several years and have now become more important of variants of BSE which are not vCJD, some of which people believe have more of a linkage to sporadic CJD. We also do not look for these things.

So, I think that in looking at what we say about what should be done, although this has no practical application right now to what the FDA is going to do about saying we can't use this blood or that blood, I think it is a much broader problem. I also agree with people in the audience who came and said that CJD is not a reportable disease in many places, and I think this is very frustrating in terms of knowing what is really going on in our population. So, I would like to add that.

PAPER MILL REPORTING 301 495-5831 164

DR. HOGAN: I think those are most important points that a lot of us agree with, and I know that the staff is looking at some of those in the future. What we are specifically charged with today is a little bit less encompassing issue but, nonetheless, exactly what you say should be considered.

SNIP...

MR. TEMPLIN: I just want to make two comments. I am sort of troubled that we don't know how much is actually infectious. A comment too about what Dr. Manuelidis said about cattle. If a farmer has cattle that he thinks may e

PAPER MILL REPORTING 301 495-5831 166

infectious he is going to throw it out in the back 40 and cover it up or throw it on the compost pile and never report it to the government because he is going to lose everything he or she owns.

DR. HOGAN: I think we are going to have some speakers this afternoon that are going to address the current USDA situation. So, we will have questions for them at that point. Miss Hamilton?

MS. HAMILTON: I have a comment about what Dr. Manuelidis said to a question. It troubles me because a few years ago there was a lot of hype about the downed cattle that were getting through and being used in food for animals and what-not, and now we don't hear anything else about it, and she was saying that there is no surveillance in that area at all. My big question is why.

DR. HOGAN: Well, we will ask the USDA this afternoon, but I am not sure that zero is correct. I think it has been lowered significantly from its initial stages but it is not zero. Dr. Kreindel?

DR. KREINDEL: We are going to have a presentation on the USDA surveillance, but we do have surveillance and our surveillance is according to international standards.

PAPER MILL REPORTING 301 495-5831 167

You know, it is not surveillance that really protects the US population. You know, we do have surveillance and there was a lot of surveillance going on. We called that surveillance enhanced surveillance. We are going to have information about that. We still have surveillance going on, you know, at the level requested by international standards but we do cover a lot of mitigations about sequential interlocking that really prevent, you know, if any BSE is present to be recycled.

DR. HOGAN: Thank you. Perhaps we will defer the discussion of surveillance till this afternoon. Do any of the statistics experts on the panel have anything to say relative to the mathematical accuracy of this model, since all those equations make me dizzy?

SNIP...then the BSe picks up on page 205 with the mathmatical formula's and the junk science of the OIE, but then on page 216 please see the questions on BSE testing in the USA by Dr. Manuelidis ;

DR. MANUELIDIS: I am just curious if you can explain to me the difference between the testing that is going on now in Europe with all the other variants or other strains of BSE, the test that is used, and whether the USDA still refuses to sort of use tests that other countries use, and what might our tests have that may be different and are they still restricted, or what is the rationale for that?

DR. HUGHES: Well, the USDA uses tests that have been validated.

DR. MANUELIDIS: I believe that the tests have been validated for the European and the Japanese stuff, they all use a standard test. So, I am curious about why the USDAB-there was the import I think you were referring to where the Japanese stopped importing food because, as I understood it and this is, of course, from places like The New York Times that may be totally wrong but as I understood it, the USDAB-this must have been about three or four years ago, said that they refused to use the test even though the plant was willing to use it. They said they had their own tests and they said they would only use their own tests.

PAPER MILL REPORTING 301 495-5831 217

Maybe you can clarify that for me and tell me what the difference is between the tests, and whether you think that you can pick up the variants of BSE, not just the UK version of BSE. If there is really a difference in the sensitivity of the tests, if any independent side-by-side comparison has been done.

DR. KREINDEL: I am not sure I can answer your question but I think you are referring to the fact that they wanted to test all animals, rather than following the USDA requirements for testing.

DR. HUGHES: The question was why don't we test all animals.

DR. MANUELIDIS: There is a test that is used in Europe and in Japan. It is used all over I think. It is a bioride[?] test and what the plant was willing to do, I understood from The New York Times, was to test their animals according to that protocol. The USDA said no, even though everybody else uses it, we want to use our own test. Then they never really did those tests. So, what I am really getting at is are our tests in the USDA as sensitive and as comprehensive even if we don't test every animal--

PAPER MILL REPORTING 301 495-5831 218

DR. HUGHES: Yes.

DR. MANUELIDIS: -Bfor all the variants of BSE and on what basis? Have you ever picked up any cases of BSE-H or BSE-L? Would you have an independent control that shows you that you can pick up these things with the tests as currently employed? Have there been any blind controls where an animal has a little bit of this or that just to see if you can pick it up out of a group?

DR. HUGHES: I think what you might be referring to is the Creekstone case.

DR. MANUELIDIS: Yes.

DR. HUGHES: Okay. Of course, I can't comment on current litigation but, basically, the USDA is unwilling to, you know, have a test be validated as a food safety test. Again, this gets back to what I spoke about earlier, that the BSE test really isn't a food safety test. It is possible to test an animal for BSE and have it be negative and still have the animal be positive for BSE. So, using that to put on a package label is just very confusing and kind of disingenuous to the public because it gives them a false sense of security about it. Our main focus for protecting human health is on other

PAPER MILL REPORTING 301 495-5831 219

mitigation measures, such as the feed ban the FDA has in place; removal of specified risk materials. So, the tissues that we know are likely to contain agent never make it into the food chain in the first place. So, that is the basis of the refusal to allow that private company to do their own testing.

DR. MANUELIDIS: I don't want to be difficult because BSE is not my specialty, minus the vCJD version of it, but as I understand, some of the BSE cases, like the typical UK BSE case, have been found in muscle where muscle has been found to be infectious. So, the food ban wouldn't really deal with those. That is why I was asking what is the test. If you did a side-by-side comparison with blind controls would you be able to pick up what Europeans and Japanese pick up? That is really what I am asking.

DR. HUGHES: And I am afraid I can't answer that, and I am not sureB-you know, the experts on that would be the folks at NVSL that are responsible for validating the test and choosing which test we use. But evidently they are not convinced that the other tests are better than what we use currently. But, again, I am sorry, I am not the expert

PAPER MILL REPORTING 301 495-5831 220

in that particular category.

snip...

SEE FULL TEXT 346 PAGES ;



http://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/UCM171810.pdf



Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)



http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html



Monday, June 01, 2009 Biochemical typing of pathological prion protein in aging cattle with BSE

SOMETHING TO PONDER ???

O.K. confusious asks, IF all these new atypical BSEs i.e. new strains of mad cow disease is just an 'OLD COW PRION DISEASE', why then can not the 'old human prion disease' such as the sporadic CJD, be from an 'old cow prion disease', same as the nvCJD 'young people mad cow disease' (which also happens in 74 year old), but why cannot the 'old cow prion diseases', i.e. l-BSE, h-BSE, and ibncBSE, cause the 'old people prion disease', which looks like sporadic CJD. seems that is what some of the pathology is showing ???

OH, that probably makes too much sense, and that the only answer could be that it's all just a happenstance of bad luck and or a spontaneous event, that just happens out of the clear blue sky $$$

IF this is the case, then where are all the SPONTANEOUS BSE CASES OF MAD COW DISEASE IN THE U.S.A., AND WHERE HAVE THEY BEEN BURIED IN THE USA OVER THE LAST 25 YEARS ???



http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html



Thursday, April 9, 2009

Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed



http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html



http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html#comments



Sunday, April 12, 2009 r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada



http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html



http://prionunitusaupdate2008.blogspot.com/2009/04/cjd-foundation-sides-with-r-calfers-no.html#comments



Tuesday, July 14, 2009

U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST

WHERE did we go wrong $$$




http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html



10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

Date: March 21, 2007 at 2:27 pm PST

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

___________________________________

PRODUCT

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.

REASON

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI

___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/bbs/topics/enforce/2007/ENF00996.html



NEW URL



http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm



Thursday, March 19, 2009

MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$



http://madcowfeed.blogspot.com/2009/03/millions-and-millions-of-pounds-of-mad.html



Sunday, May 10, 2009

Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)



http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html



Wednesday, July 1, 2009

Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)



http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html



Tuesday, July 14, 2009

U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST

WHERE did we go wrong $$$



http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html



Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie. Emerg Infect Dis. 2009 Aug; [Epub ahead of print]



http://nor-98.blogspot.com/2009/07/transgenic-mice-expressing-porcine.html



Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009



http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html



i am no doctor, i have no phd's, and I am president and ceo of nothing. ...TSS

wasted days and waste nights...freddy fender

stupid is, as stupid does...forest gump

still sadly disgusted...

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



Wednesday, July 15, 2009

TSEAC 21st Meeting Friday, June 12, 2009 (BSE TESTING USA ???) TRANSCRIPT



http://tseac.blogspot.com/2009/07/tseac-21st-meeting-friday-june-12-2009.html



Tuesday, April 21, 2009

Doctor Antonio Ruiz Villaespesa, pathologist and CJD researcher deceased because of Creutzfeldt-Jakob Disease SPAIN



http://cjdusa.blogspot.com/2009/04/doctor-antonio-ruiz-villaespesa.html



April 20, 2009

National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)

National Prion Disease Pathology Surveillance Center Cases Examined1

(December 31, 2008)

Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

1996 & earlier 42 32 28 4 0 0

1997 115 68 59 9 0 0

1998 93 53 45 7 1 0

1999 115 69 61 8 0 0

2000 151 103 89 14 0 0

2001 210 118 108 9 0 0

2002 258 147 123 22 2 0

2003 273 176 135 41 0 0

2004 335 184 162 21 0 13

2005 346 193 154 38 1 0

2006 380 192 159 32 0 14

2007 370 212 185 26 0 0

2008 383 228 182 23 0 0

TOTAL 30715 17756 1490 254 4 2

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 acquired in Saudi Arabia; 5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.

Rev 2/13/09 National



http://www.cjdsurveillance.com/pdf/case-table.pdf



http://www.cjdsurveillance.com/resources-casereport.html



http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45



*5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; *6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.

Greetings,

it would be interesting to know what year these atypical cases occurred, as opposed to lumping them in with the totals only.

are they accumulating ?

did they occur in one year, two years, same state, same city ?

location would be very interesting ?

age group ?

sex ?

how was it determined that nvCJD was ruled out ?

from 1997, the year i started dealing with this nightmare, there were 28 cases (per this report), up until 2007 where the total was 185 cases (per this report), and to date 2008 is at 182. a staggering increase in my opinion, for something that just happens spontaneously as some would have us believe. i don't believe it, not in 85%+ of all sporadic CJD cases. actually, i do not believe yet that anyone has proven that any of the sporadic CJD cases have been proven to be a spontaneous misfolding of a protein. there are many potential routes and sources for the sporadic CJD's. ...TSS

Sunday, April 12, 2009

r-calf and the USA mad cow problem, don't look, don't find, and then blame Canada



http://prionunitusaupdate2008.blogspot.com/2009/04/r-calf-and-usa-mad-cow-problem-dont.html



Monday, April 20, 2009

National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)



http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html



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

Labels: , , , , , ,