Supreme Court Protects Vaccine Manufacturers, Not Injured Children there from Bruesewitz vs Wyeth

OCTOBER TERM, 2010

Syllabus

NOTE: Where it is feasible, a syllabus (headnote) will be released, as isbeing done in connection with this case, at the time the opinion is issued.The syllabus constitutes no part of the opinion of the Court but has been prepared by the Reporter of Decisions for the convenience of the reader. See United States v. Detroit Timber & Lumber Co., 200 U. S. 321, 337.

SUPREME COURT OF THE UNITED STATES

Syllabus

BRUESEWITZ ET AL. v. WYETH LLC, FKA WYETH, INC., ET AL.

CERTIORARI TO THE UNITED STATES COURT OF APPEALS FOR THE THIRD CIRCUIT

No. 09–152. Argued October 12, 2010—Decided February 22, 2011

The National Childhood Vaccine Injury Act of 1986 (NCVIA or Act) created a no-fault compensation program to stabilize a vaccine market adversely affected by an increase in vaccine-related tort litigation and to facilitate compensation to claimants who found pursuing legitimate vaccine-inflicted injuries too costly and difficult. The Act provides that a party alleging a vaccine-related injury may file a petition for compensation in the Court of Federal Claims, naming the Health and Human Services Secretary as the respondent; that the court must resolve the case by a specified deadline; and that the claimant can then decide whether to accept the court’s judgment or reject it and seek tort relief from the vaccine manufacturer. Awards are paid out of a fund created by an excise tax on each vaccine dose. As a quid pro quo, manufacturers enjoy significant tort-liability protections. Most importantly, the Act eliminates manufacturer liability for a vaccine’s unavoidable, adverse side effects. Hannah Bruesewitz’s parents filed a vaccine-injury petition in the Court of Federal Claims, claiming that Hannah became disabled after receiving a diphtheria, tetanus, and pertussis (DTP) vaccine manufactured by Lederle Laboratories (now owned by respondent Wyeth). After that court denied their claim, they elected to reject the unfavorable judgment and filed suit in Pennsylvania state court, alleging, inter alia, that the defective design of Lederle’s DTP vaccine caused Hannah’s disabilities, and that Lederle was subject to strictliability and liability for negligent design under Pennsylvania common law. Wyeth removed the suit to the Federal District Court. It granted Wyeth summary judgment, holding that the relevant Pennsylvania law was preempted by 42 U. S. C. §300aa–22(b)(1), which 2 BRUESEWITZ v. WYETH LLC

Syllabus

provides that "[n]o vaccine manufacturer shall be liable in a civil action for damages arising from a vaccine-related injury or death associated with the administration of a vaccine after October 1, 1988, if the injury or death resulted from side-effects that were unavoidable even though the vaccine was properly prepared and was accompanied by proper directions and warnings." The Third Circuit affirmed.

Held: The NCVIA preempts all design-defect claims against vaccine manufacturers brought by plaintiffs seeking compensation for injury or death caused by a vaccine’s side effects. Pp. 7–19.

(a) Section 300aa–22(b)(1)’s text suggests that a vaccine’s design is not open to question in a tort action. If a manufacturer could be held liable for failure to use a different design, the "even though" clause would do no work. A vaccine side effect could always have been avoidable by use of a different vaccine not containing the harmful element. The language of the provision thus suggests the design is not subject to question in a tort action. What the statute establishes as a complete defense must be unavoidability (given safe manufacture and warning) with respect to the particular design. This conclusion is supported by the fact that, although products-liability law establishes three grounds for liability—defective manufacture, inadequate directions or warnings, and defective design—the Act mentions only manufacture and warnings. It thus seems that the Act’s failure to mention design-defect liability is "by deliberate choice, not in advertence." Barnhart v. Peabody Coal Co., 537 U. S. 149, 168. Pp. 7–8.

(b) Contrary to petitioners’ argument, there is no reason to believe that §300aa–22(b)(1)’s term "unavoidable" is a term of art incorporating Restatement (Second) of Torts §402A, Comment k, which exempts from strict liability rules "unavoidably unsafe products." "Unavoidable" is hardly a rarely used word, and cases interpreting comment k attach special significance only to the term "unavoidably unsafeproducts," not the word "unavoidable" standing alone. Moreover, reading the phrase "side effects that were unavoidable" to exempt injuries caused by flawed design would require treating "even though"as a coordinating conjunction linking independent ideas when it is a concessive, subordinating conjunction conveying that one clause weakens or qualifies the other. The canon against superfluity does not undermine this Court’s interpretation because petitioners’ competing interpretation has superfluity problems of its own. Pp. 8–12.

(c) The structure of the NCVIA and of vaccine regulation in general reinforces what §300aa–22(b)(1)’s text suggests. Design defects do not merit a single mention in the Act or in Food and Drug Administration regulations that pervasively regulate the drug manufacturing process. This lack of guidance for design defects, combined with

3 Cite as: 562 U. S. ____ (2011) Syllabus

the extensive guidance for the two liability grounds specifically mentioned in the Act, strongly suggests that design defects were not mentioned because they are not a basis for liability. The Act’s mandates lead to the same conclusion. It provides for federal agency improvement of vaccine design and for federally prescribed compensation,which are other means for achieving the two beneficial effects of design-defect torts—prompting the development of improved designs, and providing compensation for inflicted injuries. The Act’s structural quid pro quo also leads to the same conclusion. The vaccine manufacturers fund an informal, efficient compensation program for vaccine injuries in exchange for avoiding costly tort litigation and the occasional disproportionate jury verdict. Taxing their product to fund the compensation program, while leaving their liability for design defect virtually unaltered, would hardly coax them back into the market. Pp. 13–16.

561 F. 3d 233, affirmed.

SCALIA, J., delivered the opinion of the Court, in which ROBERTS,

C. J., and KENNEDY, THOMAS, BREYER, and ALITO, JJ., joined. BREYER, J., filed a concurring opinion. SOTOMAYOR, J., filed a dissenting opinion, in which GINSBURG, J., joined. KAGAN, J., took no part in the consideration or decision of the case. _________________ _________________ 1 Cite as: 562 U. S. ____ (2011)

Opinion of the Court

NOTICE: This opinion is subject to formal revision before publication in thepreliminary print of the United States Reports. Readers are requested tonotify the Reporter of Decisions, Supreme Court of the United States, Washington, D. C. 20543, of any typographical or other formal errors, in orderthat corrections may be made before the preliminary print goes to press.

SUPREME COURT OF THE UNITED STATES

No. 09–152

RUSSELL BRUESEWITZ, ET AL., PETITIONERS v. WYETH LLC, FKA WYETH, INC., FKA WYETHLABORATORIES, ET AL.

ON WRIT OF CERTIORARI TO THE UNITED STATES COURT OFAPPEALS FOR THE THIRD CIRCUIT

[February 22, 2011]

JUSTICE SCALIA delivered the opinion of the Court.

We consider whether a preemption provision enacted inthe National Childhood Vaccine Injury Act of 1986(NCVIA)1 bars state-law design-defect claims againstvaccine manufacturers. .....



snip...please see full text ;



http://www.supremecourt.gov/opinions/10pdf/09-152.pdf





Is polio still a disease seen in the United States? The last cases of naturally occurring paralytic polio in the United States were in 1979, when an outbreak occurred among the Amish in several Midwestern states. From 1980 through 1999, there were 152 confirmed cases of paralytic polio cases reported. Of the 152 cases, eight cases were acquired outside the United States and imported. The last imported case caused by wild poliovirus into the United States was reported in 1993.



The remaining 144 cases were vaccine-associated paralytic polio (VAPP) caused by live oral polio vaccine (OPV).


http://www.cdc.gov/vaccines/vpd-vac/polio/dis-faqs.htm



How do Democrats and Republicans stand on tort reform issues?

"Tort Reform" is a very partisan issue. At both the state and national levels, Republicans overwhelmingly support tort reform and Democrats oppose it. The trial lawyer associations which represent plaintiff lawyers are major contributors to the Democrats. Insurance and medical interests contribute heavily to Republicans. In fact, the tort reform debate can be considered as an aspect of the overall political dynamic involving distribution of the nation's wealth. The most contentious issues involve medical malpractice and product liability. The result of settlements and verdicts of these cases is a transfer of wealth from groups which tend to be wealthy to victims and their lawyers. Virtually all the reform proposals ultimately attempt to limit the amount of funds which are distributed in this fashion.

http://www.newsbatch.com/tort.htm



February 18, 2011 It’s Time to Call Tort Reform What it Really Is Standing Up Against Corporate Tyranny

Jacob Diesselhorst, Nix Law Group, PLLC, Edmond, Oklahoma

I love Oklahoma. I love the people of Oklahoma, all of them. The hard-working men and woman, the elderly-who have paved the way for us and the children-who we are grooming to carry on the legacy for our state’s future.

I love the idea of democracy and freedom. This great country of ours’ was founded based on principles…certain unalienable rights that are bestowed upon all of us– The principle that us all, whether white or black, rich or poor, republican or democrat, should be treated equally and be allowed to play on a level playing field. In turn, our political system, the 3 branches of government, should continue to exemplify this ideal and support our efforts to uphold it. Unfortunately, politics in Oklahoma has deteriorated into a power struggle for control of money and resources as opposed to an effort to embody the principles of freedom, equality and justice.

Like many of us, I am disgusted by the ugly politics and lack of civility that has invaded government. Party lines are now clearly drawn, as both sides teeter for control of a system that is now broken due to the power of special interests. Special interests have infested our politics to the point now there is no way to differentiate between two. Oklahoma politics are no different. Money talks.

The Chamber, big business, big insurance and big oil have a tight grip on this State and the brass of the current leadership of the Oklahoma Republican party. Don’t take my word for it? Let the evidence speak for itself. Look at the campaign finance reports for Oklahoma’s current GOP leadership, they read like a who’s who of Oklahoma’s business community, the super-rich and the PACS (Political Action Committees) formed by the special interests that now dictate Oklahoma politics.

Unfortunately, this influence of the money and power of big business and corporations has infected Republican leadership and convinced them to pursue policy changes that do nothing to protect or assist the general public, but act only to further enrich and empower the voracious and self-serving interests of Corporations and Insurance Companies. One disturbing example of special interests’ invasion into democracy is taking place in Oklahoma right now—with the efforts of a chosen few to force more so-called “tort reform” on the people of Oklahoma.

Tort Reform (as it is called) is the effort by the Big Business wing of the Republican party (at the direction of the corporations who fund their political campaigns and reelections) to invade the sanctity of the judicial branch and legislate in the court room by taking away the autonomy of the civil jury and dictating how juries must decide cases and what evidence is and is not allowed to come in to evidence at trial.

•Politicans want to place an arbitrary, one-size-fits all hard cap of $250k on the amount of damages a civil jury can award a catstrophically injured Oklahoman for the rest of his or her lifetime no matter how severe the injuries and no matter how disgusting, reckless and wanton the conduct of the negligent Defendant.

•GOP Idealogs claim hard caps “deter frivolous lawsuits.” This is a BLATANT LIE. Frivolous lawsuits never see the light of day in Oklahoma. Numerous laws already in place require Expert Reports before lawsuits can be filed. Moreover, Hard Caps do nothing to prevent minor injury lawsuits from being filed. What arbitratry hard caps do cause—is for people with legitimate, long term catstrophic injuries (a brain injured child or a blinded teenager or a badly burned stay-at-home mom or a nursing home resident who is beaten to death and raped in his nursing home by a bad employee) from obtaining full and fair compensation for their injuries.

•Non-economic damages are meant to serve as a deterence to Corporations and individual and ensure that our highways, schools, airports, public transportaion, workplaces, products, etc.) are SAFE. CAPS ELIMINATE THIS DETERENCE and actually give corporations, bad doctors, bad nurses, truck drivers, etc. a free license to run amuck in our state with no fear of every being punished above 250k. (which is like a parking ticket to many multi-million dollar businesses, corporations and insurance companies)

•Further, Policitians want to tip the scales of justice in favor of negligent defendants by giving a negligent tortfeasor’s insurance company and CREDIT for any collateral source of insurance an injured Oklahoman has in awarding damages.

•In other words, if you are horribly injured in a trucking accident and have $150k in medical bills–the jury gets to know your health insurance company paid part of the bills, that part was written off and that part came out of your pocket. Meanwhile, the fact that the negligent trucking company, hospital, oil and gas company etc. has millions of dollars in liability insurance will remain hidden from the jury.

•Even more disturbing, if you had the forsight to purcahse disability insurance or life insurance (in the case of a wrongful death case)–the negligent corporation’s liability insurance company will also get a credit for that insurance money (even though it is from another seperate insurance company). In other words, everyone benefits in this equation (the insurance companies and negligent defendants) EXCEPT THE ONE WHO SHOULD—THE CATASTROPHICALY INJURED OKLAHOMAN.

Our civil justice system is built on a principle of a balance of power and a weighing of the evidence to determine fault, liability and damages. The scales of justice illustrate this ideal. Our court system has successfully existed for hundreds of years built around the JURY. The Jury being a group of citizens like you and me who are entrusted to hear the evidence of a particular case and work together to render a fair and reasoned verdict. Now, however, politicians, not jurors, will decide the amount of damages to award in civil cases involving human injury and death by forcing upon a one-size fits all law that caps the maximum damages at $250,000.00 and decreases any economic damages awarded (medical bills, future medical bills, disability, loss of earnings, etc.) by the amounts of any collateral source of compensation that exists to pay part of them.

In other words, “tort reform” serves to cripple the very purpose of the jury system—to leave it to the people to decide the damages to render against a defendant who has been found to be negligent, reckless or wanton in its conduct and, as a result, caused harm to another person—by taking away the right of jurors (OKLAHOMA CITIZENS) to fairly decide legal disputes.

I for one stand with the people of Oklahoma and their constitutional right to a fair jury trial by the people…not politicians. With “tort reform”—Special Interests are completing the trifecta of infecting all 3 branches of government with their greed and self-serving influence. Meanwhile, the citizens of Oklahoma stand by, unknowlingly, while their rights are taken away by corrupt politicans whose only motivation is to satisfy their biggest campaign donors (i.e., BIG BUSINESS/BIG INSURANCE) so they can hope to get relected.

Sad but true.

Politics as usual in this State cannot be allowed to continue. The very rights to which each of us is entitled now hang in the balance.

David Farnbauch at 7:55 am. (General)

http://www.sweeneylawfirm.com/blog/its-time-to-call-tort-reform-what-it-really-is.htm



Wisconsin May Cap Punitive Damages At $200000 | Tort Reform ...Jan 14, 2011 ... GOP caps punitive damages in tort reform bill - WBAY-TV Green Bay-Fox ... Whenever the Republican party issues their issues platform, they're always for the death ... 2011 Looking Like A Bad Year For Civil Justice (JL) ...

www.tortdeform.com/.../2011/.../wisconsin_may_cap_punitive_dam.html



Justinian Lane Wisconsin May Cap Punitive Damages At $200,000 Continuing the “2011 will be a bad year for civil justice” theme:

The Senate judiciary committee voted 3-2 on Friday to cap punitive damages at $200,000 or twice the amount of compensatory damages, whichever is greater. Current state law does not lay out any caps on punitive damages.

Source: Wis. GOP caps punitive damages in tort reform bill - WBAY-TV Green Bay-Fox Cities-Northeast Wisconsin News

Capping punitive damages at $200k will only encourage corporations to sell profitable but defective products. If it weren’t for punitive damage awards well in excess of $200k, Johns Manville might still be pumping out asbestos products.

I don’t understand Republican ideology. On one hand, most of them support the death penalty. But on the other hand, they don’t like punitive damages. How can you rationalize putting a man to death for committing a crime, but not allowing the family of his victims to take more than $200k?

http://www.tortdeform.com/archives/2011/01/wisconsin_may_cap_punitive_dam.html



http://www.wisbar.org/AM/Template.cfm?Section=News&Template=/CM/ContentDisplay.cfm&ContentID=99772




Archives for February 2011 >

Arbitrary Damage Caps Reward Negligent and Wrongful Actors and Punish the Innocent Citizens of Oklahoma

Posted by Jacob Diesselhorst on February 17, 2011

In 2009 (less than 2 years ago), Oklahoma passed what the then-newly-annointed Republican Majority Senate and House Leadership coined "Landmark Comprehensive Lawsuit Reform."

Per the Oklahoma GOP's own Press Release of May 11, 2009--

“ The agreement is multi-faceted, including several key components of reform which will improve health care access to all Oklahomans, as well as assuring small business’ health and viability in the state.

”“I’m very pleased with the agreement,” said Glen Coffee (the then Republican Senate Majority Leader and now, somehow, Secretary of State (We will save that for another day). In May 2009, Coffee proclaimed “Republicans have promised reform of the legal system, the people expect us to deliver, and we have in fact delivered. The spirit of cooperation exhibited by all parties in this negotiation was gratifying, and is indicative of what can be done when people negotiate in good faith toward a mutually beneficial goal,” Coffee continued. “We look forward to sending this historic reform to Governor Henry to ratify the hard work all the parties have accomplished for the state.”

Current House Speaker Benge (who is now acting like 2009 never happened in pushing the GOP's new Corporate Welfare and Lawsuit Immunity laws) said back in 2009 about the then passed broadsweeping lawsuit reform:

“We have said since the beginning of session that lawsuit reform was one of our top priorities, and this agreement represents a huge victory for the people of Oklahoma today. All interested parties have worked together to make this deal a reality and I am proud of the collaboration that has occurred. This legislation will ensure access to the courts for all who have legitimate claims, but will also bring some certainty to a system that has recently become a hindrance to economic development in our state. I look forward to Gov. Henry signing this bill.”

”Dan Sullivan, a prominent lawyer for insurance companies and large corporations in Oklahoma and GOP Representative from Tulsa, also said in 2009:

“This agreement provides additional protections to the medical and business community from frivolous suits while protecting the right to a trial by a jury of their peers for those that are truly injured.

”HOW SOON WE FORGET. Now, the Oklahoma GOP Big Business Republicans, drunk with power in Oklahoma, having swept their way into the Governor's office and total, unfettered control of Oklahoma, plans to tip the scales of justice completely over in favor of negligent and reckless defendant tort feasors by passing the most broadsweeping and unconstitional civil justice changes in modern US History. These laws should not and in fact do not appeal to social minded and reasonable Conservative Oklahomans. See Example 1 and Example 2.

The Oklahoma GOP is slithering these bills through at the Capital with very little fanfare and Oklahoma is just sitting back while the bandits are making away with the take. In fact, Most Oklahomans do not know about these additional draconian changes and clearly do not know that not a single one of the "reforms" the GOP are now proposing favor individual Oklahomans- they all favor negligent and reckless civil defendants.

ARBITRARY $250K DAMAGE CAPS THAT RESTRICT JURY AWARDS NO MATTER HOW BAD A DEFENDANT ACTS AND HOW HORRIBLY AND PERMANENTLY AN INNOCENT OKLAHOMAN IS INJURED OR MAIMED = NO ACCOUNTABILITY.

And who bears the burden of this Corporate Bailout/Corporate Welfare?---regular Oklahomans- You, me, our kids, our parents, especially the must vulnerable of all:

•children •the elderly •stay at home moms ' •lower wage earners like pastors, fireman, police officers, teachers, etc. According to the Oklahoma GOP, The most damages a jury can ever award these type of Oklahomans, no matter how catastrophic and long-term their injuries may be, is only 250k. 90% of Oklahomans would never support this type of law--yet it will likely sail through the on the backs of the politicians the Chamber put in place, right onto the desk of Mary Failing who will not even read it before she signs it.

After these horrific and unconstitutional bills become law, Oklahomans who have LEGITIMATE CIVIL CASES and whose only avenue for justice is the COURTHOUSE, will be the one's left out in the cold with no way to get JUSTICE for their loss of quality of life---pain and suffering, disability, inability to earn a living, etc.

The Oklahoma GOP's new, so-called "Tort Reform" rewards negligent corporations cutting corners for profits, bad nursing homes, foreign produce manufacturers like drug companies and medical device companies, bad doctors, unsafe truck drivers, drunk drivers, texting drivers etc. and their multi-billion dollar Insurance Company allies. All this at the expense of your constitutional right to a non-biased and fair trial by jury of your peers- Oklahoma citizens.

How about we let Oklahoma juries sort out legitimate civil disputes and not well-greased and bought-and-paid-for politicians (who talk out of both sides of their mouths depending on what year it is) and whose only interests they apparently protect are those of the corporate donors who got them elected and will keep them in office.

Tags:anthony sykes, lawsuit reform, mary fallin, nix law group, oklahoma law, rob johnson, tort reform

http://www.oklahomainjurylawadvocate.com/2011/02/



Sunday, January 30, 2011

Vaccines and Transmissible Spongiform Encephalopathy the Prion Disease, what if ?

COMMERCIAL IN CONFIDENCE

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/vaccines-and-transmissible-spongiform.html



http://www.whale.to/v/singeltary.html



http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.html




please note ;

PPo2-26:

Transmission of Classical and Atypical (L-type) Bovine Spongiform Encephalopathy (BSE) Prions to Cynomolgus macaques

Fumiko Ono,1 Yoshio Yamakawa,2 Minoru Tobiume,3 Yuko Sato,3 Harutaka Katano,3 Kenichi Hagiwara,2 Iori Itagaki,1 Akio Hiyaoka,1 Katuhiko Komatuzaki,1 Yasunori Emoto,1 Hiroaki Shibata,4 Yuichi Murayama,5 Keiji Terao,4 Yasuhiro Yasutomi4 and Tetsutaro Sata3

1The Corporation for Production and Research of Laboratory Primates; Tsukuba City, Japan; 2Departments of Cell Biology and Biochemistry; and 3Pathology; National Institute of Infectious Diseases; Tokyo, Japan; 4Tsukuba Primate Research Center; National Institute of Biomedical Innovation; Tsukuba City, Japan; 5Prion Disease Research Team; National Institute of Animal Health; Tsukuba City, Japan

Key words: L-type BSE, cBSE, cynomolgus macaques, transmission

BSE prion derived from classical BSE (cBSE) or L-type BSE was characterized by inoculation into the brain of cynomolgus macaques. The neurologic manifestation was developed in all cynomolgus macaques at 27–43 months after intracerebral inoculation of brain homogenate from cBSE-affected cattle (BSE JP/6). Second transmission of cBSE from macaque to macaque shortened incubation period to 13–18 months. cBSE-affected macaques showed the similar clinical signs including hyperekplexia, tremor and paralysis in both primary and second transmission.

Two macaques were intracerebrally inoculated brain homogenate from the L-type BSE-affected cattle (BSE JP/24). The incubation periods were 19–20 months in primary transmission.

The clinical course of the L-type BSE-affected macaques differed from that in cBSE-affected macaques in the points of severe myoclonus without hyperekplexia. The glycoform profile of PrPSc detected in macaque CNS was consistent with original pattern of either cBSE or L-typeBSE PrPSc, respectively. Although severe spongiform change in the brain was remarkable in all BSE-affected macaques, severe spongiform spread widely in cerebral cortex in L-type BSE-affected macaques. Heavy accumulation of PrPSc surrounded by vacuola formed florid plaques in cerebral cortex of cBSE-affected macaques. Deposit of PrPSc in L-type BSE-affected macaque was weak and diffuse synaptic pattern in cerebrum, but large PrPSc plaques were evident at cerebellum. MRI analysis, T2, T1, DW and flair sequences, at the time of autopsy revealed that brain atrophy and dilatation of cerebral ventricles were significantly severe in L-type BSE-affected macaques. These results suggest that L-type BSE is more virulent strain to primates comparing to cBSE.

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




Saturday, January 29, 2011

Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate

Jpn. J. Infect. Dis., 64 (1), 81-84, 2011


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html




Wednesday, February 16, 2011 IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES

IN CONFIDENCE


http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html




Vaccines and Transmissible Spongiform Encephalopathy the Prion Disease, what if ?

COMMERCIAL IN CONFIDENCE

3.2 Minute 5.3 - 5.4 Bovine Spongiform Encephalopathy

It was reported that some replies had been received from Companies using pituitary glands in their products. Copies of the BSE document had also been sent to DHSS and NIBSC.

and then another 3 + pages of blank space. ...TSS



http://collections.europarchive.org/tna/20080102164813/http://www.bseinquiry.gov.uk/files/yb/1988/09/06005001.pdf




COMMERCIAL IN CONFIDENCE

BSE - CURRENT POSITION WITH VETERINARY LICENCED PRODUCTS (MA.1968)

There are three areas of particular concern, vaccines (including emergency vaccines), pharmaceuticals which are covered by MA licences and unlicenses hormonal products produced under exemptions claimed under (Section 9(2) Medicines Act).

1) Vaccines



http://collections.europarchive.org/tna/20080103033809/http://www.bseinquiry.gov.uk/files/yb/1988/10/06005001.pdf




NOT FOR PUBLICATION

another 6 pages of blank space. ...TSS



http://collections.europarchive.org/tna/20080103032658/http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf




http://collections.europarchive.org/tna/20080103032631/http://www.bseinquiry.gov.uk/files/yb/1988/11/04003001.pdf




http://collections.europarchive.org/tna/20080103033926/http://www.bseinquiry.gov.uk/files/yb/1988/04/00007001.pdf




COMMERCIAL IN CONFIDENCE


http://collections.europarchive.org/tna/20080103034137/http://www.bseinquiry.gov.uk/files/yb/1988/07/00007001.pdf




COMMERCIAL IN CONFIDENCE

Medicines Act - Veterinary Products Committee



http://collections.europarchive.org/tna/20080103034140/http://www.bseinquiry.gov.uk/files/yb/1988/09/00004001.pdf




COMMERCIAL IN CONFIDENCE

NOT FOR PUBLICATION

COMMITTEE ON SAFETY OF MEDICINES

another 6 pages or so that are blank. ...TSS



http://collections.europarchive.org/tna/20080102185137/http://www.bseinquiry.gov.uk/files/yb/1989/01/26007001.pdf




http://collections.europarchive.org/tna/20080102184613/http://www.bseinquiry.gov.uk/files/yb/1989/01/30001001.pdf




COMMERCIAL IN CONFIDENCE

NOT FOR PUBLICATION

COMMITTEE ON SAFETY OF MEDICINES

WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY

7.2.1. Products with bovine brain/lymphoid tissue as ingredients and administered by injection...[111]

7.2.2 Products with bovine ingredients (other than brain/lymphoid tissue) and administered by injection...[135]

7.2.3 Tissue implants, open wound dressings, surgical materials, dental and opthalmic products with bovine ingredients...[27]

7.2.4. Products with bovine ingredients and administered topically...[5]

7.2.5 Products with bovine ingredients and administered orally...[9]

7.2.6 Products with other animal/insect/bird ingredients and administered:

a. by injection a: 117

b. by topically b: 6

c. orally c: 8

7.2.7 Products with materials produced from animal material by chemical processes, eg stearic acid, gelatin and lanolin...[156]

With two exceptions, the replies to date have not given any immediate cause for concern, although 176 products do not conform to the CSM/VPC guidelines.

8. The first exception was from which gave very limited information about a very large number of homoepathic medicines with material obtained from cattle and a number with material from the brain. Of these, 53 were injectable products of which 20 were derived from cattle brain. A list of these products is attached as Appendix 1 to Annex D. The second exception relates to the product, 'Surgical Catgut', which is sourced from UK bovine intestines and will contain lymphoid material...



see full text ;



http://collections.europarchive.org/tna/20080102164420/http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf




COMMERCIAL IN CONFIDENCE


http://collections.europarchive.org/tna/20080102164744/http://www.bseinquiry.gov.uk/files/yb/1988/10/00003001.pdf




MANAGEMENT IN CONFIDENCE


CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS



http://collections.europarchive.org/tna/20080102184729/http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf





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

Date: Tue, 9 Jan 2001 16:49:00 -0800

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de

[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.

[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?

[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]

[host Richard] could you repeat the question?

[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?

[not sure whom ask this] what group are you with?

[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.

[not sure who is speaking] could you please disconnect Mr. Singeltary

[TSS] you are not going to answer my question?

[not sure whom speaking] NO

from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again;

[unknown woman] what group are you with?

[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now?

at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference.


snip...full text ;


http://bse-atypical.blogspot.com/2010/01/14th-international-congress-on.html




The documents below were provided by Terry S. Singeltary Sr on 8 May 2000.

They are optically character read (scanned into computer) and so may contain typos and unreadable parts.

TIP740203/l 0424 CONFIDENTIAL

snip...

The responses by the companies were presented by Ms Turner and were categorised by MCA standards, the products that were discussed were all low volume usage products eg sutures, heart valves.

8. As the responses included some materials of human origin it was decided that more information should be sought about CJD. There had been 2 recent deaths reported associated with human growth hormone. These were being investigated.

snip...

http://www.mad-cow.org/00/may00_news.html#aaa



5.3.3 The greatest risk, in theory, would be from parenteral injection of material derived from bovine brain or lymphoid tissue. Medicinal products for injection or surgical implantation which are prepared from bovine tissues, or which utilise bovine serum albumin or similar agents in their manufacture, might also be capable of transmitting infectious agents. All medicinal products are licensed under the Medicines Act by the Licensing Authority following guidance, for example from the Committee on Safety of Medicines (CSM), the Committee on Dental and Surgical Materials (CDSM) and their subcommittees. The Licensing Authority have been alerted to potential concern about BSE in medicinal products and will ensure that scrutiny of source materials and manufacturing processes now takes account of BSE agent.



see all 76 pages ;


http://collections.europarchive.org/tna/20080102132706/http://www.bseinquiry.gov.uk/files/ib/ibd1/tab02.pdf




EXPORT OF BRITISH BIOLOGICAL PHARMACEUTICALS...

snip...please see full text ;

Sunday, January 30, 2011

Vaccines and Transmissible Spongiform Encephalopathy the Prion Disease, what if ?

COMMERCIAL IN CONFIDENCE

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/vaccines-and-transmissible-spongiform.html





TSS



Saturday, February 26, 2011

Supreme Court Protects Vaccine Manufacturers, Not Injured Children there from Bruesewitz vs Wyeth


http://vcjdtransfusion.blogspot.com/2011/02/supreme-court-protects-vaccine.html

The risk of variant Creutzfeldt-Jakob disease among UK patients with bleeding disorders, known to have received potentially contaminated plasma products

The risk of variant Creutzfeldt-Jakob disease among UK patients with bleeding disorders, known to have received potentially contaminated plasma products




S. M. A. ZAMAN1, F. G. H. HILL2,9, B. PALMER3, C. M. MILLAR4,9, A. BONE1, A. M. MOLESWORTH1, N. CONNOR1, C. A. LEE5, G. DOLAN6, J. T. WILDE7,9, O. N. GILL1, M. MAKRIS8,9



Article first published online: 23 FEB 2011



DOI: 10.1111/j.1365-2516.2011.02508.x



© 2011 Blackwell Publishing Ltd



Keywords: haemophilia; inherited bleeding disorders; risk assessment; UK plasma products; variant Creutzfeldt-Jakob disease




Summary. The risk of variant Creutzfeldt-Jakob disease (vCJD) from potentially infected plasma products remains unquantified. This risk has been assessed for 787 UK patients with an inherited bleeding disorder prospectively followed-up for 10–20 years through the UK Haemophilia Centre Doctors’ Organisation (UKHCDO) Surveillance Study. These patients had been treated with any of 25 ‘implicated’ clotting factor batches from 1987 to 1999, which included in their manufacture, plasma from eight donors who subsequently developed clinical vCJD. Variant CJD infectivity of these batches was estimated using plasma fraction infectivity estimates and batch-manufacturing data. Total potential vCJD infectivity received by each patient has been estimated by cumulating estimated infectivity from all doses received during their lifetime. Of 787 patients, 604 (77%) were followed-up for over 13 years following exposure to an implicated batch. For these 604 patients, the estimated vCJD risk is =1% for 595, =50% for 164 and 100% for 51. This is additional to background UK population risk due to dietary exposure. Of 604 patients, 94 (16%) received implicated batches linked to donors who developed clinical vCJD within 6 months of their donations. One hundred and fifty-one (25%) had received their first dose when under 10 years of age. By 1st January 2009, none of these patients had developed clinical vCJD. The absence of clinical vCJD cases in this cohort to date suggests that either plasma fraction infectivity estimates are overly precautionary, or the incubation period is longer for this cohort than for implicated cellular blood product recipients. Further follow-up of this cohort is needed.


http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2516.2011.02508.x/abstract




Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate



Emmanuel E. Comoy1*, Cristina Casalone2, Nathalie Lescoutra-Etchegaray1, Gianluigi Zanusso3, Sophie Freire1, Dominique Marcé1, Frédéric Auvré1, Marie-Magdeleine Ruchoux1, Sergio Ferrari3, Salvatore Monaco3, Nicole Salès4, Maria Caramelli2, Philippe Leboulch1,5, Paul Brown1, Corinne I. Lasmézas4, Jean-Philippe Deslys1



1 Institute of Emerging Diseases and Innovative Therapies, CEA, Fontenay-aux-Roses, France, 2 Istituto Zooprofilattico Sperimentale del Piemonte, Turin, Italy, 3 Policlinico G.B. Rossi, Verona, Italy, 4 Scripps Florida, Jupiter, Florida, United States of America, 5 Genetics Division, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America



Abstract



Background Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne transmission of prions from slaughtered cattle with classical Bovine Spongiform Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic in aging cattle, were recently identified at slaughterhouses throughout Europe and North America, raising a question about human susceptibility to these new prion strains.



Methodology/Principal



Findings Brain homogenates from cattle with classical BSE and atypical (BASE) infections were inoculated intracerebrally into cynomolgus monkeys (Macacca fascicularis), a non-human primate model previously demonstrated to be susceptible to the original strain of cBSE. The resulting diseases were compared in terms of clinical signs, histology and biochemistry of the abnormal prion protein (PrPres). The single monkey infected with BASE had a shorter survival, and a different clinical evolution, histopathology, and prion protein (PrPres) pattern than was observed for either classical BSE or vCJD-inoculated animals. Also, the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine.



Conclusion/Significance



Our results point to a possibly higher degree of pathogenicity of BASE than classical BSE in primates and also raise a question about a possible link to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning epidemic of classical BSE, the occurrence of atypical strains should temper the urge to relax measures currently in place to protect public health from accidental contamination by BSE-contaminated products.



Citation: Comoy EE, Casalone C, Lescoutra-Etchegaray N, Zanusso G, Freire S, et al. (2008) Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate. PLoS ONE 3(8): e3017. doi:10.1371/journal.pone.0003017



Editor: Neil Mabbott, University of Edinburgh, United Kingdom



Received: April 24, 2008; Accepted: August 1, 2008; Published: August 20, 2008



Copyright: © 2008 Comoy et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Funding: This work has been supported by the Network of Excellence NeuroPrion.



Competing interests: CEA owns a patent covering the BSE diagnostic tests commercialized by the company Bio-Rad.



* E-mail: emmanuel.comoy@cea.fr



http://www.plosone.org/article/info:doi/10.1371/journal.pone.0003017




Session I - Prions: Structure, Strain and Detection (II)



Searching for BASE Strain Signature in Sporadic Creutzfedlt-Jakob Disease



Gianluigi Zanusso



Department of Neurological and Visual Sciences, Section of Clinical Neurology University of Verona, Verona, Italy.



Bovine amyloidotic spongiform encephalopathy (BASE) is a newly recognized form of bovine prion disease, which was originally detected in Italy in 2004 as an effect of active surveillance. BASE or BSE L-type (L is referred to the lower electrophoretic PrPSc migration than classical BSE) has now been reported in several countries, including Japan. All field cases of BASE were older than 8 years and neurologically normal at the time of slaughtered. By experimental transmission, we defined the disease phenotype of cattle BASE, which is quite distinct from that seen in typical BSE and characterized by mental dullness and amyotrophy. Surprisingly, following intraspecies and interspecies transmission the incubation period of BASE was shorter than BSE. The relatively easy transmission of BASE isolate as well as the molecular similarity with sporadic Creutzfeldt-Jakob disease (sCJD) have raised concern regarding its potential passage to humans. Tg humanized mice Met/Met at codon 129 challenged with both BSE and BASE isolates, showed a resistance to BSE but a susceptibility to BASE at a 60% rate; in addition, BASE-inoculated Cynomolgus (129 Met/Met) had shorter incubation periods than BSE-inoculated primates. In this study we compared the biochemical properties of PrPSc in Cynomolgus and in TgHu Met/Met mice challenged with BSE and BASE strains, by conventional SDS-PAGE analysis and 2D separation. The results obtained disclose distinct conformational changes in PrPSc, which are dependent on the inoculated host but not on the codon 129 genotype.



This work was supported by Neuroprion contract n. FOOD CT 2004 -506579 (NOE)


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




P02.35



Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE



Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden



Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.




http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf




P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS



Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA



Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C. The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.



III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)



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




PRION 2010



International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria




PPo3-11:



Blood Transmission Experiments in Primates: Squirrel Monkeys (the Baxter Study)



Paul Brown, James Ironside, Susan Gibson, Robert G. Will, Thomas R. Kreil and Christian Abee



Plasma and buffy coat samples from 2 sCJD and 3 vCJD cases were inoculated i.c. and i.v. into a total of 21 squirrel monkeys. Pooled brain from the 3 vCJD patients titered 106 LD50/g (i.c.). Whole blood from each of 4 monkeys inoculated with 10% vCJD brain homogenate was transfused i.v. to individual recipient monkeys at approximately 3-month intervals during the incubation and clinical stages of disease in the donor animals. Plasma, RBC’s, platelets, and purified leukocytes from 6 chimpanzees infected with either human sCJD or GSS were inoculated i.c. and i.v. into 12 monkeys. In the entire group of monkeys inoculated with blood or blood components, only a single neuropathologically-verified transmission occurred within a 5-year observation period, in an animal inoculated with leukocytes from a pair of GSS-infected chimpanzee.



Conclusions. In a primate model highly susceptible to TSE (the squirrel monkey), infectivity was not detected (<10 i.c. LD50/ml) in plasma or buffy coat from 2 sCJD and 3 vCJD patients, or in whole blood from 1st passage vCJD in monkeys. We did, however, detect infectivity in one monkey inoculated with purified leukocytes from chimpanzee-passaged GSS, and observed what appeared to be a ‘triggering’ of symptomatic disease by physiological stress in chimpanzees subjected to plasmapheresis under general anaesthesia.




PPo4-20:




All Clinically Relevant Components, from Prion Infected Blood Donors, can Cause Disease Following a Single Transfusion



Sandra McCutcheon,1 Fiona E. Houston,2 Anthony R. Alejo-Blanco,1 Christopher de Wolf,1 Boon Chin Tan,1 Anthony Smith,3 Nora Hunter,1 Valerie S. Hornsey,4 Ian R. MacGregor,4 Christopher V. Prowse,4 Marc Turner5 and Jean C. Manson1



1The Roslin Institute; Roslin, Edinburgh UK; 2The University of Glasgow; Glasgow, UK; 3The Institute for Animal Health; Compton, Berkshire UK; 4National Science Laboratory; Scottish National Blood Transfusion Service (SNBTS); Edinburgh, UK; 5University of Edinburgh and SNBTS; Edinburgh, UK



Key words: blood, prion, BSE, transfusion



Introduction. To date, there have been over 220 cases of vCJD worldwide, likely acquired directly from bovine sources. There is concern that human to human transmission from individuals sub-clinically infected with vCJD may amplify/prolong a vCJD epidemic. The area of greatest concern in this respect is blood transfusion, of which there have been several reported cases. Here we examined which blood components are likely to pose the greatest risk of transmitting vCJD via blood transfusion using our sheep BSE model.



Results. 67% of donors have been confirmed as having BSE. We have recorded 25 positive transmissions of BSE following transfusion of non-leucodepleted blood components and 2 transmissions resulting from the transfusion of leucoreduced red cells and leucoreduced plasma.



Conclusion. We show that all components, prepared to the same criteria as used in human medicine, contain sufficient levels of infectivity to cause disease in recipients following a single blood transfusion. Leucoreduction of plasma and red cell concentrates does not remove infectivity. These data indicate the importance of devising appropriate control measures to minimise the risk of human to human transmission of vCJD by blood transfusion. Department of Health, UK (007/0162).



Methods. Sheep were orally infected with bovine BSE brain homogenate. We collected two full-sized donations of whole blood, before the onset of clinical signs. The following components were transfused into naive recipients: whole blood, red cell concentrates buffy coat, plasma and platelet units. We also transfused leucoreduced plasma, platelets and red cells. We collected a unit of whole blood from selected primary recipients for transfusion into secondary recipients.




PPo4-21:



The Risk of Variant Creutzfeldt-Jakob Disease (vCJD) Among UK Patients with Bleeding Disorders, Known to Have Received Clotting Factors Linked to Donors who Subsequently Developed vCJD



Syed M.A. Zaman,1 Nicky Connor,1 Noel Gill,1 Carolyn M. Millar,2,6 Mike Makris,3,6 Benedict Palmer4 and Frank G.H. Hill5,6



1CJD Section, Health Protection Agency Centre for Infections; London, UK; 2Department of Haematology; Imperial College; London, UK; 3University of Sheffield; Royal Hallamshire Hospital; Sheffield, UK; 4National Haemophilia Database; Manchester, UK; 5The Children’s Hospital NHS Foundation Trust; Birmingham, UK; 6Members of the Transfusion Transmitted Infection Working Party of the UK; Haemophilia Centre Doctors’ Organisation (UKHCDO); Sheffield, South Yorkshire UK



The risk of Creutzfeldt-Jakob Disease (vCJD) from potentially infected plasma products remains un-quantified. This risk has been assessed for 787 UK bleeding disorder patients prospectively followed-up for 10–20 years through the UK Haemophilia Centre Doctors’ Organisation (UKHCDO) Surveillance Study. These patients were treated with any of 25 ‘implicated’ clotting factor batches from 1987–1999, which included in their manufacture plasma from eight donors who subsequently developed vCJD. VCJD infectivity of these batches was estimated using plasma fraction infectivity estimates and batch manufacturing data. The quantity of implicated batches received by these patients was obtained. Total vCJD infectivity received by each patient has been estimated by cumulating infectivity from all doses received in their lifetime. Of 787 patients, 604 (77%) were followed-up for over 13 years since exposure to an implicated batch. By end 2008, none of these patients had developed vCJD. For these 604 patients, the estimated vCJD risk is <1% for 595, <50% for 164, and 100% for 51. This is additional to the background UK population risk due to dietary exposure. Of 604 patients, 94 (16%) received implicated batches linked to donors who developed vCJD within six months of their donations. 151 (25%) had received their first dose under 10 years of age. The absence of clinical vCJD cases in this cohort to date suggests that either plasma fraction infectivity estimates are overly precautionary, or the incubation period is longer for this cohort than for implicated cellular blood product recipients. Further follow up of this cohort is needed to answer these questions.




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




FC5.1.1



Transmission Results in Squirrel Monkeys Inoculated with Human sCJD, vCJD, and GSS Blood Specimens: the Baxter Study



Brown, P1; Gibson, S2; Williams, L3; Ironside, J4; Will, R4; Kreil, T5; Abee, C3 1Fondation Alliance BioSecure, France; 2University of South Alabama, USA; 3University of Texas MD Anderson Cancer Center, USA; 4Western General Hospital, UK; 5Baxter BioSience, Austria



Background: Rodent and sheep models of Transmissible Spongiform Encephalopathy (TSE) have documented blood infectivity in both the pre-clinical and clinical phases of disease. Results in a (presumably more appropriate) non-human primate model have not been reported.



Objective: To determine if blood components (red cells, white cells, platelets, and plasma) from various forms of human TSE are infectious.



Methods: Blood components were inoculated intra-cerebrally (0.1 ml) and intravenously (0.5 ml) into squirrel monkeys from 2 patients with sporadic Creutzfeldt- Jakob disease (sCJD) and 3 patients with variant Creutzfeldt-Jakob disease (vCJD). Additional monkeys were inoculated with buffy coat or plasma samples from chimpanzees infected with either sCJD or Gerstmann-Sträussler-Scheinker disease (GSS). Animals were monitored for a period of 5 years, and all dying or sacrificed animals had post-mortem neuropathological examinations and Western blots to determine the presence or absence of the misfolded prion protein (PrPTSE).



Results: No transmissions occurred in any of the animals inoculated with blood components from patients with sporadic or variant CJD. All donor chimpanzees (sCJD and GSS) became symptomatic within 6 weeks of their pre-clinical phase plasmapheresis, several months earlier than the expected onset of illness. One monkey inoculated with purified leukocytes from a pre-clinical GSS chimpanzee developed disease after 36 months.



Conclusion: No infectivity was found in small volumes of blood components from 4 patients with sporadic CJD and 3 patients with variant CJD. ***However, a single transmission from a chimpanzee-passaged strain of GSS shows that infectivity may be present in leukocytes, and the shock of general anaesthesia and plasmspheresis appears to have triggered the onset of illness in pre-clinical donor chimpanzees.




FC5.1.2



Interim Transmission Results in Cynomolgus Macaques Inoculated with BSE and vCJD Blood Specimens



Lasmezas, C1; Lescoutra, N2; Comoy, E2; Holznagel, E3; Loewer, J3; Motzkus, D4; Hunsmann, G4; Ingrosso, L5; Bierke, P6; Pocchiari, M5; Ironside, J7; Will, R7; Deslys, JP2 1Scripps Florida, Infectology, USA; 2CEA, France; 3PEI, Germany; 4DPZ, Germany; 5Istituto Superiore di Sanita, Italy; 6SMI, Sweden; 7CJD Surveillance Unit, UK



BSE and vCJD transmitted to cynomolgus macaques reproduce many features of human vCJD, including clinical symptoms, neuropathological hallmarks of vCJD, PrPres electrophoretical pattern and, most importantly, the wide distribution of infectivity in peripheral organs. The latter characteristic distinguishes vCJD from sCJD in both humans and cynomolgus macaques, and prompted us to use this non-human primate model for further investigations of vCJD and its risk for human health. The occurrence of four vCJD infections in humans transfused with blood from patients who later developed vCJD has raised concern about blood transfusion safety in countries with vCJD. In this collaborative European study, we investigated the infectivity of blood components and whole blood administered by intracerebral (ic) and intravenous (iv) routes. Buffy-coat and whole blood was inoculated by ic and iv route, respectively, from two vCJD patients and from two clinical vCJD-inoculated macaques. Transfusions were also performed from whole blood and blood leucodepleted according to hospital practice standards from two clinical BSE inoculated macaques. Blood infectivity during the preclinical phase is being examined in orally infected macaques. Whole blood was collected and transfused from one such animal two years after oral challenge, whereas buffy-coat and plasma from two animals at 2 and 4.5 years post-challenge, respectively, have been inoculated by the ic route. This is an ongoing study in which recipient animals continue to be observed at various times post-inoculation. So far, we have had one positive transmission in one animal transfused 65 months earlier with 40 ml of whole blood from a vCJD macaque (the characteristics of the disease in this animal will be shown in a separate poster by E. Comoy). This positive transmission reproduces transfusion transmission of vCJD in humans, with an incubation of 5.5 years compatible with incubation periods observed in humans.



http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf






Saturday, September 5, 2009



TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS



snip...



But the first thing is our own study, and as I mentioned, it's a Baxter primate study, and those are the major participants. And the goal was twofold, and here is the first one: to see whether CJD, either sporadic or familial -- actually it turns out to be the familial CJD is incorrect. It really should be the Fukuoka strain of Gerstmann-Straussler-Scheinker disease. So it's really GSS instead of familial CJD -- when passaged through chimps into squirrel monkeys using purified blood components, very pure blood components.



So this addresses the question that was raised just recently about whether or not red cell infectivity that's been found in rodents is really in the red cells or is it contaminated.



We prepared these samples with exquisite care, and they are ultra-ultra-ultra purified. There's virtually no contamination of any of the components that we looked at ? platelets, red cells, plasma, white cells -- with any other component.



These are a sort of new set of slides, and what I've tried to do is make them less complicated and more clear, but I'm afraid I haven't included the build. So you'll just have to try and follow what I explain with this little red pointer.



There were three initial patients. Two of them had sporadic CJD. One of them had Gerstmann-Straussler-Scheinker syndrome. Brain tissue from each individual patient was inoculated intracerebrally into a pair of chimpanzees. All right?



From those chimps, either plasma or ultra purified -- in fact, everything is ultra-purified. I'll just talk about purified plasma, purified white cells -- were inoculated intracerebrally and intravenously to get the maximum amount of infective load into a pair of squirrel monkeys.



The same thing was done for each of these three sets. This monkey died from non-CJD causes at 34 months post inoculation.



Let me go back for a second. I didn't point out the fact that these were not sacrificed at this point. These chimpanzees were apheresed at 27 weeks when they were still asymptomatic. In this instance, we apheresed them terminally when they were symptomatic.



And before I forget, I want to mention just a little sidelight of this. Chimpanzees in our experience -- and I think we may be the only people that have ever inoculated chimpanzees, and that's no longer a possibility, so this was 20, 30 years ago -- the shortest incubation period of any chimpanzee that we have ever seen with direct intracerebral inoculation is 13 months.



So we chose 27 weeks, which is about seven months, and incidentally typically the incubation period is more like 16 or 18 months. The shortest was 13 months. We chose the 27th week, which is about six and a half months, thinking that this would be about halfway through the incubation period, which we wanted to check for the presence or absence of infectivity.



But within four weeks after the apheresis, which was conducted under general anesthesia for three or four hours apiece, every single one of the six chimpanzees became symptomatic. That is another experiment that I would love to conclude, perhaps because this is simply not heard of, and it very much smells like we triggered clinical illness. We didn't trigger the disease, but it certainly looks like we triggered symptomatic disease at a point that was much earlier than one would have possibly expected.



Maybe it will never be done because it would probably open the floodgates of litigation. There's no end of little things that you can find out from CJD patients after the fact. For example, the neighbor's dog comes over, barks at a patient, makes him fall down, and three weeks later he gets CJD. So you have a lawsuit against the neighbor.



I mean, this is not an unheard of matter, but I do think that physical stress in the form of anesthesia and four hours of whatever goes on with anesthesia, low blood pressure, sometimes a little hypoxemia looks like it's a bad thing.



So here we have the 31st week. All of the chimps are symptomatic, and here what we did was in order to make the most use of the fewest monkeys, which is always a problem in primate research, we took these same three patients and these six chimps. Only now we pooled these components; that is to say, we pooled the plasma from all six chimps. We pooled ultra-purified white cells from all six chimps because here we wanted to see whether or not we could distinguish a difference between intracerebral route of infection and intravenous route of infection.



With respect to platelets and red blood cells, we did not follow that. We inoculated both intracerebral and intravenously, as we had done earlier because nobody has any information on whether or not platelets and red cells are infectious, and so we wanted again to get the maximum.



This is an IV versus IC goal. This one, again, is just getting the maximum load in to see whether there is, in fact, any infectivity in pure platelets, in pure red cells.



And of all of the above, the only transmission of disease related to the inoculation was in a squirrel monkey that received pure leukocytes from the presymptomatic apheresis. So that goes some way to address the question as to whether or not it's a matter of contamination. To date the red cells have not been -- the monkeys that receive red cells have not been observed for more than a year because that was a later experiment.



So we still can't say about red cells, but we're about four and a half years down the road now, and we have a single transmission from purified leukocytes, nothing from plasma and nothing from platelets.



That was the first part of the experiment. The second part was undertaken with the cooperation of Bob Will and others supplying material to us. These were a couple of human, sporadic cases of CJD and three variant cases of CJD from which we obtained buffy coat and plasma separated in a normal way. That is, these are not purified components.



The two cases of sporadic CJD, the plasma was pooled from both patients. The buffy coat was pooled from both patients, and then inoculated intracerebrally and intravenously into three squirrel monkeys each. This is a non-CJD death five years after inoculation. The other animals are still alive.



For variant CJD we decided not to pool. It was more important to eliminate the possibility that there was just a little bit of infectivity in one patient that would have been diluted to extinction, if you like, by mixing them if it were to so occur with two patients, for example, who did not have infectivity. So each one of these was done individually, but the principle was the same: plasma and buffy coat for each patient was inoculated into either two or three squirrel monkeys. This is, again, a non-CJD related death.



In addition to that, we inoculated rain as a positive control from the two sporadic disease cases of human -- from the two human sporadic cases at ten to the minus one and ten to the minus three dilutions. We have done this many, many times in the past with other sporadic patients. So we knew what to expect, and we got exactly what we did expect, namely, after an incubation period not quite two years, all four monkeys developed disease at this dilution and at the minus three dilution, not a whole lot of difference between the two.



Now, these are the crucial monkeys because each one of these monkeys every three to four months was bled and the blood transfused into a new healthy monkey, but the same monkey all the time. So this monkey, for example, would have received in the course of 21 months about six different transfusions of blood from this monkey into this monkey, similarly with this pair, this pair, and this pair. So you can call these buddies. This is sort of the term that was used. These monkeys are still alive.



In the same way, the three human variant CJD specimens, brain, were inoculated into four monkeys, and again, each one of these monkeys has been repeatedly bled at three to four month intervals and that blood transfused into a squirrel monkey, the same one each time. Ideally we would love to have taken bleeding at three months and inoculated a monkey and then let him go, watch him, and then done the same thing at six months. It would have increased the number of monkeys eightfold and just unacceptably expensive. So we did the best we could.



That, again, is a non-CJD death, as is this.



This was of interest mainly to show that the titer of infectivity in brain from variant CJD is just about the same as it from sporadic. We didn't do a minus five and a minus seven in sporadic because we have an enormous experience already with sporadic disease in squirrel monkeys, and we know that this is exactly what happens. It disappears at about ten to the minus five. So the brain titer in monkeys receiving human vCJD is identical to the brain titer in monkeys that have been inoculated with sporadic CJD.



That's the experiment. All of the monkeys in aqua are still alive. They are approaching a five-year observation period, and I think the termination of this experiment will now need to be discussed very seriously in view of a probable six-year incubation period in the U.K. case. The original plan was to terminate the experiment after five years of observation with the understanding that ideally you would keep these animals for their entire life span, which is what we used to do when had unlimited space, money, and facilities. We can't do that anymore.



It's not cheap, but I think in view of the U.K. case, it will be very important to think very seriously about allowing at least these buddies and the buddies from the sporadic CJD to go on for several more years because although you might think that the U.K. case has made experimental work redundant, in point of fact, anything that bears on the risk of this disease in humans is worthwhile knowing, and one of the things we don't know is frequency of infection. We don't know whether this case in the U.K. is going to be unique and never happen again or whether all 13 or 14 patients have received blood components are ultimately going to die. Let's hope not.



The French primate study is primarily directed now by Corinne Lasmezas. As you know, the late Dominique Dromont was the original, originally initiated this work, and they have very active primate laboratory in France, and I'm only going to show two very simple slides to summarize what they did.



The first one is simply to show you the basis of their statement that the IV route of infection looks to be pretty efficient because we all know that the intracerebral route of infection is the most efficient, and if you look at this where they inoculated the same infective load either intracerebrally or intravenously, the incubation periods were not substantially different, which suggests but doesn't prove, but doesn't prove that the route of infection is pretty efficient.



Lower doses of brain material given IV did extend the incubation period and presumably it's because of the usual dose response phenomenon that you see in any infectious disease.



With a whopping dose of brain orally, the incubation period was even lower. Again, just one more example of inefficiency of the route of infection and the necessity to use more infective material to get transmissions.



And they also have blood inoculated IV which is on test, and the final slide or at least the penultimate slide shows you what they have on test and the time of observation, that taken human vCJD and like us inoculated buffy coat, they've also inoculated whole blood which we did not do.



So to a great extent their studies are complementary to ours and makes it all worthwhile.



We have about -- oh, I don't know -- a one to two-year lead time on the French, but they're still getting into pretty good observation periods. Here's three-plus years.



They have variant CJD adapted to the macaque. That is to say this one was passaged in macaque monkeys, the cynomolgus, and they did the same thing. Again, we're talking about a study here in which like ours there are no transmissions. I mean, we have that one transmission from leukocytes, and that's it.



Here is a BSE adapted to the macaque. Whole blood, and then they chose to inoculate leukodepleted whole blood, in both instances IV. Here they are out to five years without a transmission.



And then finally oral dosing of the macaque, which had been infected with -- which was infected with BSE, but a macaque passaged BSE, whole blood buffy coat and plasma, all by the IC route, and they're out to three years.



So with the single exception of the leukocyte transmission from our chimp that was inoculated with a sporadic case of CJD or -- excuse me -- with a GSS, Gerstmann-Straussler, in neither our study nor the French study, which are not yet completed have we yet seen a transmission.



And I will just close with a little cartoon that appeared in the Washington Post that I modified slightly lest you get too wound up with these questions of the risk from blood. This should be a "corrective."



(Laughter.)



DR. BROWN: Thanks.



Questions?



CHAIRPERSON PRIOLA: Yes. Any questions for Dr. Brown? Dr. Linden.



DR. LINDEN: I just want to make sure I understand your study design correctly. When you mention the monkeys that have the IV and IC inoculations, the individual monkeys had both or --



DR. BROWN: Yes, yes, yes. That's exactly right.



DR. LINDEN: So an individual monkey had both of those as opposed to some monkeys had one and some had the other?



DR. BROWN: Correct, correct. Where IC and IV are put down together was IC plus IV into a given monkey.



DR. LINDEN: Into a given monkey. Okay.



And the IC inoculations, where were those given?



DR. BROWN: Right parietal cortex, Southern Alabama.



(Laughter.)



DR. BROWN: Oh, it can't be that clear. Yeah, here, Pierluigi.



CHAIRPERSON PRIOLA: Dr. Epstein.



DR. BROWN: Pierluigi always damns me with feint praise. He always says that's a very interesting study, but. I'm waiting for that, Pierluigi.



I think Jay Epstein --



DR. GAMBETTI: I will say that there's an interesting study and will say, but I just --



(Laughter.)



DR. GAMBETTI: -- I just point of review. You talk about a point of information. You say that -- you mention GSS, I guess, and the what, Fukuowa (phonetic) --



DR. BROWN: Yes, Fukuoka 1.



DR. GAMBETTI: Fukuowa, and is that from the 102, if I remember correctly, of the --



DR. BROWN: Yes, that is correct.



DR. GAMBETTI: Because that is the only one that also --



DR. BROWN: No, it's not 102. It's 101. It's the standard. It's a classical GSS. Oh, excuse me. You're right. One, oh, two is classical GSS. It's been so long since I've done genetics. You're right.



DR. GAMBETTI: Because that is the only one I know, I think, that I can remember that has both the seven kv fragment that is characteristic of GSS, but also the PrPsc 2730. So in a sense, it can be stretching a little bit compared to the sporadic CJD.



DR. BROWN: Yeah, I think that's right. That's why I want to be sure that I made you aware on the very first slide that that was not accurate, that it truly was GSS.



There's a GSS strain that has been adapted to mice, and it's a hot strain, and therefore, it may not be translatable to sporadic disease, correct. All we can say for sure is that it is a human TSE, and it is not variant. I think that's about it.



DR. GAMBETTI: I agree, but this is also not perhaps the best --



DR. BROWN: No, it is not the best. We understand --



DR. GAMBETTI: -- of GSS either.



DR. BROWN: Yeah. If we had to do it over again, we'd look around for a -- well, I don't know. We'd probably do it the same way because we have two sporadics already on test they haven't transmitted, and so you can take your pick of what you want to pay attention to.



Jay?



DR. EPSTEIN: Yes, Paul. Could you just comment? If I understood you correctly, when you did the pooled apheresis plasma from the six chimps when they were symptomatic at 31 weeks, you also put leukocytes into squirrel monkeys in that case separately IV and IC, but in that instance you have not seen an infection come down in squirrel monkey, and the question is whether it's puzzling that you got transmission from the 27-week asymptomatic sampling, whereas you did not see transmission from the 31-week sampling in symptomatic animals.



DR. BROWN: Yes, I think there are two or three possible explanations, and I don't know if any of them are important. The pre-symptomatic animal was almost symptomatic as it turned out so that we were pretty close to the period at which symptoms would being, and whether you can, you know, make much money on saying one was incubation period and the other was symptomatic in this particular case because both bleedings were so close together. That's one possibility.



The other possibility is we're dealing with a very irregular phenomenon and you're not surprised at all by surprises, so to speak so that a single animal, you could see it almost anywhere.



The third is that we, in fact, did just what I suggested we didn't want to do for the preclinical, namely, by pooling we got under the threshold. See?



You can again take that for what it's worth. It is a possible explanation, and again, until we know what the levels of infectivity are and whether by pooling we get under the threshold of transmission, we simply cannot make pronouncements.



CHAIRPERSON PRIOLA: Dr. DeArmond.



DR. DeARMOND: Yeah, it was very interesting data, but the --



(Laughter.)



DR. BROWN: I just love it. Go ahead.



DR. DeARMOND: Two comments. The first one was that the GSS cases, as I remember from reading your publications -- I think Gibbs was involved with them -- when you transmitted the GSS into animals, into monkeys, perhaps I think it was chimps, the transmission was more typical of CJD rather than GSS. There were no amyloid plaques. It was vacuolar degeneration so that you may be transmitting a peculiar form, as I criticized once in Bali and then you jumped all over me about.



DR. BROWN: I may do it again.



DR. DeARMOND: Calling me a bigot and some other few things like that.



(Laughter.)



DR. BROWN: Surely not. I wouldn't have said that.



DR. DeARMOND: So there could be something strange about that particular --



DR. BROWN: Yeah. I think you and Pierluigi are on the same page here. This may be an unusual strain from a number of points of view.



DR. DeARMOND: The other question though has to do with species barrier because the data you're showing is kind of very reassuring to us that it's hard to transmit from blood, but the data from the sheep and from the hamsters and some of the work, I think, that has been done by others, that it's easy in some other animals to transmit, hamster to hamster, mouse to mouse.



Could you comment on the --



DR. BROWN: That's exactly why we went to primates. That's exactly it, because a primate is closer to a human than a mouse is, and that's just common sense.



And so to try and get a little closer to the human situation and not totally depend on rodents for transferrable data, that is why you would use a primate. Otherwise you wouldn't use them. They're too expensive and they cause grief to animal care study people and protocol makers and the whole thing.



Primate studies are a real pain.



DR. DeARMOND: But right now it's inconclusive and you need more time on it.



DR. BROWN: I believe that's true. I think if we cut it off at six years you could still say it was inconclusive, and cutting it off at all will be to some degree inconclusive, and that's just the way it is.



DR. DeARMOND: So what has to be done? Who do you have to convince, or who do we all have to convince to keep that going?



DR. BROWN: Thomas?



Without trying to be flip at all, the people that would be the first people to try to convince would be the funders of the original study. If that fails, and it might for purely practical reasons of finance, then we will have to look elsewhere because I really don't want to see those animals sacrificed, not those eight buddies. Those are crucial animals, and they don't cost a whole lot to maintain. You can maintain eight -- well, they cost a lot from my point of view, but 15 to $20,000 a year would keep them going year after year.



CHAIRPERSON PRIOLA: Dr. Johnson.



DR. JOHNSON: Yeah, Paul, I'm intrigued as you are by the shortening of the incubation period. Have you in all of the other years of handling these animals when they were transfused, when they were flown out to Louisiana at night -- a lot of the stressful things have happened to some of these chimps. Have you ever noticed that before or is this a new observation?



DR. BROWN: Brand new.



MR. JOHNSON: Brand new. Okay.



CHAIRPERSON PRIOLA: Bob, did you want to say something? Dr. Rohwer.



DR. ROHWER: The Frederick fire, wasn't that correlated with a lot of --



DR. BROWN: Not that I k now of, but you may --



DR. ROHWER: Well, that occurred shortly after I came to NIH, and what I remember is that there were a whole bunch of conversions that occurred within the few months following the fire. That was fire that occurred adjacent to the NINDS facility, but in order to protect it, they moved the monkeys out onto the tarmac because they weren't sure it wouldn't burn as well.



DR. BROWN: Well, if you're right, then it's not brand new, but I mean, I'm not sure how we'll ever know because if I call Carlton and ask him, I'm not sure but what I would trust the answer that he gives me, short of records.



You know, Carlot is a very enthusiastic person, and he might say, "Oh, yeah, my God, the whole floor died within three days," but I would want to verify that.



On the other hand, it may be verifiable. There possibly are records that are still extant.



DR. ROHWER: Actually I thought I heard the story from you.



(Laughter.)



DR. BROWN: You didn't because it's brand new for me. I mean, either that or I'm on the way



(Laughter.)



CHAIRPERSON PRIOLA: Dr. Bracey.



DR. BRACEY: I was wondering if some of the variability in terms of the intravenous infection route may be related to intraspecies barriers, that is, the genetic differences, the way the cells, the white leukocytes are processed, whether or not microchimerism is established, et cetera.



DR. BROWN: I don't think that processing is at fault, but the question, the point that you raise is a very good one, and needless to say, we have material with which we can analyze genetically all of the animals, and should it turn out that we get, for example, -- I don't know -- a transmission in one variant monkey and no transmissions in another and a transmission in three sporadic monkeys, we will at that point genetically analyze every single animal that has been used in this study, but we wanted to wait until we could see what would be most useful to analyze.



but the material is there, and if need be, we'll do it.



CHAIRPERSON PRIOLA: Okay. Thank you very much, Dr. Brown.



I think we'll move on to the open public hearing section of the morning.



snip...



http://www.fda.gov/ohrms/dockets/ac/04/transcripts/4019t1.DOC




snip...



see full text ;




http://tseac.blogspot.com/2009/09/tseac-meeting-february-12-2004-baxter.html





Thursday, August 12, 2010



USA Blood products, collected from a donor who was at risk for vCJD, were distributed July-August 2010


http://creutzfeldt-jakob-disease.blogspot.com/2010/08/usa-blood-products-collected-from-donor.html





Sunday, August 01, 2010



Blood product, collected from a donors possibly at increased risk for vCJD only, was distributed USA JULY 2010



http://vcjdtransfusion.blogspot.com/2010/08/blood-product-collected-from-donors.html





14th ICID International Scientific Exchange Brochure -



Final Abstract Number: ISE.114



Session: International Scientific Exchange



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



T. Singeltary



Bacliff, TX, USA



Background:



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



Methods:



12 years independent research of available data



Results:



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



Conclusion:



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



page 114 ;




http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf





International Society for Infectious Diseases Web: http://www.isid.org/



please see full text ;


http://transmissiblespongiformencephalopathy.blogspot.com/





Wednesday, September 08, 2010



Emerging Infectious Diseases: CJD, BSE, SCRAPIE, CWD, PRION, TSE Evaluation to Implementation for Transfusion and Transplantation September 2010



http://vcjdtransfusion.blogspot.com/2010/09/emerging-infectious-diseases-cjd-bse.html




Wednesday, February 2, 2011

Detection of prion infection in variant Creutzfeldt-Jakob disease: a blood-based assay



http://transmissiblespongiformencephalopathy.blogspot.com/2011/02/detection-of-prion-infection-in-variant.html




Monday, February 7, 2011



FDA's Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???




http://tseac.blogspot.com/2011/02/fdas-currently-recommended-policies-to.html





Monday, September 13, 2010



atypical BSE strains and sporadic CJD strains, is there a connection and why shouldn't there be $



http://bse-atypical.blogspot.com/2010/09/atypical-bse-strains-and-sporadic-cjd.html




Saturday, January 29, 2011

Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate



Jpn. J. Infect. Dis., 64 (1), 81-84, 2011



http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html




Tuesday, September 14, 2010



Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)


http://tseac.blogspot.com/2010/09/transmissible-spongiform_14.html





Sunday, May 10, 2009



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



TO : william.freas@fda.hhs.gov



May 8, 2009



Greetings again Dr. Freas, TSEAC et al,



I would kindly, once again, wish to comment at this meeting about the urgent actions that need to be taken asap, to the Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009. Due to my disability from my neck injury, I will not be attending this meeting either, however I hope for my submission to be read and submitted. ...



IN reply to ;



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





Friday, February 11, 2011



Creutzfeldt-Jakob disease (CJD) biannual update (2010/1) Emerging infections/CJD


http://creutzfeldt-jakob-disease.blogspot.com/2011/02/creutzfeldt-jakob-disease-cjd-biannual.html




TSS