Saturday, August 01, 2009

Cases of Early-Onset Sporadic Creutzfeld-Jakob Disease in Michigan

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*

snip...

In 2001, two additional CJD patients 26 and 28 years of age were reported from a single state (Table 2) (34). The patients grew up in adjacent counties and had illness onset within several months of each other. As a result of this fact and their unusually young age, a possible environmental source of infection, including exposure to CWD-infected venison, was considered. One of the patients died after an illness lasting 5–6 months that was characterized by progressive aphasia, memory loss, social withdrawal, vision disturbances, and seizure activity leading to status epilepticus and induced coma. Histopathologic, immunohistochemical, and Western blot testing of brain biopsy and autopsy samples confirmed a CJD diagnosis. The patient’s disease phenotype corresponded to the MM2 sporadic CJD subtype reported by Parchi et al. (35). This patient did not hunt, and family members provided no history of regularly eating venison. The patient may have occasionally eaten venison originating from the Upper Peninsula of Michigan while away from home during his college years. However, ongoing surveillance has not detected CWD in Michigan deer (36).

The second patient died from an illness lasting ˜16 months. The patient’s illness began with behavioral changes, including unusual outbursts of anger and depression. Confusion, memory loss, gait disturbances, incontinence, headaches, and photophobia also developed. Western blot analysis of frozen brain biopsy tissue confirmed a prion disease diagnosis. Immunohistochemical analysis of brain tissue obtained after the patient’s death

showed prion deposition consistent with GSS. Aprion protein gene analysis could not be performed because appropriate samples were lacking. However, prion protein gene analysis of a blood sample from one of the patient’s parents indicated a GSS P102L mutation. The patient did not hunt but may have eaten venison from Michigan once when he was 1–2 years old. The GSS diagnosis greatly reduced the likelihood that the two patients reported from adjacent counties had disease with a common origin. Recently, rare neurologic disorders resulting in the deaths of three men who participated in “wild game feasts” in a cabin owned by one of the decedents created concern about the possible relationship of their illnesses with CWD (Table 2) (37). Two of the patients reportedly died of CJD, and the third died from Pick’s disease. More than 50 persons were identified as possibly participating in these feasts; the three patients were the only participants reported to have died of a degenerative neurologic disorder. Reanalysis of autopsy brain tissues from the three patients at the National Prion Disease Pathology Surveillance Center indicated that two of them had no evidence of a prion disease by immunohistochemical analysis. CJD was confirmed in the third patient, who had clinicopathologic, codon 129, and prion characteristics similar to the most common sporadic CJD subtype (MM1/MV1) (35). This patient participated in the feasts only once, perhaps in the mid-1980s. In addition, the investigation found no evidence that the deer and elk meat served during the feasts originated from the known CWD-endemic areas of Colorado and Wyoming.

In 2003, CJD in two deer and elk hunters (54 and 66 years of age) was reported (38). The report implied that the patients had striking neuropathologic similarities and that their illness may represent a new entity in the spectrum of prion diseases. A third patient (63 years of age), who was also purported to have been a big game hunter, was subsequently reported from the same area. However, none of the three patients were reported to have eaten venison from the CWD-endemic areas of the western United States. The 66- year-old patient hunted most of his life in Washington State. Although information about the 54-year-old patient was limited, there was no evidence that he hunted in CWD-endemic areas. The third patient was not a hunter but ate venison harvested from Pennsylvania and Washington. The neuropathologic changes, Western blot profile, and genotype at codon 129 of the three patients each fit the MM1, VV1, or VV2 sporadic CJD subtype, indicating absence of phenotypic similarity among the cases or atypical neuropathologic features (35). To date, only two nonfamilial CJD cases with a positive history of exposure to venison obtained from the known CWD-endemic areas have been reported. One of the patients was a 61-year-old woman who grew up in an area where this disease is known to be endemic, and she ate venison harvested locally. She died in 2000, and analysis of autopsy brain specimens confirmed that the patient’s CJD phenotype fit the MM1 subtype, with no atypical neuropathologic features. The second patient was a 66-yearold man who was reported to have eaten venison from two deer harvested in a CWD-endemic area. Both deer tested negative for CWD, and the patient’s illness was consistent with the MM1 CJD phenotype.




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




Archive Number 20020430.4061

Published Date 30-APR-2002

Subject PRO/AH/EDR> CJD, sporadic? - USA (Michigan)

CJD, SPORADIC? - USA (MICHIGAN)

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A ProMED-mail post

<http://www.promedmail.org>

ProMED-mail is a program of the International Society for Infectious Diseases <http://www.isid.org>

[see also: CJD (new var.), suspected - USA (FL) ex UK 20020419.3989 CJD (new var.) - UK: update Apr 2002 20020404.3877 CJD (new var.) - France: sixth case 20020418.3983 CJD (new var.), suspected case - Italy (Sicily) (03) 20020210.3528 CJD (new var.) - China (Hong Kong): confirmed 20020222.3604 2001 ---- Chronic wasting disease, cervid - USA: human risk? 20010126.0193 CJD (new var.), incidence & trends - UK 20011115.2816 CJD (new var.), incidence & trends - UK (02) 20011124.2875 CJD (new var.) - UK: 9th Annual Report 20010706.1293 CJD (new var.) - UK: regional variation 20010628.1231 CJD (new var.) - UK: regional variation (02) 20010907.2145 1999 ---- CJD (new var.), human - Ireland 19990715.1192]

[1] Date: Sat, 27 Apr 2002 20:28:05 -0400 From: Terry Allen <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000043/!x-usc:mailto:tallen@igc.org>

Source: Abstract presented at American Academy of Neurology meeting, Denver, 13-20 Apr 2002

Cases of Early-Onset Sporadic Creutzfeld-Jakob Disease in Michigan

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

Amanda C. Peltier, Patience H. Reading, Karen Kluin, SharinSakurai, Ahmad Beydoun, Jonathan Edwards, Pierluigi Gambetti, Norman L. Foster Ann Arbor , MI; Cleveland, OH

OBJECTIVE: To describe the clinical, pathological and genetic features in 2 young men who developed sporadic Creutzfeldt-Jakob disease (CJD) concurrently in Michigan.

BACKGROUND: Sporadic CJD typically occurs in the 6th and 7th decades of life and is rarely reported in persons younger than 30, except with exposure to bovine spongiform encephalopathy (BSE) or pituitary extract derived human growth hormone (HGH). BSE has not been found in the US.

DESIGN/METHODS: Case Reports.

RESULTS: In our hospital, 2 young men, ages 26 and 28, who were unknown to each other and had lived their entire lives in Michigan, developed rapidly progressive dementia and were simultaneously evaluated. Neither had traveled to countries with known BSE, received HGH, eaten venison or elk, or had a family history of dementia. The first patient had a 2-month history of progressive aphasia, social withdrawal, and memory difficulties. An EEG performed on admission revealed waxing and waning rhythmic spike and wave discharges. He was treated for nonconvulsive status epilepticus, which became convulsive during his hospital course. His seizures were refractory to medical therapy despite multiple anticonvulsants, including midazolam coma. His EEG became more periodic and he never recovered responsiveness even as medication was tapered. A brain biopsy and subsequent postmortem examination following his death 5 months after the onset of symptoms showed spongiform changes. The scrapie prion protein (PrPsc) was distributed in a cluster pattern as revealed by immunohistochemistry. Genetic analysis and immunoblot established that this patient had the MM2 subtype of sporadic CJD. Treatment with quinacrine had no benefit.

The second patient had a 10-month history of progressive memory loss, inappropriate behavior, violent outbursts, and difficulty performing his job. He had bradykinesia and rigidity on examination. There were no periodic discharges on EEG and CSF protein 14-3-3 was negative. Following a brain biopsy showing spongiform changes he developed startle myoclonus. The presence of PrPsc type 1 was confirmed with immunoblot and immunostaining.

Both patients had abnormal MRI scans with increased signal in the basal ganglia and cerebral cortex on T2- and diffusion-weighted images.

CONCLUSIONS: These cases expand the spectrum of sporadic CJD to include younger age of onset than previously suspected and cases presenting as non-convulsive status epilepticus. The appearance of CJD in 2 individuals within a few months of each other in southeastern Michigan may indicate that very early-onset CJD is more common than previously believed. Alternatively, other unrecognized risk factors may exist. It is important to consider CJD in young people with progressive behavioral and cognitive disturbances, even in the absence of typical EEG or CSF abnormalities.

Supported By: This study was supported by NIH grant AG14359 and grant CCU 515004 to the National Prion Disease Pathology Surveillance Center and the Michigan Alzheimers Disease Research Center (NIH grant P50-AG0871).

Kathy Stone Media Relations Manager American Academy of Neurology 1080 Montreal Avenue St. Paul, Minnesota 55116 USA ph: 651-695-2763 fax: 651-695-2791 <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000043/!x-usc:mailto:kstone@aan.com>

-- Terry J. Allen <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000043/!x-usc:mailto:tallen@igc.org>

****** [2] Date: Mon 29 Apr 2002 8:29 PM From: Terry Allen <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000043/!x-usc:mailto:tallen@igc.org> Source: USA Today 29 Apr 2002 Page 7D

Michigan brain-disease deaths 'unusual, disturbing' -

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Last fall 2 young men, ages 26 and 28, died in the same Michigan hospital of a rare brain disease that occurs mainly in elderly people. The incident, which raised fears that the human form of mad cow disease, or something similar, had emerged in the USA, prompted a swift investigation by federal health officials, but doctors familiar with the cases say there is no evidence to support that fear. They say autopsies and other tests indicate the victims died from so-called "classic" forms of Creutzfeldt-Jakob disease (CJD).

While the cases are "highly unusual and disturbing," says University of Michigan neurologist Norman Foster, the data show that the forms of CJD suffered by the young men are ones seen previously in older individuals. CJD occurs at the rate of about one person per million per year, almost always in people over age 60. What doctors feared is that a new form of CJD, possibly similar to a variant that emerged in the mid-1990s in the United Kingdom and linked to consumption of mad-cow-infected beef, had struck.

Unlike classic CJD, the new variant, vCJD, strikes mainly young adults. It has killed more than 100 people. The only known case of vCJD in the USA was diagnosed recently in a 22-year-old British woman living in Florida, who is thought to have contracted the disease in England. Mad cow disease has not been detected in cattle in the USA, but a similar disease in deer and elk is spreading in the Midwest. Chronic wasting disease (CWD) is fatal to deer and elk but is not known to cause illness in humans.

Lawrence Schoenberger of the Centers for Disease Control and Prevention in Atlanta says the agency sent investigators to Michigan in late August 2001, when the victims were still alive. "The key thing here is the 2 were right together. We were worried that there was maybe a common exposure, but our investigation revealed that was not the case." The men lived in adjacent counties but did not know each other, he says.

In the rare cases when CJD strikes before age 30, it is often caused by a hereditary form of the disease, says Foster, and "tests are continuing to see if that may be a factor in these cases." But extensive family interviews determined that neither man had a family history of dementia, nor had they eaten venison or elk meat or visited countries where mad cow disease has been detected.

"We feel as comfortable as anyone can that this is not related to either CWD or (mad cow disease)," says Foster, who treated the patients at the University of Michigan Medical Center in Ann Arbor. Not everyone is comfortable. "I discount the statement that these 2 young people, dying at the same time in the same hospital in southeast Michigan, did not eat venison, after living their entire lives in that state," says John Stauber of the Center for Media & Democracy and co-author of Mad Cow USA.

He suspects a new American variant of CJD, perhaps related to chronic wasting disease, may be emerging. "Any attempt to portray these CJD deaths as some sort of 'normal' occurrence that has simply, to date, gone unobserved is absurd," Stauber says. Current estimates of only 5 cases per billion of CJD in people 30 and younger may be incorrect, says Foster, who co-wrote a report on the cases presented this month at a meeting of the American Academy of Neurology.

"The fact that they both occurred at the same time in a relatively small population suggests that (CJD in younger people) may be more common than previously suspected," Foster says. Doctors don't expect to see it in young people, so misdiagnosis may occur. " Any young individual with progressive neurologic disease should be considered for CJD."

He says the cases also underscore the need for a national system to seek out and report all cases of CJD. "There certainly is the possibility that other cases have been seen and not diagnosed, or even if diagnosed, not reported."

[Byline: Anita Manning]

-- Terry j allen <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000043/!x-usc:mailto:tallen@igc.org>

[At present a link between CWD and CJD in the USA or Canada has not been established. Unfortunately, reviewing the UK and European experience, it would not be a surprise if such a link were identified. Clearly we are very early in our understanding of prion disease and early in our identification of the full range and spectrum of the prion disease presently manifested as CWD in cervids in North America. The occurrence of 2 cases of sporadic CJD in unrelated individuals below the age of 30 is unusual and warrants the scrutiny it has been receiving. We await more information as it becomes available.

Some useful reference for our readers:

1: Belay ED, Gambetti P, Schonberger LB, Parchi P, Lyon DR, Capellari S, McQuiston JH, Bradley K, Dowdle G, Crutcher JM, Nichols CR. Creutzfeldt-Jakob disease in unusually young patients who consumed venison. Arch Neurol. 2001 Oct;58(10):1673-8.

2. Brown P, Will RG, Bradley R, Asher DM, Detwiler L. Perspective: Bovine Spongiform Encephalopathy and Variant Creutzfeldt-Jakob Disease: Background, Evolution, and Current Concerns. EID 7(1) Jan-Feb 2001 <http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm>

3. Holman RC, Khan AS, Belay ED, Schonberger LB. Dispatches: Creutzfeldt-Jakob Disease in the United States, 1979-1994: Using National Mortality Data to Assess the Possible Occurrence of Variant Cases. EID 2(4) Oct-Dec 1996 <http://www.cdc.gov/ncidod/eid/vol2no4/holman2.htm>

4. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Research letter: Creutzfeldt-Jakob Disease in the United States: 1979-1998. JAMA 284(18) 8 Nov 2000 <http://jama.ama-assn.org/issues/v284n18/ffull/jlt1108-6.html>

5. Surveillance for Creutzfeldt-Jakob Disease. MMWR, 45(31):665-668 9 Aug 1996 <http://www.cdc.gov/mmwr/preview/mmwrhtml/00043220.htm> - Mod.MPP] ..................................lm/mpp/pg/lm

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Monday, July 27, 2009



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

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 $$$

SNIP...

Monday, July 27, 2009

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



http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.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




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




TSS

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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: , , , , , ,

Tuesday, August 12, 2008

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

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

From: TERRY SINGELTARY
To: TERRY SINGELTARY
Sent: Friday, August 08, 2008 5:30 PM
Subject: Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007



Biosafety in Microbiological and Biomedical Laboratories*

U.S. Department of Health and Human Services Public Health Service

Centers for Disease Control and Prevention and National Institutes of Health

Fifth Edition 2007

U. S. Government Printing Office Washington: 2007

Section VIII-H: Prion Diseases

Transmissible spongiform encephalopathies (TSE) or prion diseases are neurodegenerative diseases which affect humans and a variety of domestic and wild animal species (Tables 1 and 2).1,2 A central biochemical feature of prion diseases is the conversion of normal prion protein (PrP) to an abnormal, misfolded, pathogenic isoform designated PrPSc (named for “scrapie,” the prototypic prion disease). The infectious agents that transmit prion diseases are resistant to inactivation by heat and chemicals and thus require special biosafety precautions. Prion diseases are transmissible by inoculation or ingestion of infected tissues or homogenates, and infectivity is present at high levels in brain or other central nervous system tissues, and at slightly lower levels in lymphoid tissues including spleen, lymph nodes, gut, bone marrow, and blood. Although the biochemical nature of the infectious TSE agent, or prion, is not yet proven, the infectivity is strongly associated with the presence of PrPSc, suggesting that this material may be a major component of the infectious agent.

A chromosomal gene encodes PrPC (the cellular isoform of PrP) and no PrP genes are found in purified preparations of prions. PrPSc is derived from PrPC by a posttranslational process whereby PrPSc acquires a high beta-sheet content and a resistance to inactivation by normal disinfection processes. The PrPSc is less soluble in aqueous buffers and, when incubated with protease (proteinase K), the PrPC is completely digested (sometimes indicated by the “sensitive” superscript, PrPsen) while PrPSc is resistant to protease (PrPres). Neither PrP-specific nucleic acids nor virus-like particles have been detected in purified, infectious preparations.

OCCUPATIONAL INFECTIONS

No occupational infections have been recorded from working with prions. No increased incidence of Creutzfeldt-Jakob disease (CJD) has been found amongst pathologists who encounter cases of the disease post-mortem.

NATURAL MODES OF INFECTION

The recognized diseases caused by prions are listed under Table 1 (human diseases) and Table 2 (animal diseases). The only clear risk-factor for disease transmission is the consumption of infected tissues such as human brain in the case of kuru, and meat including nervous tissue in the case of bovine spongiform encephalopathy and related diseases such as feline spongiform encephalopathy. It is also possible to acquire certain diseases such as familial CJD by inheritance through the germline.

Agent Summary Statements – Prion Diseases

TABLE 1

THE HUMAN PRION DISEASES

DISEASE ABBREVIATION MECHANISM OF PATHOGENESIS

Kuru Infection through ritualistic cannibalism Creutzfeldt-Jakob disease CJD Unknown mechanism Sporadic CJD sCJD Unknown mechanism; possibly somatic mutation or spontaneous conversion of PrPC to PrPSc Variant CJD vCJD Infection presumably from consumption of BSE-contaminated cattle products and secondary bloodborne transmission Familial CJD fCJD Germline mutations in PrP gene Iatrogenic CJD iCJD Infection from contaminated corneal and dural grafts, pituitary hormone, or neurosurgical equipment Gerstmann-Sträussler- Scheinker syndrome GSS Germline mutations in PrP gene Fatal familial insomnia FFI Germline mutations in PrP gene TABLE 2 THE ANIMAL PRION DISEASES DISEASE ABBREVIATION NATURAL HOST MECHANISM OF PATHOGENESIS Scrapie Sheep, goats and mouflon Infection in genetically susceptible sheep Bovine spongiform encephalopathy BSE Cattle Infection with prion-contaminated feedstuffs Chronic wasting disease CWD Mule deer, white-tailed deer and Rocky Mountain elk Unknown mechanism; possibly from direct animal contact or indirectly from contaminated feed and water sources Exotic ungulate encephalopathy EUE Nyala, greater kudu and oryx Infection with BSE-contaminated feedstuffs Feline spongiform encephalopathy FSE Domestic and wild cats in captivity Infection with BSE-contaminated feedstuffs Transmissible mink encephalopathy TME Mink (farm raised) Infection with prion-contaminated feedstuffs

Agent Summary Statements – Prion Diseases

Species-specificity of prions. Most TSE agents, or prions, have a preference for infection of the homologous species, but cross-species infection with a reduced efficiency is also possible. After cross-species infection there is often a gradual adaptation of specificity for the new host; however, infectivity for the original host may also be propagated for several passages over a time-span of years. The process of cross-species adaptation can also vary among individuals in the same species and the rate of adaptation and the final species specificity is difficulty to predict with accuracy. Such considerations help to form the basis for the biosafety classification of different prions.

LABORATORY SAFETY

Biosafety level classification In the laboratory setting prions from human tissue and human prions propagated in animals should be manipulated at BSL-2. BSE prions can likewise be manipulated at BSL-2. Due to the high probability that BSE prions have been transmitted to humans, certain circumstances may require the use of BSL-3 facilities. All other animal prions are considered BSL-2 pathogens. However, when a prion from one species is inoculated into another the resultant infected animal should be treated according to the guidelines applying to the source of the inoculum. Contact APHIS National Center for Import and Export at (301) 734- 5960 for specific guidance.

Although the exact mechanism of spread of scrapie among sheep and goats developing natural scrapie is unknown, there is considerable evidence that one of the primary sources is oral inoculation with placental membranes from infected ewes. There has been no evidence for transmission of scrapie to humans, even though the disease was recognized in sheep for over 200 years. The diseases TME, BSE, FSE, and EUE are all thought to occur after the consumption of prion-infected foods.1,2 The exact mechanism of CWD spread among mule deer, white-tailed deer and Rocky Mountain elk is unknown. There is strong evidence that CWD is laterally transmitted and environmental contamination may play an important role in local maintenance of the disease.2

Human prion diseases In the care of patients diagnosed with human prion disease, Standard Precautions are adequate. However, the human prion diseases in this setting are not communicable or contagious.3 There is no evidence of contact or aerosol transmission of prions from one human to another. However, they are infectious under some circumstances, such as ritualistic cannibalism in New Guinea causing kuru, the administration of prion-contaminated growth hormone causing iatrogenic CJD, and the transplantation of prion-contaminated dura mater and corneal grafts. It is highly suspected that variant CJD can also be transmitted by blood transfusion.4 However, there is no evidence for bloodborne transmission of non-variant forms of CJD. Familial CJD, GSS, and FFI are all dominantly inherited prion diseases; many different mutations of the PrP gene have been shown to be genetically linked to the development of inherited prion disease. Prions from many cases of inherited prion disease have been transmitted to apes, monkeys, and mice, especially those carrying human PrP transgenes.

SPECIAL ISSUES

Inactivation of prions Prions are characterized by resistance to conventional inactivation

Agent Summary Statements – Prion Diseases

procedures including irradiation, boiling, dry heat, and chemicals (formalin, betapropiolactone, alcohols). While prion infectivity in purified samples is diminished by prolonged digestion with proteases, results from boiling in sodium dodecyl sulfate and urea are variable. Likewise, denaturing organic solvents such as phenol or chaotropic reagents such as guanidine isothiocyanate have also resulted in greatly reduced but not complete inactivation. The use of conventional autoclaves as the sole treatment has not resulted in complete inactivation of prions.5 Formalin-fixed and paraffin-embedded tissues, especially of the brain, remain infectious. Some investigators recommend that formalin-fixed tissues from suspected cases of prion disease be immersed for 30 min in 96% formic acid or phenol before histopathologic processing (Table 3), but such treatment may severely distort the microscopic neuropathology.

The safest and most unambiguous method for ensuring that there is no risk of residual infectivity on contaminated instruments and other materials is to discard and destroy them by incineration.6 Current recommendations for inactivation of prions on instruments and other materials are based on the use of sodium hypochlorite, NaOH, Environ LpH and the moist heat of autoclaving with combinations of heat and chemical being most effective (See Table 4).5,6

Surgical procedures Precautions for surgical procedures on patients diagnosed with prion disease are outlined in an infection control guideline for transmissible spongiform encephalopathies developed by a consultation convened by the WHO in 1999.6 Sterilization of reusable surgical instruments and decontamination of surfaces should be performed in accordance with recommendations described by the CDC (www.cdc.gov) and the WHO infection control guidelines.6 Table 4 summarizes the key recommendations for decontamination of reusable instruments and surfaces. Contaminated disposable instruments or materials should be incinerated.

Autopsies Routine autopsies and the processing of small amounts of formalin-fixed tissues containing human prions can safely be done using BSL-2 precautions.7 The absence of any known effective treatment for prion disease demands caution. The highest concentrations of prions are in the central nervous system and its coverings. Based on animal studies, it is likely that prions are also found in spleen, thymus, lymph nodes, and intestine. The main precaution to be taken by laboratorians working with prion-infected or contaminated material is to avoid accidental puncture of the skin.3 Persons handling contaminated specimens should wear cutresistant gloves if possible. If accidental contamination of unbroken skin occurs, the area should be washed with detergent and abundant quantities of warm water (avoid scrubbing); brief exposure (1 minute to 1N NaOH or a 1:10 dilution of bleach) can be considered for maximum safety.6 Additional guidance related to occupational injury are provided in the WHO infection control guidelines.6 Unfixed samples of brain, spinal cord, and other tissues containing human prions should be processed with extreme care at least in a BSL-2 facility.

Bovine spongiform encephalopathy Although the eventual total number of variant CJD cases resulting from BSE transmission to humans is unknown, a review of the epidemiological data from the United Kingdom indicates that BSE transmission to humans is not efficient.8 The most prudent approach is to study BSE prions at a minimum in a BSL-2 facility. When performing necropsies on large animals where there is an opportunity that the worker may be accidentally splashed or have contact with high-risk materials (e.g., spinal column, brain, etc.) personnel

Agent Summary Statements – Prion Diseases

should wear full body coverage personal protective equipment (e.g., gloves, rear closing gown and face shield). Disposable plasticware, which can be discarded as a dry regulated medical waste, is highly recommended. Because the paraformaldehyde vaporization procedure does not diminish prion titers, BSCs must be decontaminated with 1N NaOH and rinsed with water. HEPA filters should be bagged out and incinerated. Although there is no evidence to suggest that aerosol transmission occurs in the natural disease, it is prudent to avoid the generation of aerosols or droplets during the manipulation of tissues or fluids and during the necropsy of experimental animals. It is further strongly recommended that impervious gloves be worn for activities that provide the opportunity for skin contact with infectious tissues and fluids. Animal carcasses and other tissue waste can be disposed by incineration with a minimum secondary temperature of 1000oC (1832oF).6 Pathological incinerators should maintain a primary chamber temperature in compliance with design and applicable state regulations, and employ good combustion practices. Medical waste incinerators should be in compliance with applicable state and federal regulations.

The alkaline hydrolysis process, using a pressurized vessel that exposes the carcass or tissues to 1 N NaOH or KOH heated to 150oC, can be used as an alternative to incineration for the disposal of carcasses and tissue.5,9 The process has been shown to completely inactive TSEs (301v agent used) when used for the recommended period of time.

TABLE 3

TISSUE PREPARATION FOR HUMAN CJD AND RELATED DISEASES

1. Histology technicians wear gloves, apron, laboratory coat, and face protection. 2. Adequate fixation of small tissue samples (e.g., biopsies) from a patient with suspected prion disease can be followed by post-fixation in 96% absolute formic acid for 30 minutes, followed by 48 hours in fresh 10% formalin. 3. Liquid waste is collected in a 4L waste bottle initially containing 600 ml 6N NaOH. 4. Gloves, embedding molds, and all handling materials are disposed as regulated medical waste. 5. Tissue cassettes are processed manually to prevent contamination of tissue processors. 6. Tissues are embedded in a disposable embedding mold. If used, forceps are decontaminated as in Table 4. 7. In preparing sections, gloves are worn, section waste is collected and disposed in a regulated medical waste receptacle. The knife stage is wiped with 2N NaOH, and the knife used is discarded immediately in a "regulated medical waste sharps" receptacle. Slides are labeled with "CJD Precautions." The sectioned block is sealed with paraffin. 8. Routine staining: a. slides are processed by hand; b. reagents are prepared in 100 ml disposable specimen cups; c. after placing the coverslip on, slides are decontaminated by soaking them for 1 hour in 2N NaOH; d. slides are labeled as "Infectious-CJD." 9. Other suggestions: a.disposable specimen cups or slide mailers may be used for reagents; b. slides for immunocytochemistry may be processed in disposable petri dishes; c. equipment is decontaminated as described above or disposed as regulated medical waste. Agent Summary Statements – Prion Diseases Handling and processing of tissues from patients with suspected prion disease The special characteristics of work with prions require particular attention to the facilities, equipment, policies, and procedures involved.9 The related considerations outlined in Table 3 should be incorporated into the laboratory's risk management for this work. TABLE 4 PRION INACTIVATION METHODS FOR REUSABLE INSTRUMENTS AND SURFACES 1. Immerse in 1 N NaOH, and heat in a gravity displacement autoclave at 121oC for 30 minutes. Clean and sterilize by conventional means. 2. Immerse in 1 N NaOH or sodium hypochlorite (20,000 ppm) for 1 hour. Transfer into water and autoclave (gravity displacement) at 121oC for 1 hour. Clean and sterilize by conventional means. 3. Immerse in 1N NaOH or sodium hypochlorite (20,000 ppm) for 1 hour. Rinse instruments with water, transfer to open pan and autoclave at 121oC (gravity displacement) or 134oC (porous load) for 1 hour. Clean and sterilize by conventional means. 4. Surfaces or heat-sensitive instruments can be treated with 2N NaOH or sodium hypochlorite (20,000 ppm) for 1 hour. Ensure surfaces remain wet for entire time period, then rinse well with water. Before chemical treatment, it is strongly recommended that gross contamination of surfaces be reduced because the presence of excess organic material will reduce the strength of either NaOH or sodium hypochlorite solutions. 5. Environ LpH (EPA Reg. No. 1043-118) may be used on washable, hard, non-porous surfaces (such as floors, tables, equipment, and counters), items (such as non-disposable instruments, sharps, and sharp containers), and/or laboratory waste solutions (such as formalin or other liquids). This product is currently being used under FIFRA Section 18 exemptions in a number of States. Users should consult with the State environmental protection office prior to use. (Adapted from www.cdc.gov, 10,11) Working Solutions 1 N NaOH equals 40 grams of NaOH per liter of water. Solution should be prepared daily. A stock solution of 10 N NaOH can be prepared and fresh 1:10 dilutions (1 part 10 N NaOH plus 9 parts water) used daily. 20,000 ppm sodium hypochlorite equals a 2% solution. Most commercial household bleach contains 5.25% sodium hypochlorite, therefore make a 1:2.5 dilution (1 part 5.25% bleach plus 1.5 parts water) to produce a 20,000 ppm solution. This ratio can also be stated as two parts 5.25% bleach to three parts water. Working solutions should be prepared daily. CAUTION: Above solutions are corrosive and require suitable personal protective equipment and proper secondary containment. These strong corrosive solutions require careful disposal in accordance with local regulations. Precautions in using NaOH or sodium hypochlorite solutions in autoclaves NaOH spills or gas may damage the autoclave if proper containers are not used. The use of containers with a rim and lid designed for condensation to collect and drip back into the pan is recommended. Persons who use this procedure should be cautious in handling hot NaOH solution (post-autoclave) and in avoiding potential exposure to gaseous NaOH, exercise caution during all sterilization steps, and allow the autoclave, instruments, and solutions to cool down before removal. Immersion in sodium hypochlorite bleach can cause severe damage to some instruments. Agent Summary Statements – Prion Diseases REFERENCES 1. Prusiner SB. Prion diseases and the BSE crisis. Science. 1997;278:245-51. 2. Williams ES, Miller MW. Transmissible spongiform encephalopathies in non-domestic animals: origin, transmission and risk factors. Rev Sci Tech Off Int Epiz. 2003;22:145- 56. 3. Ridley RM, Baker HF. Occupational risk of Creutzfeldt-Jakob disease. Lancet. 1993;341:641-2. 4. Llewelyn CA, Hewitt PE, Knight RS, et al. Possible transmission of variant Creutzfeldt- Jakob disease by blood transfusion. Lancet. 2004;7;363:417-21. 5. Taylor DM, Woodgate SL. Rendering practices and inactivation of transmissible spongiform encephalopathy agents. Rev Sci Tech Off Int Epiz. 2003;22:297-310. 6. World Health Organization. [http://www.who.int/en/]. Geneva (Switzerland): The Organization; [updated 2006 Sept 21; cited 2006 Sept 21]. 2000. WHO Infection Control Guidelines for Transmissible Spongiform Encephalopathies. Report of a WHO Consultation, Geneva, Switzerland, 23-26 March 1999. Available from:

http://www.who.int/csr/resources/publications/bse/WHO_CDS_CSR_APH_2000_3/en/


7. Ironside JW and JE Bell. The 'high-risk' neuropathological autopsy in AIDS and Creutzfeldt-Jakob disease: principles and practice. Neuropathol Appl Neurobiol. 1996;22:388-393. 8. Hilton DA. Pathogenesis and prevalence of variant Creutzfeldt-Jakob disease. Pathol J. 2006;208:134-41. 9. Richmond JY, Hill RH, Weyant RS, et al. What’s hot in animal biosafety? ILAR J. 2003;44:20-7. 10. Ernst DR, Race RE. Comparative analysis of scrapie agent inactivation methods. J. Virol. Methods. 1994; 41:193-202. 11. Race RE, Raymond GJ. Inactivation of transmissible spongiform encephalopathy (prion) agents by Environ LpH. J Virol. 2004;78:2164-5.



http://www.cdc.gov/OD/OHS/biosfty/bmbl5/BMBL_5th_Edition.pdf




No occupational infections have been recorded from working with prions ???


I beg to differ. i would say that none has been documented yet, for various reasons.

incubation time period, surveillance just to name a few. how can you document something that is not reportable, and or with an incubation period that can last as long as decades.

i am reminded of our own CJD/TSE surveillance in the USA, and or, the lack of.


USA WRITTEN CJD QUESTIONNAIRE ???


http://cjdquestionnaire.blogspot.com/




vCJD questionnaire



http://www.bseinquiry.gov.uk/report/volume8/pdf/1stquestionnaire.pdf





WHAT are officials so afraid of, as to make cjd reportable of all age groups, and to have a written CJD questionnaire ???

what are they afraid of that they may find $$$

why is it they continue to rely on 'death certificates', when they themselves say it is inaccurate $$$

same with surveillance of mad cow diseae in the USA $$$ and i think this is the reason. they dont want to find either one, and or document.

SAD THAT OLDER FOLKS SEEM TO BE EXPENDABLE IN RELATIONS TO TSEs.IF YOUR NOT YOUNG, IF IT's NOT THE UKBSENVCJD ONLY STRAIN, OR IF YOU NOT A DOG OR CAT, YOUR OUTA LUCK. YOUR SPORADIC, YOUR SPONTANEOUS, in short, your expendable, you are an acceptable death. it's a corporate decission. ...tss

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

snip...



http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf





ii. Reliance on death certificates was no help, as ‘CJD is written on death certificates in quite a reckless way!’





http://www.bseinquiry.gov.uk/files/yb/1990/02/00006001.pdf



The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.http://www.cjdfoundation.org/fact.html

POLICY IN CONFIDENCE; CONFIDENTIAL; CJD IN FARMER WITH BSE COW ie OCCUPATIONAL EXPOSURE

Subject: POLICY IN CONFIDENCE: CJD IN FARMER WITH BSE COW

POLICY IN CONFIDENCE: CJD IN FARMER WITH BSE COW

LIKELY TO ATRACT MEDIA ATTENTION



http://www.bseinquiry.gov.uk/files/yb/1992/08/13002001.pdf



http://www.bseinquiry.gov.uk/files/yb/1992/08/21002001.pdf



http://www.bseinquiry.gov.uk/files/yb/1992/08/21005001.pdf



CONFIRMED CJD IN FARMER WITH BSE COW

line to take, sporadic CJD



http://www.bseinquiry.gov.uk/files/yb/1992/10/22004001.pdf



http://www.bseinquiry.gov.uk/files/yb/1992/10/22005001.pdf



http://www.bseinquiry.gov.uk/files/yb/1992/10/22001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1992/11/05002001.pdf



http://www.bseinquiry.gov.uk/files/yb/1992/11/05003001.pdf



SECOND CASE CJD IN DAIRY FARMER



http://www.bseinquiry.gov.uk/files/yb/1993/00/00001001.pdf



CJD IN AN INDIVIDUAL OCCUPATIONALLY EXPOSED TO BSE

ii. on page 2 the sentence ''He had drunk pooled milk from the herd which included that from the affected animal'' will mislead the uninformed. It needs to be made clear that milk from a cow which is suspected to be affected with BSE cannot be drunk or added to the bulk milk produced by the rest of the herd.

iii. in the final paragraph I suggest that the phrase ''and a causal link with BSE is at most conjectural'' BE DELETED: the first paragraph of the sentence would then stand as a clear statement that the CJD case was likely to have been a CHANCE PHENOMENON.



http://www.bseinquiry.gov.uk/files/yb/1993/02/15003001.pdf



''DH is aware of a second case of CJD in a dairy farmer who has had BSE in his herd. We cannot comment on the details of the case, but we know of nothing to suggest this is anthing other than a sporadic case of CJD. .........



http://www.bseinquiry.gov.uk/files/yb/1993/07/12001001.pdf



IF PRESSED:

The numbers concerned are very small, and it is not possible to draw any conclusions from such small numbers. This issue is being considered by the Government's expert advisers....



http://www.bseinquiry.gov.uk/files/yb/1993/07/12002001.pdf



THE FARMER IS THOUGHT TO HAVE HAD AT LEAST TWO CASES OF BSE IN HIS HERD, which were diagnosed in 1992. The farmer is reported to have asssisted in calving and to have drunk milk from his herd. This does not suggest that this is anything other than a sporadic case of CJD. ...



http://www.bseinquiry.gov.uk/files/yb/1993/07/12003001.pdf



CONFIDENTIAL

CONFIRMED CASE OF CJD IN DAIRY FARMER



http://www.bseinquiry.gov.uk/files/yb/1993/07/14003001.pdf



3. Neither Dr Will nor the CJD surveillance unit intend to disclose the existence of this case or make any comment at present unless it attracts media attention.

snip...

HUMAN CASE DETAILS CONFIDENTIAL

snip...

6. CJD IN FARMERS

The second annual report on CJD surveillance in the UK, which is about to be published, gives occupational history details of 29 definite and probable CJD cases recorded in people who had a history of employment at any time in particular occupational groups of potential significance for the occurrence of the disease. The 29 cases were amongst 95 diagnosed over a 3 year period: the other 66 cases did not fall into such occupational groups.

These relevant details are:-

MEDICAL/PARAMEDICAL/DENTISTRY 7

ANIMAL LABORATORY 1

PHARMACEUTICAL LABORATORY 0

RESEARCH LABORATORY 0

FARMERS/VETERINARY SURGEONS 7

BUTCHERS/ABATTOIR WORKERS/OCCUPATION INVOLVING DIRECT CONTACT WITH ANIMAL OR CARCASES 5

OCCUPATION INVOLVING ANIMAL PRODUCTS 9

snip... full text ;



http://www.bseinquiry.gov.uk/files/yb/1993/07/19001001.pdf



Rocky Mountain oysters, mountain oysters, prairie oysters, Montana tendergroin or swinging sirloin

POLICY IN CONFIDENCE

1. The article in the Daily Mail of 12 August again raises the question of a CAUSATIVE LINK BETWEEN BSE AND CJD. This follows the death of a second farmer from CJD...

snip...

I am, however, concerned about how DH and MAFF would respont to public concern generated if there are further CJD cases among farmers.

snip...

4. Unwelcome, though it maybe to the Tyrrell Committee, I think they must be asked at their next meeting to give further thought to what they might advise the Department and MAFF if ANOTHER FARMER (or TWO) DEVELOPS CJD. OR, if a butcher or abattoir worker develops the disease.

5. Although the Committee were given plenty of advance warning about the second farmer, they may NOT BE SO FORTUNATE NEXT TIME ROUND. Some Contingency planning on the Committee's response to a further case of CJD in a farmer seems essential. At the same time the Committee should consider if there is SPECIAL RISK TO FARMERS, FOR EXAMPLE THEIR HISTORICAL HABIT OF CHEWING CATTLE NUTS, that might be implicated. .....(oh my GOD...tss)



http://www.bseinquiry.gov.uk/files/yb/1993/08/12002001.pdf



Ministers will note from this that experts are of the view, that there is unlikely to be a direct link between the cases of BSE, and the occurance of CJD in the farmer.

(NOTE CJD increasing over 3 years. ...TSS)



http://www.bseinquiry.gov.uk/files/yb/1993/08/18004001.pdf



'AGE AT ONSET' is therefore likely to be a reflection of particulary aetiological factors, about which, for sporadic CJD at least, much is yet unknown. IT has therefore been suggested that examination of the f/d i/p of other groups with TSE's, and comparison with that of CJD subsets might help to elucidate aetiological mechanisms for sporadic CJD in particular; i.e. ALMOST A REVERSAL OF THE ORIGINAL UNDERTAKING.



http://www.bseinquiry.gov.uk/files/yb/1993/08/26001001.pdf



OCCUPATIONAL EXPOSURE TO BSE AND CJD

2. The Tyrrell Committee met on 7 October and the significance of the two cases of CJD reported in dairy farmers who had BSE-affected animals on their farms was discussed at some length, AS WERE THE IMPLICATIONS OF A THIRD (OR FORTH) similar case.

3. The Committee were unable to identify any possible risk factors over and above those that they had already considered, both in general and with particular of TASTING THE FEED does continue but there was no consensus about the value of advising farmers to discontinue this practice. Feed currently in use does not pose a risk because of the ruminant-ruminant feed ban.



http://www.bseinquiry.gov.uk/files/yb/1993/10/11001001.pdf



MRC

STRAIN CHARACTERISATION OF THE CREUTZFELDT-JAKOB DISEASE AGENT BY TRANSMISSION TO MICE

In view of the CONCERN that exposue to BSE OR SCRAPIE MAY POSE A RISK TO HUMANS, it is proposed investigate the relationship between sporadic creutzfeldt-jakob disease.....



http://www.bseinquiry.gov.uk/files/yb/1993/10/12001001.pdf



3. While Committee may have no leads to pursue on why farmers might be at increased risk, I hope they understand the urgency with which they will need to respond if or when a THIRD FARMER DEVELOPS CJD.



http://www.bseinquiry.gov.uk/files/yb/1993/10/18001001.pdf



INCREASE IN SPORADIC CJD



http://www.bseinquiry.gov.uk/files/yb/1993/11/11001001.pdf



occupational



http://www.bseinquiry.gov.uk/files/yb/1994/02/16001001.pdf



Dealler gets ''dixie chicked' again ;



http://www.bseinquiry.gov.uk/files/yb/1993/11/22001001.pdf



http://www.bseinquiry.gov.uk/files/yb/1993/12/08003001.pdf



http://www.bseinquiry.gov.uk/files/yb/1993/12/10006001.pdf



http://www.bseinquiry.gov.uk/files/yb/1993/12/14003001.pdf



http://www.bseinquiry.gov.uk/files/yb/1993/12/16006001.pdf



http://www.bseinquiry.gov.uk/files/yb/1993/12/17003001.pdf



STACKING THE DECK AGAINST SPORADIC CJD AND SOUND SCIENCE

APPOINTMENTS IN CONFIDENCE

MEMBERSHIP TO SEAC

snip...

I have informed Dr Tyrrell that we have now written to Dr Hueston to invite him to serve on the Committee and he was very pleased to hear this. He was also in favour of our idea of having a deputy Chairman who could take any emergency meetings eg IF THERE WERE TO BE ANOTHER CJD CASE IN AGRICULTURE. I suggested that either Dr. WIll or Dr Kimberlin were likely candidates and he thought that this was about right. He felt that on balance he would prefer Dr Will who he thought took a more cautious line and was LESS DOGMATIC. .....



http://www.bseinquiry.gov.uk/files/yb/1993/12/01003001.pdf



http://www.bseinquiry.gov.uk/files/yb/1994/01/00005001.pdf



CHANGING SCIENCE TO FIT YOUR INDUSTRY NEEDS COVER-UP IN FULL MODE NOW

PROBLEM

7. The main findings in the case-control study were STATISTICALLY SIGNIFICANT ASSOCIATIONS BETWEEN CONSUMPTION OF VEAL OR VENISON AND THE DEVELOPMENT OF CJD (INCREASED RISKS OF 2-13x).

IP PS(L) wishes to probe this further we think it best to explain the matter VERBALLY. The problem is how to present the findings in this year's annual report in a way which avoids unnecessary public alarm and limits the scope for media scare stores. (or the facts...TSS)



http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf



A REVISED VERSION WHERE THE FOLLOWING WAS MADE TO BE REMOVED FROM SCIENTIFIC FINDINGS. ...TSS

''This year's findings show a number of associations but the strongest is for veal.''

A BIG LINE WAS DRAWN THROUGH THAT SENTENCE TO BE REMOVED DUE TO THE FOLLOWING. THIS IS THE NEXT SENTENCE ;

''This is of considerable concern given recent developments. In particular, Ministers will be particularly concerned about the European dimension given the recent troubles with the Germans.''

YOU can see the beginning of the ukbsenvCJD only theory beginning to unfold now. full text of this ukbsenvcjd only conspiracy can be seen here. ...TSS

POLICY RESTRICTED



http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf



BRITISH DEER FARMERS ASSOCIATION

OCTOBER 1994

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

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

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

snip...

The statistical results regarding the consumption of venison was put into perspective in the body of the report and was NOT MENTIONED AT ALL IN THE PRESS RELEASE. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of VENISON was highlighted only by the media i.e. in the News at one television programme.

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



http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf



see buttered and watered down report here that caters to industry instead of human safety...TSS



http://www.bseinquiry.gov.uk/files/yb/1994/10/00004001.pdf



SEE WHERE THIS ;

''This year's findings show a number of associations but the strongest is for veal.''

WENT TO THIS;

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and increased risk of CJD. When some account was taken of possible confounding, the association between veal eating and risk of CJD emerged as the strongest of these associations statistically. These findings concerning dietary history are particulary difficult to interpret for two reasons.

1. .........BSeee...........TSS

2. .........BSeee...........TSS

(I.E. BSeee = bull sh!t encephalopathy or government cover-up i.e. God save the industry at all cost, including human health. ...TSS)

THUS, the reported veal eating habits of confirmed CJD cases appear virtually identical to suspect cases later judged not to have the disease. This provides good circumstantial evidence to support the hypothesis that the apparent association between veal consumption and CJD is due to recall bias. Analysis of other apparent dietary risk factors for CJD, including venison, has provided similar evidence of recall bias.

snip...

In summary, the analysis of the dietary case-control study demonstrates a strong association between a lifetime history of veal consumption and the risk of developing Creutzfeldt-Jakob disease. HOWEVER this result may well be due to recall bias and analysis of clinical and molecular bilogical features does not provide supportive evidence for the hypothesis that veal eating is a risk factor for CJD. ...

snip...

MORE OF THIS BSeee CAN BE READ IN THE FINAL GOVERNMENT DICTATED CJD REPORT OF 1994



http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf



BSE SCIENTIST WAS 'CENSORED'

He says that when he worked at MAFF, ''the way it was structurally set up was not that science would drive the politics, but that the politics will drive the science. And that's wrong.''



http://www.bseinquiry.gov.uk/files/yb/1997/12/11001001.pdf



11/3/96 DGRC alerts DTI Ministers and CSA to discovery of nvCJD on basis of letter from MRC Chief Executive dated 11/3/96

BIRTH OF THE UKBSEnvCJD ONLY THEORY, the birth of the 'BIG LIE' begins. ...tss



http://www.bseinquiry.gov.uk/files/db/do01/tab03.pdf



REPORT OF 16 YEAR OLD GIRL WITH CJD

5. This case may raise fears of a link between BSE and CJD. Current advice is that there is no scientific evidence of a link between BSE in cattle and CJD in humans. Furthermore advice from the Spongiform Encephalopathy Advisory Committee is that they are satisified that all necessary safeguards are in place to minimise further spread of spongiform encephalopathies in animals and to prevent any risk of transmission to humans. ...



http://www.bseinquiry.gov.uk/files/yb/1994/01/14005001.pdf



To ask the Secretary of State for Health, how many people under the age of 20 years in each of the last five years have suffered from Creutzfeldt-Jakob disease; and of these how many had not had any growth treatment previously.

SUGGESTED REPLY

We are not aware of any people under the age of 20 in the UK suffering from Creutzfeldt-Jakob Disease in the last five years.



http://www.bseinquiry.gov.uk/files/yb/1994/01/20001001.pdf



STATEMENT FROM HOSPITAL



http://www.bseinquiry.gov.uk/files/yb/1994/01/20005001.pdf



http://www.bseinquiry.gov.uk/files/yb/1994/01/25001001.pdf



PREPARING FOR THE STORM 'LINE TO TAKE'



http://www.bseinquiry.gov.uk/files/yb/1994/01/25003001.pdf



BARONESS CUMBERLEGE TRYING TO MANIPULATE THE MEDIA



http://www.bseinquiry.gov.uk/files/yb/1994/01/25006001.pdf



http://www.bseinquiry.gov.uk/files/yb/1994/01/25006001.pdf



MAD COW MEAL DESTROYED MY DAUGHTERS LIFE

A TEENAGE GIRL may have caught the human form of MAD COW DISEASE by eating a contaminated burger it was claimed last night.

VICKY RIMMER, 16, has the killer Creutzfeldt-Jakob disease (CJD).



http://www.bseinquiry.gov.uk/files/yb/1994/01/25007001.pdf



GIVE ME BACK MY LIFE



http://www.bseinquiry.gov.uk/files/yb/1994/01/25008001.pdf



HUSH UP! GOVERNMENT TOLD GRAN: ''YOU MUST THINK OF THE ECONOMY''



http://www.bseinquiry.gov.uk/files/yb/1994/01/25009001.pdf



WHY IS MY GIRL DYING ? '' IT WAS LIKE SOMEBODY OLD INSIDE A YOUNG PERSON'S BODY



http://www.bseinquiry.gov.uk/files/yb/1994/01/25010001.pdf



I have interviewed Mrs Rimmer at my constituency surgery

IF there is nothing to hide, why is there so much SECRECY? WHY is the Government and other Bodies trying to stop any CHANCE OF PEOPLE CONNECTING THE TWO DISEASES. The B.S.E. problem is obvious, but if the correct measures are taken, surely the problem could be contained, however, as it stands the lack of investigation and interest of the possibility of B.S.E. and C.J.D. being linked is open for speculation and surely someone has to account for peoples lives! WHY is so much trouble being taken to convice people that B.S.E. and C.J.D. are not linked? Guilty Conscience perhaps ? - or cover up?

HOUSE OF COMMONS

FROM BARRY JONES, M.P.

22 FEBRUARY 1994



http://www.bseinquiry.gov.uk/files/yb/1994/02/22009001.pdf



Alleged Case of Creutzfeld Jakob Disease: Victoria Rimmer.

(now story changes that biopsy shows she does not have CJD...tss)



http://www.bseinquiry.gov.uk/files/yb/1994/06/06004001.pdf



now story changes to ;

Advice

7. The Parliamentary Secretary is invited to note the recent statements made on __________ and the present position which remains that CJD cannot be confirmed, in this case at this stage.



http://www.bseinquiry.gov.uk/files/yb/1994/06/08004001.pdf



3. The Medical Director at ___________________ Hospital advised the Department on 6 June that the results of ___________________ brain biopsy had been received and that it showed NO EVIDENCE OF CJD. ______________ Hospital subsequently issued a statement to the press to this effect and this was publicised widely in the press (doc 1). News coverage which followed suggested that the statement made by ________________ Hospital had been misleading (doc 2). Enquires have been made of the Medical Director at _______________ Hospital who has CONFIRMED THAT THE STATEMENT ISSUED BY THE HOSPITAL WAS ISSUED IN ERROR. The facts are that two pathology reports on the same piece of brain tissue were recieved. The first report indicated that CJD was unlikely, The second report indicated that CJD was possible, PERHAPS EVEN LIKELY, but that no definitive diagnosis could be made before a post mortem was undertaken.



http://www.bseinquiry.gov.uk/files/yb/1994/06/08006001.pdf



(ONLY PROBLEM IS, VICKY RIMMER, 16, DID NOT DIE FROM nvCJD, SHE DIED FROM SPORADIC CJD, the same damn thing. ...TSS)

IN light of Asante/Collinge et al findings that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD;

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To: "[log in to unmask]"

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.

I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best wishes.

Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:

[log in to unmask] (until 9/12/02)

New e-mail: [log in to unmask] (active from now)

____________________________________

snip...

full text ;



http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm



WHAT ABOUT U.S.A. ???

CJD YOUNG PEOPLE

in the USA, a 16 year old in 1978;

ALSO IN USA;

(20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. see second url below)

in France, a 19 year old in 1982;

in Canada, a 14 year old of UK origin in 1988;

in Poland, cases in people aged 19, 23, and 27 were identified in a retrospective study (published 1991), having been originally misdiagnosed with a viral encephalitis;

Creutzfeldt's first patient in 1923 was aged 23.



http://www.bseinquiry.gov.uk/files/yb/1995/10/27013001.pdf



20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. A 19 year old died from sCJD in France in 1985. There is no evidence of an iatrogenic cause for those cases....



http://www.bseinquiry.gov.uk/files/yb/1995/10/04004001.pdf



NOW BACK TO THOSE FARMERS WITH BSE HERDS THAT DIED FROM SPORADIC CJD

CJD FARMERS WIFE 1989



http://www.bseinquiry.gov.uk/files/yb/1989/10/13007001.pdf



http://www.bseinquiry.gov.uk/files/yb/1989/10/13003001.pdf



cover-up of 4th farm worker ???



http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf



http://www.bseinquiry.gov.uk/files/yb/1995/10/20006001.pdf



CONFIRMATION OF CJD IN FOURTH FARMER



http://www.bseinquiry.gov.uk/files/yb/1995/11/03008001.pdf



now story changes from;

SEAC concluded that, if the fourth case were confirmed, it would be worrying, especially as all four farmers with CJD would have had BSE cases on their farms.

to;

This is not unexpected...

was another farmer expected?



http://www.bseinquiry.gov.uk/files/yb/1995/11/13010001.pdf



4th farmer, and 1st teenager



http://www.bseinquiry.gov.uk/files/yb/1996/02/27003001.pdf



2. snip...

Over a 5 year period, which is the time period on which the advice from Professor Smith and Dr. Gore was based, and assuming a population of 120,000 dairy farm workers, and an annual incidence of 1 per million cases of CJD in the general population, a DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN an individual in the general population to develop CJD. Using the actual current annual incidence of CJD in the UK of 0.7 per million, this figure becomes 7.5 TIMES.

3. You will recall that the advice provided by Professor Smith in 1993 and by Dr. Gore this month used the sub-population of dairy farm workers who had had a case of BSE on their farms - 63,000, which is approximately half the number of dairy farm workers - as a denominator. If the above sums are repeated using this denominator population, taking an annual incidence in the general population of 1 per million the observed rate in this sub-population is 10 TIMES, and taking an annual incidence of 0.7 per million, IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than that in the general population...



http://www.bseinquiry.gov.uk/files/yb/1995/01/31004001.pdf



IN CONFIDENCE

CJD IN FARMERS WIFE

Locally, they made quite an association with BSE, since she was a farmers wife on a farm that, atypically for that area of s Yorkshire, had several BSE cases.



http://www.bseinquiry.gov.uk/files/yb/1989/10/13003001.pdf



A CASE OF CJD - (NOT FROM A BSE FARM)

Dr. R G Will has looked into the case about which I wrote a month ago, and concludes ''any connection between this patient and any bovine condition was tenuous''. No further action is called for.



http://www.bseinquiry.gov.uk/files/yb/1989/11/20011001.pdf



WE concluded that it would be a mistake to involve CDSC, since this would encourage people to believe CJD was somehow directly communicable and would increase the noise in the reporting, just as making CJD notifiable would.



http://www.bseinquiry.gov.uk/files/yb/1989/11/29003001.pdf



http://www.bseinquiry.gov.uk/files/yb/1989/12/01004001.pdf



http://www.bseinquiry.gov.uk/files/yb/1989/12/01003001.pdf



DOES ANYONE BESIDES ME SEE A PATTERN YET ???

Vickey Rimmer, 16, DID NOT DIE FROM nvCJD, she died from a form of sporadic CJD, whatever the hell that is. and there have been 16 year old die from sporadic CJD in the USA as well.

SIMPLY PUT, the ukbsenvcjd only theory was wrong from day one. the elderly are expendable, pets and kids are not.

Science was dictated by 'big buisness' after the Vickey Rimmer case with the ukbsenvcjd only myth.

YOU CAN SEE FULL TEXT ;

Thursday, July 10, 2008 A New Prionopathy OR more of the same old BSe





http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html




CONFIDENTIAL

6. CJD IN FARMERS

The second annual report on CJD surveillance in the UK, which is about to be published, gives occupational history details of 29 definite and probable CJD cases recorded in people who had a history of employment at any time in particular occupational groups of potential significance for the occurrence of the disease. The 29 cases were amongst 95 diagnosed over a 3 year period: the other 66 cases did not fall into such occupational groups.


These relevant details are:-


MEDICAL/PARAMEDICAL/DENTISTRY 7

ANIMAL LABORATORY 1

PHARMACEUTICAL LABORATORY 0

RESEARCH LABORATORY 0

FARMERS/VETERINARY SURGEONS 7

BUTCHERS/ABATTOIR WORKERS/OCCUPATION INVOLVING DIRECT CONTACT WITH ANIMAL OR CARCASES 5

OCCUPATION INVOLVING ANIMAL PRODUCTS 9

snip... full text ;


http://www.bseinquiry.gov.uk/files/yb/1993/07/19001001.pdf


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



CJD toll among farmers `too high for mere chance' August 15, 1997 PA News John von Radowitz and Andrew Woodcock Microbiologist Richard Lacey, billed in this story as the first to suggest a link between CJD and BSE seven years ago, was cited in this story as saying that the number of cattle farmers falling victim to Creutzfeld-Jakob Disease is much too high to be mere chance, adding that, "Where the CJD Surveillance Unit come unstuck is in trying to explain what happened to these six farmers. This is just too many to have occurred by chance. Unfortunately they don't want to consider the possibility that these farmers in this country and other countries were infected by cattle before BSE developed."

The story notes that professor Lacey believes sporadic CJD itself originates from a cattle infection - possibly a precursor to BSE that has not yet been detected, adding that,

"For years I have suggested that the cause is a rare disease in cattle world wide. Both BSE and the new variant CJD are a new and different disease. What has probably happened is that BSE is a variant of the old type of disease, which could have been missed because it's symptom free. It would explain why such an unusually high number of dairy farmers are being affected by CJD both here and abroad." He also said that cases of sporadic CJD had been recorded as far back as the 1920s. Professor Lacey went on to add that he thought the new variant pattern was alarming, adding, "It's rising, and that is a concern. Unfortunately we can't predict the scale of the problem. If the disease doubled each year up to the year 2020 you'd have hundreds of thousands of cases."



http://www.mad-cow.org/~tom/cousens_gore.html#toll




Prions
Iatrogenic Disease
Source of Contamination N=
n Growth Hormone 139
n Dura Mater Grafts 114
n Neurosurgery 5
n Gonadotropin 4
n Corneal Transplants 3
n Stereotactic EEG 2
Total 267
Brown et al: Neurology 2000; 55:1075


1: J Neurosci Nurs. 1991 Apr;23(2):116-9.



Recommended Biosafety Practices for Handling Prions andPrion-Infected TissuesUpdated May 2007


hazard is from accidental parenteral inoculation or ingestion. Cuts and punctures should be avoided and the use of sharp knives, scalpels, blades and needles should be minimized. If the use of sharps cannot be avoided, cut-resistant gloves should be worn (CFIA 2005). Wherever possible, the laboratory and equipment used for work with prions should be dedicated to that task alone. All employees should be informed and aware that prion research is being conducted in the lab. The entrance to the lab should allow for the separation of PPE/lab clothing and staff clothing. An exposure protocol should be developed, posted and communicated to all employees (CFIA 2005, UCSD 2002). Procedures should be in place for the effective decontamination of all waste, re-usable equipment, surfaces and other lab space (CFIA 2005, UCSD 2002).




http://www.biosafety.msu.edu/current_topic/Prions/working_with_prions.pdf





Precautions prevent spread of Creutzfeldt-Jakob disease. Mocsny N. Veterans Administration Medical Center, Cincinnati, Ohio.

In addition, there are now three cases of laboratory workers with CJD from exposure in the workplace.



http://www.ncbi.nlm.nih.gov/pubmed/1831471?ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum




NEXT ;

Q J Med 2000; 93: 617-631 © 2000 Association of Physicians

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

Commentary papers

Is there evidence for exogenous risk factors in the aetiology and spread of Creutzfeldt-Jakob disease? C. E. M. Hillier and R. L. Salmon From the Welsh Combined Centres for Public Health, University of Wales College of Medicine, Cardiff, UK

snip...

Occupational exposure: observations from case reports and series Case reports and series focus on two main occupational groups; health professionals and those who are exposed to farm animals, in particular sheep and cattle.

There are at least 26 reports of sporadic CJD in health-care workers world-wide.69–71 These include seven physicians, including a neurologist and head of an intensive care unit, two neurosurgeons, an orthopaedic surgeon and a pathologist, three dentists, a dental surgeon, nine nurses, three nursing assistants and two histopathology technicians. Clinical details are available for six of the cases.

Berger70 describes a 58-year-old physician who died of definite CJD and who, 20 years previously, had frequently performed autopsies. Weber71 described a case in a 55-year-old orthopaedic surgeon who died of definite CJD. The clinical picture was suggestive of a peripheral route of infection. Twenty years previously, he had handled both sheep and human dura mater. The specimens of dura mater were later sent to a company that sold dura mater preparations that subsequently transmitted CJD on six occasions. His wife did not remember any definite injury during the time he was working with dura mater. Schoene72 reported a case with an atypical clinical presentation including necrotizing cutaneous lesions with vasculitis in a 54-year-old neurosurgeon, which was later confirmed, as CJD, by experimental transmission. There was no definite history of exposure to any case of CJD. In a case in a pathologist,73 he is known to have performed over 14 000 autopsies, but it is not known if any of them were cases of CJD. There is no information on the dentists or nurses. One of the two histopathology technicians had been a neuropathology technician for 22 years74 and had come into contact with two cases of CJD, 16 and 11 years before the onset of her disease. The other technician75 had been exposed to animal and human brain.

A wide range of occupations have been reported among cases of sporadic CJD.6,21 Several case series quote an excess number of farmers and farmers' wives.24,30 In an Italian study,24 the incidence was three times the expected. An analysis of epidemiological surveillance data in the UK from 1970–9616 revealed a statistically significant excess of cases among dairy farm workers and their spouses and among people with greater degrees of contact with live cattle infected with BSE. No such excess was found in abattoir workers butchers or meat cutters.

snip...



http://qjmed.oxfordjournals.org/cgi/content/full/93/9/617



WHO/CDS/CSR/APH/2000.3 10 WHO Infection Control Guidelines for Transmissible Spongiform Encephalopathies Section 4.

OCCUPATIONAL INJURY 4.1

Occupational exposure Although there have been no confirmed cases of occupational transmission of TSE to humans, cases of CJD in healthcare workers have been reported in which a link to occupational exposure is suggested. Therefore, it is prudent to take a precautionary approach. In the context of occupational exposure, the highest potential risk is from exposure to high infectivity tissues through needle-stick injuries with inoculation; however exposure to either high or low infectivity tissues through direct inoculation (e.g. needle-sticks, puncture wounds, .sharps. injuries, or contamination of broken skin) must be avoided. Exposure by splashing of the mucous membranes (notably the conjunctiva) or unintentional ingestion may be considered a hypothetical risk and must also be avoided. Healthcare personnel who work with patients with confirmed or suspected TSEs, or with their high or low infectivity tissues, should be appropriately informed about the nature of the hazard, relevant safety procedures, and the high level of safety which will be provided by the proposed procedures described throughout this document.'



http://www.who.int/csr/resources/publications/bse/whocdscsraph2003.pdf



PMCID: PMC1769932

Copyright © Copyright 2003 Journal of Clinical Pathology

Health and safety at necropsy

J L Burton Correspondence to: Dr J L Burton, Academic Unit of Pathology, E-Floor Medical School, Beech Hill Road, Sheffield S10 2RX, UK; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000134/!x-usc:mailto:j.l.burton@shef.ac.uk Accepted October 16, 2002.

Transmissible spongiform encephalopathies The risk of acquiring other category 3 risk pathogens, notably the prions responsible for TSE (including v-CJD) is considerably less. However, it should be remembered that the agents responsible for TSE are extremely resilient. They are not “killed” by formalin or phenolised formalin fixation, and are resistant to routine methods of physical and chemical decontamination.3,21,81 Furthermore, v-CJD can be transmitted from archived, formalin fixed, paraffin wax embedded tissues,82 and can survive reduction to ash at 360°C.3 Decontamination requires disinfection with sodium hypochlorite (20 000 parts per million chlorine for at least one hour), 1–2M sodium hydroxide, or steam autoclaving at 134°C for at least 18 minutes.3 Given the prolonged latency of these disorders, evidence of an occupational risk to postmortem room workers remains circumstantial. However, a single case of v-CJD has been reported in a laboratory technician whose work included handling formalin fixed brains.83



http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1769932



http://www.ncbi.nlm.nih.gov/pubmed/3281004



CREUTZFELDT-JAKOB DISEASE (CJD)

The risk of occupational exposure is considered low however reported cases include one neurosurgeon, one pathologist and three pathology technicians.



http://ag.ca.gov/cci/content/bbpsafty.php#cjd



Infection Control Policy for the Management of Patients with, Suspected, or ‘At Risk’ of Having Creutzfeldt-Jakob Disease or Any Transmissible Spongiform Encephalopathy (TSE) (Interim Policy)



http://www.lcrpct.nhs.uk/site/Internet/PoliciesAndProcedures/Clinical/InfectionControlCommunityHospitals/0/CH023%20Patients%20with%20Suspected%20or%20at%20Risk%20of%20Having%20CJD%20Policy%201.pdf



Blackpool Fylde and Wyre Hospitals NHS Trust Revision No: 2 Review Date:01/02/2008 I.D. No: CORP/PROC/031 Title: Healthcare Workers Exposed To Infective Tissues And Body Fluids From Patients Known To Have, Or At High Risk Of Having A Transmissible Spongiform Encephalopathy (Tse)



http://www.bfwhospitals.nhs.uk/about/foi/part_two/cat8/documents/ic_docs/Corp_Proc_031.pdf



TRANSMISSABLE SPONGIFORM ENCEPHALOPATHIES (TSEs) POLICY LEAD DIRECTOR: Alex Horne, Medical Director POLICY APPROVED BY: Executive Management Team DATE POLICY APPROVED: June 2007 IMPLEMENTATION DATE: June 2007 REVIEW DATE: June 2009

snip...

6.0 Occupational Exposure

Although cases of CJD/vCJD have been reported in healthcare workers, there have been no confirmed cases linked to occupational exposure. It is important to take a precautionary approach. The highest potential risk is from exposure to high infectivity tissues through direct inoculation as a result of sharps injuries, puncture wounds or contamination of broken skin or exposure of the mucous membranes.

If a TSE were to develop as a result of occupational exposure, it may only become apparent decades later. It is a requirement of the COSHH regulations that employers keep a list of employees exposed to human TSE agents for 40 years following the last known exposure (for known and suspected). This list is not required for those involved in routine clinical care of patients with CJD or a related disorder, but does include those who have been involved in any invasive procedure.

An official record will be made of all incidents with infectious or potentially infectious material involving the exposure of individuals. This will apply whether or not the accident is reportable under RIDDOR.

The COSHH regulations provide the framework to control the risk from a range of hazardous substances including biological agents. Schedule 9 of the regulations includes the TSE agents.

All employees must have a clear understanding of identifiable risks to their health arising from work and the actions to be taken in dealing with situations in which exposure may occur.

If there is any incident with a known exposure of staff to potentially infectious material, then there must be an urgent incident meeting to consider up-to-date evidence on treatment options, along with infection control aspects of the incident.

This will include: Infection Control Doctor - Infection Control Nurse - Occupational Health - Consultant Communicable Disease Control - Manager of Staff Member

snip...



http://www.nelmht.nhs.uk/downloads/TSEs%20Policy%20CG036.pdf




Sunday, December 16, 2007 Risk factors for sporadic Creutzfeldt-Jakob disease Sunday, December 16, 2007 Risk factors for sporadic Creutzfeldt-Jakob disease Published Online: 11 Dec 2007

Copyright © 2007 American Neurological Association



http://creutzfeldt-jakob-disease.blogspot.com/2007/12/risk-factors-for-sporadic-creutzfeldt.html




SEAC 99th meeting on Friday 14th December 2007

snip...

© SEAC 2007

New research

4. Preliminary, unpublished results of research from the Health Protection Agency, aimed at addressing some of the uncertainties in the risk assessments, were reviewed by SEAC (SEAC 97, May 2007). The prion agent used in these studies is closely related to the vCJD agent. This research, using a mouse model, shows that following inoculation of mouse-adapted bovine spongiform encephalopathy (BSE) directly into the gut, infectivity subsequently becomes widespread in tissues of the oral cavity, including dental pulp, salivary glands and gingiva, during the preclinical as well as clinical stage of disease.

5. It is not known how closely the level and distribution of infectivity in the oral cavity of infected mice reflects those of humans infected with vCJD, as there are no comparable data from oral tissues, in particular dental pulp and gingiva, from human subclinical or clinical vCJD cases. Although no abnormal prion protein was found in a study of human dental tissues, including dental pulp, salivary glands and gingiva from vCJD cases22, the relationship between levels of infectivity and abnormal prion protein is unclear23. Infectivity studies underway using the mouse model and oral tissues that are presently available from human vCJD cases will provide some comparable data. On the basis of what is currently known, there is no reason to suppose that the mouse is not a good model for humans in respect to the distribution of infectivity in oral tissues. Furthermore, the new data are consistent with published results from experiments using a hamster scrapie model24.

6. A second set of experiments using the same mouse model showed that non-invasive and transient contact between gingival tissue and fine dental files contaminated with mouse-adapted BSE brain homogenate transmits infection very efficiently. It is not known how efficient gingival transmission would be if dental files were contaminated with infectious oral tissues and then subsequently cleaned and sterilised, a situation which would more closely model human dental practice. Further studies using the mouse model that would be more representative of the human situation, comparing oral tissues with a range of doses of infectivity, cleaned and sterilised files and the kind of tissue contact with instruments that occurs during dentistry, should be considered.

7. SEAC considered that the experiments appear well designed and the conclusions justified and reliable, while recognising that the research is incomplete and confirmatory experiments have yet to be completed. It is recommended that the research be completed, submitted for peer-review and widely disseminated as soon as possible so others can consider the implications. Nevertheless, these preliminary data increase the possibility that some oral tissues of humans infected with vCJD may potentially become infective during the preclinical stage of the disease. In addition, they increase the possibility that infection could potentially be transmitted not only via accidental abrasion of the lingual tonsil or endodontic procedures but a variety of routine dental procedures.

20 Department of Health (2006) Dentistry and vCJD: the implications of a carrier-state for a self-sustaining epidemic. Unpublished. 21 SEAC (2006) Position statement on vCJD and endodontic dentistry.



http://www.seac.gov.uk/statements/statement0506.htm



22 Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343. 23 SEAC 90 reserved business minutes.

Implications for transmission risks

snip...PLEASE SEE DISTURBING FINDINGS FULL TEXT HERE ;


http://seac992007.blogspot.com/



Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in Endodontic Practice in Absence of Adequate Prion Inactivation

Nadège Bourvis1,2, Pierre-Yves Boelle1,2,3, Jean-Yves Cesbron4,5,6, Alain-Jacques Valleron1,2,3*

1 Université Pierre et Marie Curie-Paris6, Unité de Recherche Epidémiologie-Systèmes d'information-Modélisation, UMR S 707, Paris, France, 2 INSERM, U707, Paris, France, 3 Assistance Publique-Hôpitaux de Paris (AP-HP), Unité de Santé Publique, Hôpital St Antoine, Paris, France, 4 Laboratoire Adaptation et de Pathogénie des Micro-organismes, Université Joseph Fourier, UMR 5163, Grenoble, France, 5 Centre National de la Recherche Scientifique (CNRS), UMR 5163, Grenoble, France, 6 Centre hospitalier universitaire (CHU) de Grenoble, Laboratoire d'Immunologie, Grenoble, France

Abstract

Background

Experimental results evidenced the infectious potential of the dental pulp of animals infected with transmissible spongiform encephalopathies (TSE). This route of iatrogenic transmission of sporadic Creutzfeldt-Jakob disease (sCJD) may exist in humans via reused endodontic instruments if inadequate prion decontamination procedures are used.

Methodology/Principal Findings

To assess this risk, 10 critical parameters in the transmission process were identified, starting with contamination of an endodontic file during treatment of an infectious sCJD patient and ending with possible infection of a subsequent susceptible patient. It was assumed that a dose-risk response existed, with no-risk below threshold values. Plausible ranges of those parameters were obtained through literature search and expert opinions, and a sensitivity analysis was conducted. Without effective prion-deactivation procedures, the risk of being infected during endodontic treatment ranged between 3.4 and 13 per million procedures. The probability that more than one case was infected secondary to endodontic treatment of an infected sCJD patient ranged from 47% to 77% depending on the assumed quantity of infective material necessary for disease transmission. If current official recommendations on endodontic instrument decontamination were strictly followed, the risk of secondary infection would become quasi-null.

Conclusion

The risk of sCJD transmission through endodontic procedure compares with other health care risks of current concern such as death after liver biopsy or during general anaesthesia. These results show that single instrument use or adequate prion-decontamination procedures like those recently implemented in dental practice must be rigorously enforced.

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http://www.plosone.org/article/info:doi/10.1371/journal.pone.0001330



http://www.plosone.org/article/fetchObjectAttachment.action;jsessionid=A92C286CBD5A9668069613D3CD070D90?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0001330&representation=PDF



Conclusions 14. Preliminary research findings suggest that the potential risk of transmission of vCJD via dental procedures may be greater than previously anticipated. Although this research is incomplete, uses an animal model exposed to relatively high doses of infectivity, and there are no data from infectivity studies on human oral tissues, these findings suggest an increased possibility that vCJD may be relatively efficiently transmitted via a range of dental procedures. Ongoing infectivity studies using human oral tissues and the other studies suggested here will enable more precise assessment of the risks of vCJD transmission through dental procedures.

15. Guidance was issued to dentists earlier this year recommending that endodontic files and reamers be treated as single use which, provided it is adhered to, will remove any risk of a self-sustaining epidemic arising from re-use of these instruments. To minimise risk it is critical that appropriate management and audit is in place, both for NHS and private dentistry.

16. It is also critical that a detailed and comprehensive assessment of the risks of all dental procedures be conducted as a matter of urgency. While taking into account the continuing scientific uncertainties, this will allow a more thorough consideration of the possible public health implications of vCJD transmission via dentistry and the identification of possible additional precautionary risk reduction measures. The assessment will require continued updating as more evidence becomes available on the transmissibility of vCJD by dental routes, and on the prevalence of infection within the population. A DH proposal to convene an expert group that includes dental professionals to expedite such an assessment is welcomed. Given the potential for transmission via dentistry, consideration should be given to the urgent assessment of new decontamination technologies which, if proved robust and effective, could significantly reduce transmission risks.

SEAC June 2007

References 1Smith et al. (2003) Prions and the oral cavity. J. Dent. Res. 82, 769-775.

2Smith et al. (2005) Residual protein levels on reprocessed dental instruments. J. Hosp. Infect. 61, 237-241.

3Everington et al. (2007) Dental treatment and risk of variant CJD – a case control study. Brit. Den. J. 202, 1-3.

4Department of Health. (2003) Risk assessment for vCJD and dentistry.

5 Department of Health (2006) Dentistry and vCJD: the implications of a carrier-state for a self-sustaining epidemic. Unpublished.

6SEAC (2006) Position statement on vCJD and endodontic dentistry.


http://www.seac.gov.uk/statements/statement0506.htm



7Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343.

8SEAC 90 reserved business minutes.

9Ingrosso et al. (1999) Transmission of the 263K scrapie strain by the dental route. J. Gen. Virol. 80, 3043-3047.

10Department of Health (2006) Dentistry and vCJD: the implications of a carrier-state for a self-sustaining epidemic. Unpublished.

11Clarke & Ghani (2005) Projections of future course of the primary vCJD epidemic in the UK: inclusion of subclinical infection and the possibility of wider genetic susceptibility R. J. Soc. Interface. 2, 19-31.

12SEAC Epidemiology Subgroup (2006) position statement of the vCJD epidemic.


http://www.seac.gov.uk/statements/st...06subgroup.htm



13DH (2007) Precautionary advice given to dentists on re-use of instruments


http://www.gnn.gov.uk/environment/fu...partment=False




Page updated: 8 June, 2007



http://www.seac.gov.uk/statements/state-vcjd-dentrstry.htm




Subject: MASTER DENTIST FALLS VICTIM TO CJD Date: March 31, 2007 at 1:27 pm PST

''It was in the cards a long time ago,'' she says. ''We've put it in the hands of God.''

- Crystal Harmon can be reached at 894-9643 or by e-mail at mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000134/!x-usc:mailto:charmon@bc-times.com.



http://www.mlive.com/news/bctimes/index.ssf?/base/news-9/1175181333132150.xml&coll=4



Occupational risk factors for the sporadic form of Creutzfeldt-Jakob disease. Cocco PL, Caperna A, Vinci F. Dipartimento di Sanità Pubblica, Sezione di Medicina del Lavoro, Università di Cagliari, via San Giorgio 12, 09124 Cagliari. mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000134/!x-usc:mailto:coccop@pacs.unica.it

1: Med Lav. 2003 Jul-Aug;94(4):353-63.

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CJD cases represented a wide variety of occupations (159) and industries (147). Among occupations and industries, for which previous reports suggested potential exposure to a transmissible spongiform encephalopathy (TSE) agent, the OR for CJD was significantly increased among butchers (OR = 6.8, 95% C.I. 1.5, 30.1, based on 4 cases and 3 controls), and persons working in offices of physicians (OR = 4.6, 95% C.I. 1.2, 17.6 based on 5 cases and 4 controls). Nine other occupations and seven other industries, for which no previous suggestion existed in the literature, also showed significant associations. Overall, our results suggest that occupational exposures are not an important source of sCJD infection. However, as the excess among butchers and some workers in health occupations was consistent with previous reports, more indepth research is warranted to address the hypothesis.




http://www.ncbi.nlm.nih.gov/pubmed/14526494




Saturday, December 08, 2007 Transfusion Transmission of Human Prion Diseases


http://vcjdblood.blogspot.com/2006/12/vcjd-case-study-highlights-blood.html





Thursday, July 24, 2008Prion diseases are efficiently transmitted by blood transfusion in sheep Submitted April 18, 2008 Accepted June 28, 2008



http://vcjdblood.blogspot.com/2008/07/prion-diseases-are-efficiently.html



Saturday, January 20, 2007 Fourth case of transfusion-associated vCJD infection in the United Kingdom


http://vcjdtransfusion.blogspot.com/2007/01/fourth-case-of-transfusion-associated.htmlhttp://vcjdblood.blogspot.com/



OCCUPATIONAL EXPOSURE FROM TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES TSEs IN THE USA


let me count the ways. ...tss



Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007.



http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf




Scrapie



http://scrapie-usa.blogspot.com/




NOR-98



http://nor-98.blogspot.com/2008_04_01_archive.html




Friday, July 18, 2008
TSE risk assessment from carcasses of ovine and caprine animals below 6 months of age from TSE infected flocks intended for human consumption


http://nor-98.blogspot.com/2008/07/tse-risk-assessment-from-carcasses-of.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.

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

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full text ;




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





Transmissible Mink Encephalopathy TME




http://transmissible-mink-encephalopathy.blogspot.com/






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

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