==================================================================
Everyone who can build a website should acquire this data and put it on
their own websites. As you can see, it is in an organized format,
follows logically and follows the crime in sequential order.
This is the data that IDSA refused to turn over to the Connecticut Attorney
General because they did not want a federal judge to see it.
What is meant
by "scientifically valid"
by Kathleen Dickson, Analytical Chemist (formerly Pfizer)
·
FDA's Rules on the VALIDATION of an Analytical Method
Specificity (only detects one thing)
Accuracy (data from known concentrations is all over the place, but
never should detect "none" as is the case with Lyme Western Blotting and the
Lyme ELISA, especially)
Limit of Detection (the opposite of Steere's "receiver operating
characteristic" below)
Precision (system has integrity in performance)
Ruggedness (anyone can run the test with their own equipment and get
the same results)
Linearity (concentration range of analyte for which the test is
valid) in and out of matrix
As far as we can tell, there
are plenty of personal spirochetes for whom humans are allowed to be hosts,
as long as we don’t call any of them “Lyme Disease,” since that’s trade
marked concept, is meant to be associated LYMErix® (Dearborn =
RICO), and is the imaginary autoimmune arthritis in a knee invented by
CDC officer
Allen Steere while he was in Europe in the
early 1990s. We will get to a more specific description of what exactly
“Lyme Disease” is in later chapters, but first one must acquire
scientific-validity-speak.
In this book we will freely make up new words. We’re
talking “medicine,” here, and as most people know, new diseases are being
invented all the time, with the same frequency as BigPharma and
psychiatry expand products and associated diseases, while BigInsurance
attempts to narrow the definitions of those diseases. For example,
Pfizer invented “erectile dysfunction,” while BigInsurance invented that the
“antiphospholipid syndrome” should replace “Lupus,” raising the bar on how
many antibodies one may have in order to have an “illness.” BigInsurance
and BigPharma together invent vector-borne diseases, since Kaiser-Permanente
and SmithKline established the “American Lyme Disease Foundation” or the ALDF.com at
New York Medical College in New York in association with, primarily, Yale.
... See the rest of the Chapter 1 explainer on how science is actually
done
HERE. You will see that Yale (Fikrig and
Flavell) know how to validate a method and have done so.
The above is
the very essential graphic for interpreting Steere's Elephant Diagnostics
Rule (from
Chp 3). He tried to assert that the higher the antibody concentration,
the more "valid" the test, falsely claiming that by "narrowing the number of
persons who will test positive," that makes his test more SPECIFIC,
and claimed that "the higher the concentration of antibodies in the blood
makes the test more SENSITIVE," when as we know, SENSITIVITY is a function
of LIMIT of DETECTION or the ability of the test to detect very low
concentrations of analyte.
The new
Steere fantasy term "receiver operating characteristic" is not a
criterion for the validation of an analytical method. It means the opposite
of sensitivity or the goal of detecting increasingly lower quantities of the
specific analyte in question with reliability.
What this scientific nonsense by Steere means is that we
can throw out all data generated by the Steere/Dearborn method, including
the
Klempner report. If the Klempner report is thrown out, IDSA has no
basis for their "guidelines" other than their own former handiwork [Chapters
1 (crooks know how to validate methods of detection),
3 (no one agreed with Steere at
Dearborn, but this 'two-tiered' testing schema was approved anyway by the
interest-conflicted parties),
5 (crooks are playing a shell game with the RNA and DNA primers),
7 (the RICO patents tell a different story and they also tell the
"MONOPOLY" story as regards the "No-OspA/B in the standard because of the
OspA vaccines")
8 (the 1989 IDSA Reviews tells an opposing story from
today's),
9 (Biomarkers and ALS-, MS-, and Lupus-like like outcomes discovered
by the crooks, who then made them undetectable at Dearborn and deployed
scientifically bogus psychiatry),
10 (Mark Klempner's obvious crimes),
11 (crooks all reported persistence past treatment),
14 (crooks are aware of the viability of the cyst form and that they
should be using a rodent-spinal fluid infectivity test to assess antibiotic
efficacies),
17 (crooks' own data on Congenital
Lyme), and probably over
the 4 reports by the crooks that show they could not actually read
their Western Blots in LYMErix-vaccinated people but did not report this to
the FDA] - the very data they refused to turn over to CT Attorney Richard
Blumenthal for nearly 2 years after his subpoena.
This is obvious libel, not to mention,
extremely vicious:
The above is, in fact, the outline of the indictment for
murder. MURDER and not manslaughter or negligence because of
the deliberate derogatory libel, slander, and false statements made about us
in the press and in conferences. The
harassment, the false criminal charges, the
perjury, the anonymous internet harassment (a federal crime), the stalking,
the
Munchausen's accusations, the wiretapping,
the deployment of the moron child protective services, false reports to the
medical boards, and the deployment of the IRS, show "intent to cause harm."
Or, the
www.ALDF.com, now having taken over
www.IDSociety.org - since all the MDs associated with IDSA now happen to
have been exposed to the whole world as morons to not have read their own
previous reports - is a "racketeering-influenced and corrupt organization."
As Yale's Durland Fish admits, his gang "...tried to
shut him down."
Durland Fish- Hilarious Courant Interview
"I
need more than rumors to attack!!" surely as regards the
wiretapping later performed by Edward
McSweegan which he later said under oath at
the depositions, was information to libel the Lyme.org, obtained via
"clairvoyance" or "wishful thinking." (You can read more about their
criminal antics,
HERE, on the Chapter 2, McSweegan and Barry
Goldwater page)
IDSA finally caved to Blumenthal after everyone interested
witnessed Yale's Eugene Shapiro lie his face off in the new movie,
UNDER OUR SKIN about congenital Lyme.
http://www.youtube.com/watch?v=sxWgS0XLVqw
Yale and Allen Steere are the authors of several reports on congenital Lyme,
including Yale's famous congenital Lyme autopsy where they reported that the
cause of the infant's
death was the congenital Lyme brain damage. The mother and baby
were "seronegative," treated for Lyme, and they mentioned the "remarkable
lack of inflammation" in the autopsy.
Hence, a person can have a disease, the disease could cause damage, and the
damage could be caused by mechanisms other than inflammation.
In the agreement with Richard Blumenthal,
you can see that IDSA very strongly wants to avoid criminal charges.
The diagnostic standard for "Lyme disease" is bogus
science and was meant to screen out all the neurologic cases of Lyme disease
in the first step, the ELISA (only detects late Lyme arthritis), since those
are the patients who need the expensive,
relapsing, intravenous ceftriaxone.
Looking further into who is involved in the deliberate
maltreatment of "Lyme Disease" victims:
NIH's Phil Baker and the crooked bankers and the
crooked CDC...
ALDF_BOARD.htm
(BigBankers, very big bankers)
I'm thinking there is a lot of money to recover cuz we're
talking the biggest people with the biggest money:
THE CABAL:
www.aldf.com = Serving both BigInsurance - who happens to reside
right at that cabal's headquarters,
Kaiser-Permanente at New York Medical College, Valhalla, NY, literally
training MDs as well as giving them tuition reimbursements if
they will agree to become Kaiser-Drones - and presumably, ALDF.com's
venture cap investors/ supporters:
Anthony J. Walton, British banker of the Wal-Mart empire,
Philip "controversy" Morris, CFR's
Mortimer "Run-Awaaaay" Zuckerman,
CFR's
AIG Greenbergs,
Gleason, LLC, etc and now
www.otrglobal.com , or "Off the Record Research," which is an
international spy ring for hire, and is now spying on ILADS.org's new
"research" group
lyme-disease-research-database (You can get more real data, free,
here, and have the bonus expertise of a BigPharma analytical chemist :))
Remember, MDs learn all they know from
BigPharma at Lunch!
It could be that they're all just plain stupid, but then
why was Corixa was given an
NIH Biodefense Contract and soon thereafter, Corixa was absorbed by
SmithKline?? I'm thinking we're entitled to know what the
biotech-investor-banker-insiders know about the bioweapons and the HLA data
and the vaccines-damage secrecy...
"TLR2 may form heterodimers with TLR6 to identify
diacylated lipoproteins, while TLR2 works in concert with TLR1 to recognize
triacylated lipoproteins such as OspA."
http://www.ncbi.nlm.nih.gov/pubmed/12804162?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Yes, we know Erol. That's LYMErix Disease® and/or Chronic
Lyme Disease- the disease associated with the immune suppression caused by
tolerization to Pam3Cys or the shed or
blebbed lipoproteins or the HIV gp120 and gp41 antigens and the Foot and
Mouth Disease Pam3Cys antigens and the mycoplasma Pam3Cys antigens. That's
why Corixa only mentioned TLR4, here in their advertisement?
RICO Patent Weaponeer David Persing's Corixa neglects
to mention in his NIH BIOWEAPONS CONTRACT the immune-suppressing effects of
these very antigens, Pam3Cys lipopeptides, only found in the goodies known
to be messed with on Plum Island.
Presumably that's what Gary Wormser was talking about when
he, too, revealed that LYMErix or OspA vaccination suppressed the immune
response:
Gary Wormser reporting the blunting of
the immune response in vaccinated animals:
http://www.ncbi.nlm.nih.gov/pubmed/10865170?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
"OspA interferes with the response of lymphocytes
to proliferative stimuli including a blocking of cell cycle phase
progression."
Oh.
FAAABulous, Gar'.
I'm thinking the whole world is watching their shenanigans
and is entitled to return the favor.
PNAC "Race-specific
bioweaponeering," pg 60
HIV & African fetuses
PLUM ISLAND
On this homepage is Chp 3 of
Crime Disease, where Steere goes to Europe (1992) to come up with the
bogus 2-tiered blood testing standard. (Borreliosis is a disease of immune
suppression, in reality, with little or no antibodies late in the disease.)
The IDSA/ALDF Lyme crooks claim that B31 is the American "prototypical" Lyme
strain, when it has little or no OspC in it. Therefore strain B31 is
the American strain from the BigInsurance perspective, since brain
infections require the expensive drug intravenous ceftriaxone. The IDSA
"guidelines" are all about the non-treatment of "Lyme disease," because
Kaiser-Permanente helped set up this cabal at New York Medical College,
Valhalla, New York.
See the reality of OspC in strain
B31 in the
Central RICO Patents.
Dattwyler and Luft (copied into this homepage, Chapter 3 of
Crime Disease): "Treat on tick bite to prevent brain invasion"
NEWS-
SUNY's Ben Luft (good guy) on his new OspC patent;
You can't talk about OspC as a vaccine for Lyme
without mentioning that Lyme is a brain disease.
John Dunn, at Brookhaven (Luft and Dattwyler) discusses OspC as the
invasiveness antigen (into the brain) resulting in the Multiple Sclerosis
version of Lyme- a condition that IDSA denies exists. See Chp
8,
10, and
11 of Crime Disease, on the 1989 IDSA reviews, Mark Klempner, and the
perpetrators on "persistence in the brain" for a clear picture of this
scientific FRAUD. (Use the left navigation bar.)
Connecticut Democrat James Amann interfered with our request for action on
Lyme as a cause of Multiple Sclerosis, because Amann makes his own personal
money as an MS Society fundraiser. We think Amann will be running for CT
Governor next- don't allow it. His staff is rude and obnoxious. Amann only
cares about himself. Lyme is a cause of a syndrome identical to MS in
25-36% of all cases of MS and likely half of all Lou Gehrig's Disease
cases. See the
Dictionary of Connecticutisms for more on the asshole James Amann and
his staff.
CDC officer and former head of the Rocky Mountain NIH
Bioweapons lab, Alan Barbour on OspC as the neurotropism antigen-
MEDLINE (National Irresponsible Library duh
Medicine)
http://mmbr.asm.org/cgi/reprint/50/4/381?view=long&pmid=3540570
- by Alan Barbour, CDC officer
Plum Island evolutionary bottleneck:
From
http://www.jstage.jst.go.jp/article/mandi/48/7/501/_pdf
How amazing!!!!! Lyme and West Nile virus, AFRICAN
DISEASES, both first appeared in America within 20 miles of Plum Island!!
And Yale's Durland Fish just happens to perform such
AFRICAN DISEASES in US ticks tricks ("research") right on Plum Island,
still, to this day!!
Fish tries out African Swine Fever in pig (and probably other) ticks on
MedLine
Swine African Swine Virus plasmid found in Borrelia
burgdorferi DNA
says CDC officer Alan Barbour. Hmm. Bacteriophage-vectored DNA of the
Swine Fever poxvirus type, and bacteriophage-vectored DNA of the Mycoplasmal,
Foot and Mouth Disease, and E. coli OspA-type (not to mention HIV), both
found in this "evolutionary bottleneck" of New England Relapsing Fever ??.
Tully, JG on MedLine
Shope, RE on MedLine
Like usual, the CDC is rather stupid to suggest "Lyme came
from Europe" and that there "have been no accidental releases from Plum
Island," because all that that will do is lead to demonstrating that there
is less likelihood of the natural evolution of tropical diseases emerging at
the Connecticut and Long Island coasts, especially when we have already
proven that all 4 diseases, Foot and Mouth, Borreliae, mycoplasmas,
and E. coli - all being things KNOWN to be objects of
such "study" on Plum Island and all VOILA!! HIV has the same Pam3Cys antigen
common to all the others messed with there.
If we could believe these insane people, they would have
injected us with the common, immune-suppressing bioweapon, OspA or Pam3Cys
(whether they knew it or not and not is a great possibility given how stupid
these IDSA/ALDF/Yale/NYMC people are). They literally wanted to turn humans
into walking canisters of tick-disinfectant, they so wanted
the royalties and the blood from the LYMErix RICO scam (the chapter on
exactly how they did it is below on this homepage).
People have asked me what is the purpose of Phil Baker as
the new head of the ALDF.com. That means they intend to shut down all
avenues of inquiry.
Like usual, that won't happen, because the structure of
OspA is right here on this homepage (scroll down through Chp 3, of Cryme
Disease,
HERE) and people can verify independently
that it is nearly identical to the gp120 and gp41 antigens in HIV. People
can independently verify what's in these crooks' patents.
http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=138
I hope to be remembered as the disease designer for
Borrelia gimmeabreakii,LYMERIX Disease®, Plum Island Slyme®,
Retrochondria, Femzalgia, - all the diseases that the crooks say are
syndromes of hypochondria but are really the result research fraud and the
epidemic of cognitive impairment in the AMA.
Jorge Benach demonstrating the cross-reacting
antibodies caused by Borreliosis attacking the nodes of Ranvier, potentially
affecting nerve conduction.
http://iai.asm.org/cgi/reprint/63/10/4130?view=long&pmid=7558329
I find it hard to
believe that all of us'n
internet culters knew ahead of time that
that specific antibody- one of course not detected in Lyme Western blotting
or any other common diagnostic test for Lyme at the present time because
that would be too much like not working for BigInsurance - yet that is their
assertion as regards the source of our complaints.
Benach of course, wrote
a letter to the Editor of the New York Times
where he stated
that indeed we chronic Lymers are crazy and that Steere has the science on
his side, when Steere says we're just crazy and don't have a real disease.
We think this is
utterly hilarious, because why waste your reputation over a
nutcase like Allen Steere?
http://query.nytimes.com/gst/fullpage.html?res=9F05EFDE173CF933A05756C0A9669C8B63
May 30, 2000
A Lyme Battle Rages
To the Editor:
The May 23 article depicts the sad state of affairs regarding the
''bitter medical debate over Lyme disease.'' Who would have thought back in
the late 70's when Dr. Allen Steere described the clinical syndrome that we
know today as Lyme disease that he would be the subject of complaints by
patients who do not agree with his diagnoses.
Increasingly, groups of patients (who may or may not have Lyme
disease) are attempting to impose their will on governmental agencies
charged with health care and research, and thus to subvert the scientific
process. The ''bitter debate over Lyme disease'' is not that at all; it is a
debate between science and ignorance, with science on the side of Dr.
Steere.
DR. JORGE L. BENACH
Stony Brook, N.Y.
The writer is the director of the Center for Infectious Disease and a
professor at SU
Oh.
Maybe someone forgot to tell Benach how
science was actually performed. He can read Chapters 1 and 3 of Cryme
Disease. Either that or he can change the FDA's rules for the validation of
an analytical method to make it all like Steere's "ROC" Elephant Rule
diagnostics, although I think Homelame Stupidity would at that point step
in.
lol
Soon to be Published in
hard copy: Lyme Cryme
A must have for every doctor * * * * Find it on Amazon!
Yet another
fictitious disease: "Lyme Disease"
By Kathleen Dickson, Analytical Chemist (formerly Pfizer)
|
INTRODUCTION,
CRYME DISEASE (Murphy's
Law: It could only have happened in
Corrupticut)
CHAPTER 1,
WHAT IS SCIENTIFIC VALIDITY?
CHAPTER 2,
McSWEEGAN and BARRY GOLDWATER
(naturally, a Corrupticut native)
CHAPTER 3,
STEERE, in EUROPE, CREATES "CRYME
DISEASE"
CHAPTER 4,
THE REAL OUTCOME OF LYMERIX- WHAT I
SHOWED the FDA(the whole 30 pages)
on the FDA's website
NIH's Edward McSweegan's Near-SPONTANEOUS
COMBUSTION-Experience in response to my demonstrating to the FDA that LYMErix was
never proven to be a vaccine because the testing for Lyme is
bogus.
CHAPTER 5,
PRIMERSHELLGAME
CHAPTER 6,
RICO PATENTS (tell a
different story from the public one)
CHAPTER 7,
RUSSIAN SCIENTISTS at NYMC
(speaking about their "non-intracellular intracellular
spheroplasts")
CHAPTER 8,
1989 IDSA REVIEWS,
("treatment endpoint is unknown," and other self-ass-biting)
LINK TO MEDLINE, ALL, "Reviews of Infectious
Diseases" (the former name of the IDSA journal), 1989
Supplement 6; The status summary that lead to the creation
of the ALDF.com cabal at New York Medical College and
Kaiser-Permanente's takeover of "Lyme Disease"
CHAPTER
9,
BIOMARKERS of DISEASE (by
the crooks)
CHAPTER 10,
KLEMPNER ("a bogus
article")
CHAPTER 11,
PERSISTENCE in the BRAIN-
by the crooks
CHAPTER
12,
CROOKS DEPLOY the MUMBO-JUMBO DUMBOS
(Scientific Fraud With Intent to Cause Harm)
CHAPTER 13,
CDC STAFF COMPLICIT PATENT PROFITEERS
CHAPTER 14,
IDSA AWARE THAT the CYST/SPHEROPLAST
is VIABLE
CHAPTER 15,
PLUM ISLAND SLYME (OspA) AND
IMMUNE-SUPPRESSION
CHAPTER 16,
OSPA VACCINES and the FRAUD UPON the
GOVERNMENT
(Qui
Tam)
CHAPTER 17,
CONGENITAL LYME and CONGENITAL
SYPHILIS
CHAPTER 18,
UCONN'S CHILD ABUSE HERE and in the
CZECH REPUBLIC
CHAPTER 19, YALE'S EUGENE SHAPIRO and his PERJURY at
the CHARLES RAY JONES TRIAL
CHAPTER 20,
YALE'S JAMES PHILLIPS, SY HERSH, and
the UNIBOMBER CHEMIST
CHAPTER 21,
YALE'S PATRICIA LEEBENS and JOHN
DCF-ROWLANDGATE'S JUVEY JAILS RICO
CHAPTER 22, THE CORRUPTICUT UNIONS, the DEMS, and
JAMES AMANN vs
MULTIPLE SCLEROSIS
CHAPTER 23,
THE DISTRICT of CORRUPTICUT USDOJ,
PORNOGRAPHY, and BANTAM LAKE
CHAPTER 24,
CORRUPTICUT'S OWN BUSH CRIME FAMILY
(Kissinger, & the Vosslerockefellers vs the
Darkefellers)
CHAPTER 25,
ASHKENAZI NEOSCHIZOPHRENICS and their TWINS, THE LYME CRIMINALS
CHAPTER 26,
THE PHILOSOPHY of the UNEXPLAINED (Dr Michael A. Schwartz and Allen Steere)
CHAPTER 27,
THE HISTORY of RELAPSING FEVER
GLOSSARY |
|
Chapter 3 of
Cryme
Disease ;
CDC "officer" Allen
Steere went to Europe to set up the FALSE CLAIM that his method (we
call it simply "Dearborn," the two-tiered ELISA/Western Blot schema)
to diagnose a "case" of "Lyme Disease" was scientifically valid, and
the resultant RICO or monopoly on grants, vaccines, tests, and test
kits for vector-borne diseases (an "enterprise" called the
www.aldf.com ),
in cahoots with Kaiser-Permanente. Kaiser bailed out the
financially floundering New York Medical College, and is still
there, training MDs who are
provided to
the New York State Medical Board as "experts" against the
realists.
What Allen Steere did
in Europe in 1992-3, revealed in this chapter, resulted in the 1994
CDC Dearborn, MI, farce of a conference and the bogus testing which
facilitated the intended monopoly. OspA
or the LYMErix "vaccine," is the key to the "controversy."
Compare what Allen Steere
did (discussed in this chapter) at the same time, 1992, to what
Fikrig and Magnarelli were doing as regards enhancing a
flagellin method, in 1992, discussed in
CHAPTER 1.
The CDC apparently thinks we
can't see that the 1986-Steere roll-out of "10-11 bands that
occur over months to years" is not equal to the 1993-Steere or
the 1994 Dearborn version: "most of the 10-11 bands occur
together in first few months of Lyme infection and we don't know
what happens after that, since we're only talking about EARLY LYME
diagnosis."
If Lyme is a Relapsing Fever
organism, then some aspect of it gave it that name. That something
was the spirochetes' chronic production of new surface antigens,
rendering previously made antibodies, useless. This is the same
process by which
Alan Barbour "selects" "mutants."
Barbour (or anyone) can grow some spirochetes in a dish with the
antibodies specific to the surface antigens he wants to pharm
out of the bug. In a chronically infected mammal, there
will always be spirochetes producing new surface antigens that are
changing all the time. Whenever new antigen is produced, new
antibodies are produced, and those new antibodies are IgM type. If
Alan Barbour selects mutants, and antibodies do no good, then a
vaccine is impossible, especially if it is true as Yale's
veterinarian Stephen Bartold (and all the older, pre-Steere
literature) says, that these spirochetes are coated in a slime layer
which keeps them protected from immunological attack (REF):
"He finds that
during the early stages of infection, B. burgdorferi avoids
immune detection by decreasing its expression of surface
proteins or cloaking its expressed surface proteins under a
layer of slime. "It's using some sort of stealth-bomber-type
mechanism," he says. Or, using another diversionary tactic
called blebbing, the spirochete can pinch off bits of its
membrane in order to release its surface proteins. Explains
Barbour: "It's like a bacterial Star Wars defense program," in
which released surface proteins might intercept incoming host
antibodies keeping the spirochetes safe from immunological
attack."
--
1996, The Crooks.
We, the victims of these
crimes and incompetence, are aware that the specific Lyme Disease
cabal established itself at New York Medical College in 1990,
after the publication of the
1989 Reviews of Infectious Diseases
(the former journal of the Infectious Diseases Society of America)
special supplement on spirochetal disease (Supplement 6). Allen
Steere began publishing obvious research garbage about "Chronic
Lyme" disease around that time. Anyone following these sequence of
events in the crime would find it hard to believe that the crime of
"Lyme Disease and LYMErix®" was any accident or the result of
research stupidity. It is research fraud.
The overall driving force
behind these crimes was to TAKE all the funding money
and OWN and GRAB all the DNA and
LIE and TRASH the Lyme victims and
DESTROY all the Lyme treaters with a ferocity never seen
before or imagined. The behavior of the Lyme disease criminals
knows no unethical limits. They will and did cross every red line.
The evil here is insidious and large, and
very, very deliberate.
DEARBORN and the 1986- and
1993- versions of Allen Steere:
The current (2006-2007)
CDC-sanctioned testing for hard-tick Relapsing Fever had been
changed by the perps into the non-existent entity “Lyme
Disease” in 1994 at the CDC's Dearborn, MI, meeting with some
goofball labs- standards entity which is apparently brainless and
powerless.
The CDC's 1994 Dearborn
"two-tiered" testing criteria is meant for the diagnosis of “early
Lyme,” or within the second month of illness to less than six months
into illness.
"Two tiered" testing means:
First, one has an ELISA test or a general, or slop-o-metric,
screening test to detect the concentration of antibodies in the
blood to see if the victim has late stage chronic severe arthritis
in a knee with the very, very high antibody concentration. (Steere's
kind of autoimmune Lyme is a genetically-linked hypersensitivity
reaction, like asthma or Type 1 diabetes).
If one has a positive
ELISA result, one may then proceed to Western Blotting, but the
problem is that the ELISA screens out all but the extraordinary
cases of a loud, red, swollen arthritis in a knee and misses all
of the neurologic or regular Lyme cases.
That is, in order to have
"Early Lyme," one must first have "Late Lyme Arthritis in a
knee," according to Allen Steere and the ALDF.com cabal and is
now the CDC's accepted testing protocol.
We don't know of any more
highly regulated testing anywhere in the US. If you, the lab
owner, decided to perform actually scientifically valid testing
for Lyme, the CDC will come after you and try to shut you down.
You will recall from the
Hartford Courant interview interview
with Yale's Durland Fish:
"He proceeds down the
list, name by name: "Totally bogus." "He killed one of his
patients." "They tried to shut him down." Words like
"crackpot," "wacko," "buffoon" and "fraud" pepper his
discourse.
The two tiered testing schema was designed to SCREEN OUT all
the neurologic cases of Lyme with the first test. Some
insurance companies even state that they won't pay for a Western
Blot if the ELISA is negative. This is scientific fraud with
intent to cause harm since Lyme progresses into all sorts of
very severe neurological diseases and death.
The Lyme ELISA only detects
late Lyme arthritis, with a full-blown swollen knee. Late Lyme
arthritis in a knee is caused by a hypersensitivity or allergy
reaction or too many antibodies to OspA. The too-many-antibodies
against OspA allegedly cross reacted with knee tissue, but now Allen
Steere's mob say that OspA is a superantigen for certain persons.
That is, people with a certain genetic background will super-bind
the OspA antigen into their HLA molecules, causing an almost toxic
level of antibodies (chronic stimulation) or the antibodies exist as
a free, toxic immune complex (antibody is bound to the free
antigen), and suffer the associated immune response (downstream
mechanisms after antibody production that is tissue-damaging).
Other researchers counter that if the Steere superantigen model was
true, the phenomenon would not be limited to a knee.
Again, if a Lyme victim passes
that test, the ELISA, and has a late Lyme arthritis in
a knee, they may graduate on to having a Lyme Western Blot test. As
explained in the first few chapters, one does not validate a test by
saying, for example, "Only 7 ton elephants may be diagnosed as
elephants, and that 200 pound baby elephants may not diagnosed and
treated as elephants." You can still see the baby elephant and know
it is an elephant by its specific features, and know it is
there (that being the point of "diagnosis" or "identification" of
the offending organism).
And this is where these
evil-and-viciousness-relatedly stupid Lyme criminals are really
scary-
Lyme is a bioweapon in the
"stealth disabler" class, causing
immune-suppression-related and/or immune-dysregulation-related
outcomes as we will see in the
Plum Island and
OspA Chapters. Thankfully we
can't sneeze it on each other (but spirochetes can be inhaled as
we will see).
We will see in later chapters
that the pathology associated with the presence of spirochetes is
hardly limited to the production of cross-reacting antibodies. In
other words, no one cares if they have "too many OspA antibodies,"
they only care to know if what is making them sick is something
treatable with something so simple as antibiotics.
Again, 5 of the of the 10-11
early-Lyme, pre-1987-Steere, antibodies which occur "over
months to years" must now - after 1994 and after the
bogus CDC Dearborn MI conference - occur within the first ~6 months
of infection in order to be a case of "Lyme Disease," since that's
what CDC-type conferences are about.
That is, where once Lyme was
thought to be a Relapsing Fever, characterized by "changing and
expanding IgM antibodies that occurred over a fairly long time and
represented persisting infection," it suddenly has been changed to:
"5 of 10 IgG bands have to all occur at once" for a
person to be able to have a diagnosable (treatable) case of "Lyme
Disease."
When the CDC's 1994 Dearborn
conference was proposed and announced, some labs thought it was
about standardizing the method and not to create a new
interpretative platform. That is, to any real scientist, to
"standardize a method" means, 1) Everyone uses the same equipment
and concentration of components in the electrophoretic gel, 2) the
standard should be the same (use low passage strains of
SPECIFIC organisms; Borrelia that express OspA, B, C, Borrelia-specific
flagellin and other specific known antigens that produce antibodies
in most humans), 3) Everyone should agree that the assay of the
proposed analytes is a method that does not co-elute more
than one analyte. The method should be validated in that the
concentration of one analyte is not erroneously added to at the same
retention time or kilodalton apparent molecular weight by another
(masked) analyte.
The following is the
publication of the self-alleged results of the CDC's Dearborn, MI,
self-alleged conference:
Notice to Readers
Recommendations for Test Performance and Interpretation from the
Second National Conference on Serologic Diagnosis of Lyme Disease
The Association of State
and Territorial Public Health Laboratory Directors, CDC, the Food
and Drug Administration, the National Institutes of Health, the
Council of State and Territorial Epidemiologists, and the National
Committee for Clinical Laboratory Standards cosponsored the Second
National Conference on Serologic Diagnosis of Lyme Disease held
October 27-29, 1994. Conference recommendations were grouped into
four categories: 1) serologic test performance and interpretation,
2) quality-assurance practices, 3) new test evaluation and
clearance, and 4) communication of developments in Lyme disease (LD)
testing. This report presents recommendations for serologic test
performance and interpretation, which included substantial changes
in the recommended tests and their interpretation for the
serodiagnosis of LD.
A two-test approach for
active disease and for previous infection using a sensitive enzyme
immunoassay (EIA) or immunofluorescent assay (IFA) followed by a
Western immunoblot was the algorithm of choice. All specimens
positive or equivocal by a sensitive EIA or IFA should be tested by
a standardized Western immunoblot. Specimens negative by a sensitive
EIA or IFA need not be tested further. When Western immunoblot is
used during the first 4 weeks of disease onset (early LD), both
immuno- globulin M (IgM) and immunoglobulin G (IgG) procedures
should be performed. A positive IgM test result alone is not
recommended for use in determining active disease in persons with
illness greater than 1 month's duration because the likelihood of a
false-positive test result for a current infection is high for these
persons. If a patient with suspected early LD has a negative
serology, serologic evidence of infection is best obtained by
testing of paired acute- and convalescent-phase serum samples. Serum
samples from persons with disseminated or late-stage LD almost
always have a strong IgG response to Borrelia burgdorferi antigens.
It was recommended that an
IgM immunoblot be considered positive if two of the following
three bands are present: 24 kDa (OspC) * , 39 kDa (BmpA), and 41 kDa
(Fla) (1). It was further recommended that an that IgG immunoblot be
considered positive if five of the following 10 bands are present:
18 kDa, 21 kDa (OspC) *, 28 kDa, 30 kDa, 39 kDa (BmpA), 41 kDa (Fla),
45 kDa, 58 kDa (not GroEL), 66 kDa, and 93 kDa (2).
The details of both plenary
sessions and the work group deliberations are included in the
publication of the proceedings, which is available from the
Association of State and Territorial Public Health Laboratory
Directors; telephone (202) 822-5227.
References
Engstrom SM, Shoop E,
Johnson RC. Immunoblot interpretation criteria for serodiagnosis of
early Lyme disease. J Clin Microbiol 1995;33:419-22.
Dressler F, Whelan JA,
Reinhart BN, Steere AC. Western blotting in the serodiagnosis of
Lyme disease. J Infect Dis 1993;167:392-400.
The apparent molecular mass of
OspC is dependent on the strain of B. burgdorferi being tested. The
24 kDa and 21 kDa proteins referred to are the same.
Disclaimer
All MMWR HTML versions of articles are electronic conversions from
ASCII text into HTML. This conversion may have resulted in character
translation or format errors in the HTML version. Users should not
rely on this HTML document, but are referred to the electronic PDF
version and/or the original MMWR paper copy for the official text,
figures, and tables. An original paper copy of this issue can be
obtained from the Superintendent of Documents, U.S. Government
Printing Office (GPO), Washington, DC 20402-9371; telephone: (202)
512-1800. Contact GPO for current prices.
**Questions or messages
regarding errors in formatting should be addressed to
mmwrq@cdc.gov.
The CDC apparently thinks we can't
see that the 1986-Steere roll-out of "10-11 bands that occur over
months to years" is not equal to the 1994 Dearborn version: "most
of the 10-11 bands occur together in first few months of Lyme infection
and we don't know what happens after that, since we're only talking
about EARLY LYME diagnosis."
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=3531237
full text link
:
J Clin Invest. 1986 Oct;78(4):934-9.
Links
Antigens of Borrelia
burgdorferi recognized during Lyme disease. Appearance of a new
immunoglobulin M response and expansion of the immunoglobulin G
response late in the illness.
Craft JE,
Fischer DK,
Shimamoto GT,
Steere AC.
Using immunoblots, we
identified proteins of Borrelia burgdorferi bound by IgM and IgG
antibodies during Lyme disease. In 12 patients with early disease
alone, both the IgM and IgG responses were restricted primarily to a
41-kD antigen. This limited response disappeared within several
months. In contrast, among six patients with prolonged illness, the
IgM response to the 41-kD protein sometimes persisted for months to
years, and late in the illness during arthritis, a new IgM response
sometimes developed to a 34-kD component of the organism. The IgG
response in these patients appeared in a characteristic sequential
pattern over months to years to as many as 11 spirochetal
antigens. The appearance of a new IgM response and the
expansion of the IgG response late in the illness, and the lack of
such responses in patients with early disease alone, suggest that
B. burgdorferi remains alive throughout the illness. PMID:
3531237 [PubMed - indexed for MEDLINE]
As an aside,
Mark Klempner, CDC "officer,"
and now a Boston University apprentice provost, alleges that the
meaning of: "only 78 out of 1800 (4%) persons" who are
"Chronic Lyme" victims, and who all have been treated before
with antibiotics - yet still have the CDC bogus positive early
Lyme/late Lyme IgG blood testing criteria of Alien Abductee
Steere - means that the probability that a person who claims to
have Chronic Lyme "is 96% likely to be a kook." An
antibiomaniac. A Munchauser. A Lyme paranoiac. No one knows
what kind of victims Klempner captured and abused in his
"Chronic Lyme is imaginary but cured by the placebo effect of
antibiotics 'study,'" since the Steere early Lyme/Late Lyme
criteria for a "positive case of Lyme," has never been studied,
much less validated for late, treated, chronic Lyme. The
victims or class of people Mark Klempner claimed to have
assessed for antibiotic efficacy, should have been "seronegative,"
due to the host adaptation of their own particular spirochetes
and the immune suppression caused by chronic infection and the
chronic blebbing.
Amazing as it is to believe,
few people realize that the CDC IgG method to diagnose “Lyme
Disease” is only to be used in the first few months after infection,
but that also, "IgG means past infection and not a treatable case,"
according to Imugen Labs (Norwood, MA).
That is, the 1994 Dearborn
(Dressler/Steere) early Lyme criteria to be used to diagnose
early Lyme comes from an imaginary standard that was revealed
(to Allen Steere) as a series of antibodies developed against
antigens "over months to years," but IgG means old or previous
infectious, so most people will not have a treatable case of
Lyme no matter what the circumstances. IgG means past
infection. And no treatment. IgM means current. But almost no
IgM bands may be identified and reported towards a positive
test. Which means no treatment.
DANGEROUSLY SERONEGATIVE
Most MDs don't realize that
this bogus testing standard is to not be used for persons who have
been sick for more than a year because the spirochetes become “host
adapted." That is, spirochetes that arrive into a person fresh
from a tick are expressing different surface antigens than those
spirochetes which have been cohabitating with their human victims
for years. Therefore, the long-infected person produces
different antibodies than the newly-infected.
Not only are these later,
host-adapted antibodies not predictable, not detectable, and not
occurring early in the disease (and thus will yield a negative
test result), but due to the immune suppression cause by these
shed Osps (CHAPTER
15 RELATED PLUM ISLAND GOODIES) - the Alan Barbour "Star
Wars blebbing" - has the effect desensitizing its
human victims or tolerizing the immune system to them, with the
result that antibodies are not produced. The antigen presenting
molecules or HLA molecules are down-regulated. If the blebs or
the surface antigens can not be presented (presented to B cells,
which make antibodies) because the HLA (human leukocyte
presenting antigen) molecules have been removed, fewer
antibodies will be produced. This is also important because the
blebs were made into "vaccines," one of the patents for which
was owned by Alan Barbour (ImmuLyme), who said of them (besides
the "rich vein of gold from which to mine virulence
determinants" comment),
http://www.nature.com/nature/journal/v390/n6660/full/390553a0.html
"One of the
lipoproteins, OspA, has already been crystallized and
structurally characterized5,
and it is undergoing human field trials as a vaccine against
Lyme disease, although no one yet knows what it
does." - because the adverse events were
deliberately not reported to the FDA.
These late, undetectable,
antibodies are not detectable or become not detectable because 1)
everyone has their own special collection of spirochetes'
antibodies (which have become host-adapted and are constantly
undergoing antigenic variation), 2) everyone has their own
genetically-determined tendency to find certain kinds of
antigens irritating (HLA differences), although there are clearly
clusters or genetic histories are shared by peoples (see the
"race-specific bioweapons" comment in the Israeli's PNAC document),
3) many people, especially the sickest- usually "seronegative
(seronegative to the imaginary Steere Dearborn criteria case)" - are
likely to be multiply-infected with the other immune suppressing
organisms, Babesia and Ehrlichia (ref Dave Persing), and have
the neurologic kind of Lyme [since only the knee-kind tests Steere/Dearborn
positive; only the knee-kind of Lyme people make sufficient
antibodies and "may even be called immune-competent," according to
Vikay Sikand, MD (East, Lyme, Connecticut, at the 1998 LYMErix FDA
meeting)], and 4), there is now an identified mechanism of
immune suppression, the tolerization to these spirochetal
antigens, turning off the immune system to these types (triacyl
Palmitoyl 3 Cys lipopeptides like OspA,
the vaccines), rendering some people perhaps permanently
seronegative and SERONEGATIVE to OTHER INFECTIONS that
bear the same type of antigens.
We will see in the
Biomarkers chapter that it was
known in 1992, that the lymphocytes of chronic Lyme victims look
like Epstein-Barr transformed or mutated cells. That's yet
another can of worms which we think is co-related to LYMErix
outcomes and cancer. Again, the pathological outcomes of Lyme
have all been subjected to the Negative Data Rule: Don't look
for or fund the research into information you don't want to
discover or want revealed. The most well-known sufferers of the
Negative Data Rule are the Gulf War Illness Veterans.
Naturally, the keeper of this fraud is the British psychiatrist
Simon Wessely. Whether or not these Lyme crimes are bioweapons-related
or just evil, profiteering frauds tripping over their own dicks
may be resolved by looking deeper into Simon Wessely's history.
One thing we will find out about Simon Wessely is that he knows
absolute zero about ethics or integrity, but his counterparts in
the USA will be subject to the same scrutiny.
Some of the other infections
which bear these same type of antigens as LYMErix or the shed Osps
are HIV, Foot and Mouth Disease, Tuberculosis, mycobacteria, and
mycoplasma.
A huge can of worms.
Maybe the AMA can tell us
about it.
Maybe not.
Related to the immune
suppression/dysregulation outcomes and according to CDC's bioweapons
officer Alan Barbour in his US Patent 6,719,983,
http://patft1.uspto.gov/6,719,983
2.1
Methods of Treatment
"An important aspect of the invention is the recognition that
Borrelia VMP-like sequences recombine at the vls site, with the
result that antigenic variation is virtually limitless. Multiclonal
populations therefore can exist in an infected patient so that
immunological defenses are severely tested
if not totally overwhelmed."
TRANSLATION: "The Lyme
infected person's immune system could be completely overwhelmed
by their chronic infection with multiple 'clones' of
spirochetes, all of which continuously undergo antigenic
variation (negating the validity of the term "clone") creating
seventy five bahzillion different antibodies which overwhelm the
immune system. But everyone who says they're chronically ill,
but who don't have Dearborn Lyme, is a hypochondriac and please
read my totally unreferenced book entitled, 'Lyme Disease,
the Cause, the Cure and the Controversy,' and never mind the
fact that I am a CDC clone lying profiteer, since there are no
other CDC officer species."
Homo bovis excrementii
Therefore, due to antigenic
variation and likely being infected with multiple types of
spirochetes (burgdorferi, or barbouri, or wormserii,
or popeyei, etc) and over the longer term, becoming
immune-suppressed/dysregulated, the only way to see if a chronically
infected person is chronically infected using an antibody method, is
to capture some spirochetes from said chronically infected person,
grow a few, and use that current-human-spirochete-slurry
to Western Blot the same infected person and see if they have
antibodies against their own spirochetes. (But they might not, due
to the effect of OspA or Pam3Cys-related immune suppression.)
We could only expect such
stupid science from the Steere camp. We know that if they
performed such a stupid science experiment, the Steere camp
would still try to tell the patient from whom spirochetes were
extracted that their antibodies were only IgG antibodies, and
that that meant that the patient only has past-Lyme disease or
is therefore no longer infected and does not need treatment.
'Since no one ever needs
treatment. 'That being the part about Kaiser-Permanente
rescuing the financially failing New York Medical College in
return for the opportunity to train the New York Office of
Medical Conduct's "experts" on "Lyme disease" in preparation for
the Bush Senior-Karl Rove-esque harassment of Lyme treaters and
establishing the racketeering cabal, the "American
Lyme Disease Foundation."
The entire point of the
erroneous and criminal final solution dictated to us from Dearborn
"conference," is that "We should look for 5 of 10 IgG bands and
ignore most of the IgM bands, because the presence of IgM bands is a
phenomenon that demonstrates persisting infections, according to the
1986 version of Allen Steere." If every single iota of medical
malarkey from the Steere camp were an H2O molecule, we'd all have
wished we built arks and captured pairs of animal species (not
ticks).
Examples of explanations of
host-adapted spirochetes or the proof that late neurologic Lyme will
never test positive to the CDC Dearborn method (and these are
repeated in the
PRIMERSHELLGAME chapter, since the
fraud in testing by antibody is related to the fraud in testing
using DNA and RNA methods):
1)
Pachner and Brains, 1990
"The plasmid
content of N40Br was different from that of the infecting strain
implying either a highly selective process during infection or
DNA rearrangement in the organism in vivo. "
2) NIH's Dave Doward on
TRAINING SPIROCHETES TO BE CERTAIN TISSUE TROPIC:
http://iai.asm.org/cgi/content/full/69/3/1428?view=long&pmid=11179308
"By repeatedly
coincubating spirochetes with primary mouse lymphocytes
that were immobilized by adherence to immunomagnetic
beads, we were able to preferentially enrich
cultures for or against bacteria with
constitutive affinity for murine B and T cells."
3)
Using monoclonal antibodies "to select
"mutants" in vitro- Barbour
4) Antibody selection:
Fikrig discussing OspA’s uselessness
http://iai.asm.org/cgi/reprint/63/5/1658?view=long&pmid=7729870

5) "New antigen milieu"
from Fikrig re brains
http://www.pnas.org/cgi/content/full/100/26/15953
If
Fikrig claims there is new antigen expression over time as
the spirochetes host-adapt, and the Yale OspA vaccine was to
be given annually due to the fact that the IgG antibody
concentration fades (this was probably due to the immune
suppression it caused, as revealed in the Plum Island
chapter), and if Steere claims that only people with his
genetic HLA relation to Lyme arthritis maintain a high IgG
antibody concentration for "months to years," why does
Fikrig not make a public announcement that the new
antigen-antibody milieu negates the Dearborn criteria?
The usual case of a chronic
Lyme victim is that they have had chronic fatigue and neurologic/brain
signs for several years before finding their way to a specialist who
understands that the blood testing schema proposed by the 1993
version of Allen Steere, fraudulently accepted by the Centers for
Disease Confabulation and accepted by the American Medical Kool-Aid
Drunkards Association, is an elaborate concoction of nonsense
intended to set up a monopoly on testing for “Lyme Disease” around
the OspA vaccine.
Keeping in mind that the
ALDF.com camp are interested only in the profit in vector borne
diseases and not in anyone’s better health outcome, “Lyme
Borreliosis” – the serologic definition previously established by
Allen Steere and the CDC as a Relapsing Fever organism, the
diagnosis of which was to be in the performance of serial Western
Blots in order to look for "changing and expanding IgM and IgG
antibodies" - was spun into "Lyme Disease."
Time hardly flies when you're
chronically sick; imagine you're Christ on the cross with the
dislocated shoulder; imagine the agony of never having a good day
and all of these YEARS have gone by where none of the
people whose job it was to investigate and prosecute these crimes,
did so, despite being given the evidence. And so I say:
Way, way back about a hundred
years ago in 1992 , Allen Steere went to Europe with an illegal
high-passage strain of Borrelia- strain G39/40 from Guilford,
Connecticut:
.
Says Alien Steere,
from Europe: "Supernatants from
sonicated lysates of whole spirochetes were prepared as
described (20). The group 1 strain of B. burgdorferi, G39/40,
used in this study and in the previous study of US patients was
isolated from an Ixodes damini tick in Guilford, Connecticut
921). The group 2 strain, FRG [Federal Republic of
Germany], was isolated from Ixodes
ricinus near Cologne (21). The group 3 strain, IP3, was
isolated from Ixodes persulcatus near Leningrad (23). All three
strains used in this study were high
passage isolates, which were
classified by Richard Marconi (Rocky Mountain Laboratory,
Hamilton, MT) using 16S ribosomal RNA sequence
determination as described (11, 24). The recombinant
preparations of OspA and OspB used in this study were purified
maltose-binding protein-Osp fusion proteins derived from group 1
strain B31 (25). The fusion proteins contained the
full-length OspA or OspB sequence
without the lipid moiety or the signal sequence."
So, Steere did not find
too many antibodies to the B31-associated recombinant Osps A and
B in people in Europe, using G39/40 and FRG, as we will later
see. We think these shenanigans with strains and recombinants
were the reason Steere went to Europe to perform this crazy
nonsense for two reasons: European journal articles might not
be reprinted full-text online such that American researchers
could see what he had done (and they were not, I had to go to
the Yale Medical Library to get them), and Frank Dressler was a
young, innocent, inexperienced lab rat.
It makes no sense to
have done this, when Steere previously (1986) worked this
all out, no matter how you look at it. There was no
reason to go to Europe to come up with a new
antibody panel/immune response profile. There was no
reason for Americans to have accepted this from
Europe, secondly, because the CDC simultaneously claims they
lend European researchers no credibility whatsoever.
The CDC
CLAIMS that whatever happens elsewhere does not
exist... (why then did we end up with Willy Burgdorfer
from Switzerland and the German scientist, Roland
Martin?)... except for this crazy nonsense by Steere in
Europe.
The the electronegative
core in between the lipid ends and the water-soluble protein
end, is what is hyperstimulative about OspA or the Osps.
Without the lipid end, this would not be such a wild,
immunostimulatory lipoprotein. Remember, to a chemist, and now
to you the reader, what a chemical coumpound is, is what
it does. The crooks discovered, but kept secret, the
fact that OspA in it's native form was too stimulatory.
This experience with OspA led to its later modification by David
Persing at Corixa, who tried to sell an entirely new class of
lipopeptides or glycolipids or similar-looking compounds as
vaccine adjuvants.
The following are graphics
of the structure of OspA (by Mass-Spec, since you can't
recrystalize a lipid). You can see the highly densely lipidated
end (water-insoluble) is combined to the protein end
(water-soluble), by a highly electronegative cysteine core
(molecules speak to you visually; chemistry is sorta like
hieroglyphics or Chinese):


http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=259838&blobtype=pdf
and from a Korean journal:
http://www.actionlyme.org/PAM3CYS_LYME_HIV.htm

Here is Dave Persing (Lyme
testing RICO patent owner) Corixa's
"We modified OspA for use to sell in our adjuvant business
because the real OspA is too awful" advertisement which has
since been taken off the web, and Corixa has since been purchased by
SmithKline:
EMBASSIES_CORIXA_TLR_13_JULY_06.htm
And here is Dave Persing of
Corixa talking about how the native OspA proteins are too awful to
be used alone as a vaccine in another patent:
http://patft.uspto.gov/6,800,613
"While not wishing to
be bound by theory, it is believed that the efficacy of the
prophylactic and therapeutic applications described above are
based at least in part on the involvement of the mono- and
disaccharide compounds in the modulation of Toll-like receptor
activity. In particular, Toll-like receptors Tlr2, Tlr4,
and others, are believed to be specifically activated,
competitively inhibited or otherwise affected by the non-toxic
LPS derivatives and mimetics disclosed herein. Accordingly, the
methods of the invention provide a powerful and selective
approach for modulating the innate immune response pathways in
animals without giving rise to the toxicities often
associated with the native bacterial components that normally
stimulate those pathways."
In this instance they are
talking about a polysaccharide in place of the protein, but it's
the union and the opposing solubilities that are toxic or
immunostimulatory or "too immunostimulatory in the native form."
Note that one of the
claims for this modified OspA vaccine as an adjuvant or
immune-booster is that this could be used for:
7. A method in accordance with claim 2, wherein said
infectious disease is a chronic infection.
I don't know of any
"chronic infectious diseases," do you?
==========
Returning to the issue of
Allen Steere's fraudulent experiments in Europe to invent his new
idea of what a "positive" blood test for "Lyme Disease" should be:
"High-passage" is almost
exactly like George W. Bush. Too much inbreeding leads to
incompetent strains.
The National Institutes of
Health’s Rocky Mountain Labs recommended not using high passage
strains to diagnose “Lyme Disease" because they drop plasmid
expression or drop the expression of specific diagnostic antigens
(or fewer bands will show up in a Western Blot). You can't see the
antibodies in the blot even if they're in the blood because they're
not in the Western Blot antigen mix for the antibodies to bind to
and be detected.
Spirochete cultures that have
been passed many times in vitro without being pharmed back into
ticks and rodents start growing populations which have lost the
ability to infect, because they have lost the code for the surface
antigens - the speckles or the Osps or the Vmps or the Vsps - which
they use to bind surface molecules on the cells of their hosts. In
other words, they clone themselves badly. They're, like,
couch-potato spirochetes. Wimpy.
With fewer of the surface
antigens spirochetes use to invade tissue and penetrate or adhere to
cells, these spirochetes can cause less damage. Spirochetes are
parasites and must take something from the host in order to
survive. The surface antigens encoded on the plasmids help the
spirochetes find nice delicious cells to invade and steal metabolic
goodies. They do worse things like destroy cells, too, but for all
intents and purposes, they would probably not be as harmful were it
not for the immune response. This we know from the histology
studies in monkeys (non-human primates, a term that should not be
limited to the hairier guys who walk around on their knuckles, as
we've learned from exposure to Lyme crooks in addition to
spirochetes). The monkey nerve damage studies will be included in
the
Biomarkers section, which is
associated with the
1989 IDSA REVIEWS section, since the topic of how sick we are as
a result of this scam is too extensive to include with this one
really incredible topic, What Allen Steere Did in Europe.
If the surface antigens are
dropped, we can surmise that they're less invasive.
Logically, one would want to
look at what is the makeup of spirochetes, since that would suggest
what are its metabolic needs. However, these Borreliae spirochetes
can apparently adapt to any environment, any mammalian environment,
any tissue type as we have previously seen from the David Dorward
Rocky Mountain Lab tissue-tropism studies. Forward advancing
studies as to what spirochetes actually do to cause us damage has
been inhibited by the Lyme criminals who spend all their energy and
our tax-supported grant money on telling us we have no disease for
which OspA was their vaccine.
NIH Rocky
Mountain Labs, including Willy Burgdorfer, say to use low passage
strains to Western Blot because high passage strains drop
plasmids- yet high passage strains, G39/40 and FRG were used by
Steere to concoct the Dearborn standard:
http://iai.asm.org/cgi/reprint/56/8/1831?view=long&pmid=3397175

The CDC’s diagnostic standard
in 1990, before Steere went to Europe, was based on Steere’s own
original 1986 observations that Lyme was a Relapsing Fever organism
and that the antibody profile for Lyme would change over time,
producing new (IgM) antibodies when viewed via Western Blotting.
Under the pretense of “standardizing” all the US testing for Lyme in
America, in 1994, the CDC sent out invitations to numerous
labs across the country, inviting them to “contribute to the
proceedings.” However, apparently the decision had already been
made that the CDC would adopt the new Steere method- the one he
developed in Europe with bogus strains that dropped plasmids, and
thus, likely, the expression of the OspA-B plasmid- a plasmid
replaced with the "American protypical B31 strain's OspA and B
recombinant antigens," against which EUROPEANS were
blotted. This would have the effect of creating a new bogus profile
from among Steere’s victims that resulted in the current bogus CDC
IgG criteria for a positive case of “Lyme Disease” that left OspA
and B antibodies (band 31 and 34) out of the standard.
What the labs invited to the
farcical CDC 1994 Dearborn, MI, conference determined, in regard to
Steere’s new proposal for an IgG standard were:
1)
Gary Wormser at New York Medical College, "Steere’s method detected
9/59 or only 15% of all cases"

Read carefully what
Wormser says in this report:
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=266355&blobtype=pdf
He says he
is assessing the accuracy of what was later to be called the
Dearborn Method, the Dressler/Steere proposal, in the
field, and he found that the IgG method detected only 9/59 of
the Wormser cases.
2) Imugen's Dearborn
submission: "Steere’s method detected 14% of the cases"


[CAPTION] You can see from that graphic where I circled the 14% for
the January 31, 2001 FDA Vaccine Committee Hearing (CHAPTER
4), that Imugen was assessing the accuracy of the Steere/Dressler
IgG proposal, but that Imugen thought that their antigen-antibody
complex capture method was more accurate, or detected more cases.
3) Igenex, "Steere’s IgG
detected 8% of the cases" or misses 92% of the cases.
4) Wisconsin, "Steere’s
method was 15% accurate" or misses 85% of the cases.
5) The
University of Child Abuse - Larry
Zemel was referring to Lyme as comparable to juvenile rheumatoid
arthritis. Recommended adding band 50 for children’s blots.

6) Roche, "28% were
positive for every Steere band."
7) Wadsworth had some
different scoring system; did not report on accuracy of Steere
8) Ontario Ministry of
Health
9) Lutheran Hospital,
"22 % were accurate by Steere’s IgG"



Lutheran Hospital said it
would be better to standardize the method before standardizing the
interpretation of results. Lutheran Hospital clearly believed this
nonsense about Steere's "area curves" (the elephant rule, or the
Steere idea that happens to be the reverse of Limit of Detection or
Limit of Quantitation as a parameter that is supposed to suggest to
those creating and validating analytical methods and the companies
who try to sell us very sophisticated and SENSITIVE equipment that
we want to detect the LOWEST concentration of stuff, always), made
Steere's proposal INSENSITIVE, or would be inappropriate for use
on humans or would not detect as many cases of Lyme as possible.
Note that the only place
in the entire world, at the current time in history, where you
hear anything about how we could improve the
testing for Lyme, is on ActionLyme. It's a repeat or a
rebroadcast of the crooks' work from the early 1990s. Think
about what that means in terms of the integrity and competence
of your MD or any MD you know. Not a single MD in America felt
obliged to look at this data and our complaints and report this
crime to the proper authorities.

The above is the very
essential graphic for interpreting Steere's Elephant Diagnostics
Rule. He tried to assert that the higher the antibody
concentration, the more "valid" the test, falsely claiming that by
"narrowing the number of persons who will test positive," that makes
his test more SPECIFIC, and claimed that "the higher the
concentration of antibodies in the blood makes the test more
SENSITIVE," when as we know, SENSITIVITY is a function of LIMIT of
DETECTION or the ability of the test to detect very low
concentrations of analyte.
The new Steere fantasy term "receiver
operating characteristic" is not a criterion for the validation
of an analytical method. It means the opposite of sensitivity or
the goal of detecting increasingly lower quantities of analyte.
Cross apply that to what you
know from
Chapter One on Chromatography
Methods Development and Validation. No one in their right mind
would buy a chromatography detector that detects less than what you
can see with your own eyeball. No one goes hunting for viruses with
a magnifying glass. We know from Chapter One, that by 1991, Yale's
Erol Fikrig already made the most common band to ALL CASES OF
LYME, band 41, SPECIFIC by pharming sections of the DNA from Bb
flagellin into E. coli, producing a protein fragment, and comparing
the antibodies from the blood of people infected with known
spirochetal or flagellated infections and found that he had captured
a fragment of recombinant flagellin that was SPECIFIC to
Borrelia burgdorferi, or only detected Lyme-infected
patients.
Yale also claims that their
recombinant vaccine, OspA or LYMErix, was SPECIFIC enough to prevent
Lyme, so why isn't one specific antibody specific enough to detect
Lyme? Why was OspA left out of the diagnostic standard, if to have
that antibody from a vaccine, that was supposedly specific enough to
PREVENT "Lyme Disease?"
You can see how silly
Dressler/Steere is on its face. You need 5 out of 10 band in
order to be diagnosed with a case of Lyme, but you only needed
one antibody, band 31, to be PROTECTED against Lyme, according
to these loonies and accepted as a truism by the American
Medical Association and all of their related MDtards.
The reality is that each
antibody band is as ACCURATE for diagnosis as its assigned percent
specificity. If we had Steere at the helm, detecting Anthrax
during the Mossadesque Anthrax-mailing stunt in October, 2001, well,
nobody would be too happy.
10) MarDx Labs – recommended
adding bands 31 and 34, but were given Steere-Dressler positive /
arthritis-positive blood samples to qualify their test strips.
MarDx was contracted to provide blot strips for both the ImmuLyme
OspA vaccine trails and the LYMErix OspA trials. The ImmuLyme trial
started in March of 1994 before Dearborn had taken place, but the
trial administrators claimed they were using the Steere-Dressler
proposal for the interpretation of a "positive" result (or vaccine
failure).
Later we learned the same
perpetrators of the ImmuLyme trial who were using MarDx blot strips
admitted that they could not read their Western Blots in
OspA-vaccinated people:
http://www.journals.uchicago.edu/doi/pdf/10.1086/313920
Sigal: "Hmm. How
amazing. The Western Blots are unreadable in OspA-vaccinated
people, even though I reported that ImmuLyme was 92% "safe and
effective" two years ago, heh, heh, I hope nobody notices..."
http://content.nejm.org/cgi/content/abstract/339/4/216
= ImmuLyme Trial
11) CDC Atlanta, at their own
conference, talked about mouse antibodies and not human antibodies.
The mouse criteria was 2 out of three from OspC, 16 kD, 17.9 kD.
Says the CDC, "DON'T MISS THE
OPPORTUNITY TO PARTICIPATE IN THE PROCEEDINGS after which we intend
to blow you all off!! heh, heh"

So, who was there and who said
we would adopt this Steere in Europe method?
From the Dearborn booklet:

CDC officer Alan Barbour,
owner of the ImmuLyme patent, a clear conflict of interest
Ray Dattwyler who said we should perform serial Western Blots
to assess OspA outcomes.

Arthur Weinstein,
member of the
ALDF.com Kaiser cabal
Edward McSweegan, who initiated
the RICO cabal by trashing the US Navy for his good buddy Durland
Fish
CDC officer Allen Steere, formerly at Yale (owner of the
LYMErix patent) - clearly to approve his own nonsense, perhaps due
to his relationship with Imugen, one of the two main RICO labs, L2
Diagnostice being the other
Russell Johnson, formerly an
advisor to the cabal and who knew more about spirochetes than
probably anyone, edited the 1976 textbook,
Biology of Parasitic Spirochetes,
and who claimed in the very first patent for a Lyme vaccine that
Lyme was chronic due to persisting infection and he mentioned
congenital Lyme deaths in that patent. In other words, it made no
sense at all for Russell Johnson to be hanging out with these
crooks.
Raymond Ryan at the
University of Child Abuse, who published that strain B31
expresses little or no OspC.
The reason Steere's Dressler/Steere
Western Blotting recommendations performed so poorly was because
Steere decided that "Lyme disease" would be a genetically-linked
autoimmune arthritis in knee. Because Lyme disease is not a
genetically linked autoimmune arthritis in a knee, LYMErix was not a
vaccine and came off the market.
The following is an excerpt
from the Dressler/Steere report where Steere used high passage
strain G39/40 with the recombinant antigen Borrelia burgdorferi
strain B31 (no OspC in it, which means the OspC response below was
from the FRG and G39/40) bands 31 (OspA) and 34 (OspB) to leave OspA
and B out of the diagnostic standard:


[CAPTION] 1993
Dressler, Steere report where OspA and B were left out of the
diagnostic standard by using a high passage strain G39/40 (but
comparing European blood to the Osps A and B to American
strain B31) and is the basis for the current CDC IgG standard
criteria to have a diagnosis of "Lyme Disease." This is part of
the submission by Kathleen M. Dickson of southern Connecticut to the
FDA Vaccine Committee on January 31. 2001. It is part of the public
record.
As you can see, the one band
that most people had, even in the hands of Allen Steere, was band
41, in both IgM and IgG. Allen Steere did not care, ever, about
patient outcomes, as we will see in an exclusive report on Allen
Steere's abuse of the psychiatrist
Michael A. Schwartz.
The Psychoanalysis of
Allen Steere, in summary form: "DSM IV : THE EVIL, ABUSIVE
BASTARD, ALLEN STEERE, CAUSES LYME RAGE; as in 'If I see that
bastard again I am going to punch him right in the face.'"
The following snippet comes
out of the other
Steere in Europe report (Antibody
in European Lyme Borreliosis), where you can clearly see that
each manifestation of the disease has a very different antibody
panel. We claim that it is absurd to create a standard
that knowingly leaves people out of the detection ranges. We think
it is absurd to even begin to think of
creating a test for which only the people with a hypersensitivity
response are allowed to be diagnosed as positive. At Dearborn,
almost all of the IgM bands that were accepted for IgG bands were
left out of the potential contribution to identifying a case of
Lyme. (Let's face it- Lyme meningitis is the most awful case of
Lyme.) We claim that an ELISA or a titer is not only obsolete, but
not appropriate for an immune-suppressing disease, and that you only
need one specific antibody and it could be specific band 41. At
this time, by 1992-1993, Steere had already acknowledged that there
was an MS form of Lyme, and JJ Halperin has areadly proven there was
a Lou Gehrig's Disease form of Lyme:

From the report submitted by
JJ Halperin in September 1989 on what
the paired serum (blood) and spinal fluid Western Blots (the faint
pencil lines are mine) of people with the Lou Gehrig's Disease version
of "Lyme Disease":

[CAPTION] These ALS patients look
like they only have bands 41 and maybe 93, and I bet they now would test
negative to Steere's Dearborn Lyme, which will be the central homicide
charge against Allen Steere and whoever claims the Dearborn method is
either valid, accurate or sensitive, to include claims that the "ELISA
is sensitive."
"Of 19 unselected
patients with the diagnosis of amyotrophic lateral sclerosis (ALS)
living in Suffolk County, New York (an area of high Lyme disease
prevalence), 9 had serologic evidence of exposure to Borrelia
burgdorferi."
So, there is no question
that Lyme is deadly, that JJ Halperin knew it was deadly, and that
the Steere/Dearborn method would not detect these people until it
was too late and they were on their way to dead.
DELIBERATE RESEARCH FRAUD?
It is possible - check, VERY
LIKELY - that by using a bogus "high passage" strain, Steere
actually created the low percentage of patients with OspA antibodies
intentionally. Ask yourselves a question: What in the world would
be the reason for using high passage strains, if not to change the
proposed antibody panel?
The profile Steere "developed"
would not be accurate or scientifically sound no matter how you look
at it. In this Dressler/Steere table (above; given to the FDA
Vaccine Committee and is part of public record), antibodies to OspA
(band 31 kD) and OspB (34 kilodaltons) suddenly are not as prominent
as Steere first observed and reported in 1986 where he said A and B
bound prominently to antibodies in Lyme arthritis.
We suspect that
that was because they knew they were going to have an OspA vaccine
trial, and that blots were unreadable in vaccinated persons unless
Western Blotted with a strain of Bb that had no OspA-B plasmid in
it, especially since the Phase I and II trials were underway in
1993. One would suspect that somewhere along the way in the early,
Phase I and II, human trials, someone would have Western Blotted the
blood of a vaccinated human and discovered the blot-smudging
David Persing and Robert Schoen reported in
1996 and David Persing and Lenny Sigal in 2000.
We think they knew about the
blot smudging earlier than 1996.
There is no other explanation
for why Steere went to Europe with bogus high passage strains in the
first place, and why in the second place, he would have developed a
test that conveniently allowed for the RICO labs (later chapters) to
be the only people allowed to Western Blot OspA-vaccinated people
(the 1996 patent developed by David Persing of Corixa and Yale's
Robert Schoen) - a monopoly on blood and all the patentable goodies
in it. The most obvious question of all is why they thought they
should have a vaccine against "Lyme Disease" that Steere and
Dressler tried to allege is barely relevant to the infection, OspA,
as this truly "bogus
article," the Steere/Dressler panel, asserts. It looks
to be due to narrowing the disease definition to just the Steere-alleged Aspirin
disease (OspA autoimmunity) because of Steere's and the ALDF.com
cabal's association to BigInsurance - Kaiser at New York Medical
College (autoimmune knee-diseases do not require intravenous
ceftriaxone). It is also rather routine and rather obvious that one
would assess any vaccine outcome by using a different antigen than
the vaccine, if the disease is detected by an antibody test.
It wasn't until two years
after LYMErix was approved that we learned that
none of the Western Blots were readable when using a regular
normal spirochete with the OspA-B plasmid in it.
The 2000 "Whoops
we can't read our Western Blots in LYMErix vaccinated people"
report was published by the same author- David Persing, owner of
the 1996 RICO monopoly patent (the RICO monopoly patent, in
1996,
6,045,804),
and he was re-reporting the same
"unreadable blots" phenomenon that Persing reported 4 years
earlier, in 1996. Note that in between, in December 1998, the
FDA approved LYMErix and it was put on the market the following
spring. These crooks never told the FDA that they had no
way to validly assess whether or not LYMERix or ImmuLyme
prevented Lyme, but they reported 76 and 92% "safe and
effective" vaccines anyway, in the journals in 1998.
Note, and this is extremely
important:
http://www.ncbi.nlm.nih.gov/pubmed/6859726
Ann Intern
Med. 1983 Jul;99(1):76-82.
The early clinical manifestations of
Lyme disease.
Steere AC, Bartenhagen NH, Craft JE, Hutchinson GJ,
Newman JH, Rahn DW, Sigal LH,
Spieler PN, Stenn KS, Malawista SE.
Lyme disease, caused by a tick-transmitted spirochete, typically
begins with a
unique skin lesion, erythema chronicum migrans. Of 314 patients
with this skin
lesion, almost half developed multiple annular secondary
lesions; some patients
had evanescent red blotches or circles, malar or urticarial
rash, conjunctivitis,
periorbital edema, or diffuse erythema. Skin manifestations were
often
accompanied by malaise and fatigue, headache, fever and
chills, generalized
achiness, and regional lymphadenopathy. In addition, patients
sometimes had
evidence of meningeal irritation, mild encephalopathy, migratory
musculoskeletal
pain, hepatitis, generalized lymphadenopathy and splenomegaly,
sore throat,
nonproductive cough, or testicular swelling. These signs and
symptoms were
typically intermittent and changing during a period of several
weeks. The
commonest nonspecific laboratory abnormalities were a high
sedimentation rate, an
elevated serum IgM level, or an increased aspartate transaminase
level. Early
Lyme disease can be diagnosed by its dermatologic
manifestations, rapidly
changing system involvement, and if necessary, by serologic
testing.
PMID: 6859726 [PubMed - indexed for MEDLINE]
Steere first said Lyme
Borreliosis was a systemic disease and acknowledged neurologic
outcomes. Then he said in 1986, when developing his first set of
formal antibody observations, that first, band 41 (flagellin) showed
up, then next, when focusing on the arthritis cases,
http://www.jci.org/articles/view/112683/pdf


You can see from this
early Steere report that Steere did not initially believe a person
needed to have 5 of 10 bands early in the disease, but that he did
acknowledge that his preferred type of patients (arthritis patients,
people who need aspirin and not antibiotics for central nervous
system infections), continued to have a hypersensitivity response.
AND he said, a person would have antibodies earliest
in the disease against band 41, that these patients would be
seronegative to the ELISA cutoff, and that he could tell the
difference between Lyme and people with syphilis or Relapsing Fever
(not that it really matters).
Clearly his perceptions
changed drastically. Anyone with Lyme Borreliosis knows the crooks
discount completely the band 41 or anti-flagellar antibody.
In
1990, the CDC accepted Steere's
first, 1986, interpretive criteria, based on this very report. Labs
were to perform serial or sequential Western Blots to look for
new IgM antibodies, because that meant the organism was still
alive and not killed by antibiotics:

[CAPTION] As you can see with your own eyeballs, the first, CDC,
published, diagnostic standard for Lyme Disease was to perform
serial Western blots to look for any CHANGE in the antibody profile,
especially new IgM type, regardless of treatment status. New IgM
meant the bug was still alive, regardless of treatment (or
vaccination) status.
Nowadays (2006-7), Steere says
he sees antibodies against OspA as frequently as he sees antibodies
against OspC. That’s sort of amazing since these bad guys say the
prototypical strain for “Lyme Disease” - Steere's Knees-Only Disease
- is B31, which expresses little or no OspC or the brain invasion
antigen. These criminals call Lyme victims insane, when none of
us are so demented that we would could have come up with such a
bizarre story as Steere's saga with "Lyme Disease," and expect
people to believe it.
The bottom line is that in
America, no one is allowed to have neurologic Lyme disease since
that requires expensive antibiotic treatment, therefore, strain
B31- the one with low or no OspC in it - is "the American
prototypical strain."
B31 is for "No brains
allowed."
Connecticut Attorney
General Richard Blumenthal at the time of this writing (Nov
2007) would like to know what is these Lyme crooks' association
to BigInsurance and BigPharma, although he and the United States
Department oif Justice, District of Connecticut, US Attorney
Kevin O'Connor were in the fall of 2003 already provided with
the Kaiser-Permanente-New York Medical College -
SmithKline-CDC, Incorporated, hard evidence. B31 is also
for "US Attorney, District of Corrupticut" and that will be
discussed in one of the other
pornography chapters. (The
first pornography chapter is
CHAPTER
2, McSweegan and Fish's pornography.) I do not have the
benefit of that RICO data now still in the US Attorney's office
collecting dust in New Haven to cite the Kaiser-Permanente /
www.CastleConolly.com
references but I know what's there.)
Lots of phallic
symbolism for everyone, here. Not because it sells, but
because it has been rammed down our throats as an excuse for
science and healthcare.
For the 1994 CDC Dearborn
Farce, Outer Surface protein A, once thought to be the cause of Lyme
Disease (autoimmune arthritis in a knee), was left out of the
diagnostic standard. That was because it was going to be a vaccine,
and in most cases of vaccination, the vaccine antigen itself is not
used to diagnose vaccine failure for logical reasons.
Here, in 1994, the vaccine was
going to design the disease, the disease was going to be arthritis
only, and as a result of this Dearborn conference and Steere in
Europe, there came a test for the newly defined disease that leaves
out the vaccine antigen to facilitate the Yale (vaccine and
post-vaccine test) RICO enterprise.
What's different here is that
there came a "controversy," (Think BigTobacco or fraud or crime)
over what "Lyme Disease" was, ever since the publication of the
Infectious Disease Reviews Supplement 6 on Lyme and Spirochetal
Diseases, in 1989. The 1989, Sup 6 ID Reviews (CHAPTER
8) had pretty much established that Lyme was a chronic
parasitic spirochetal infection, like all the rest of the chronic
parasitic spirochetal infections.
Kaiser-Permanente pounced
on the unsuspecting priests at the Catholic Medical School, New
York Medical College, in Valhalla, New York, less than a year
later, in 1990.
All Lyme victims should
memorize three things:
1) "Lyme Disease" was
redefined by Allen Steere at the Dearborn Conference to an
autoimmune arthritis in a knee where antibodies against OspA result
in an autoimmune arthritis in a knee because OspA was intended to be
the "vaccine."
2) No one is allowed to have
"Lyme Disease," unless they have an autoimmune arthritis in a knee -
an arthritis that is so obvious that it doesn't even need a blood
test (red, raised, hot, painful). It is usually restricted to one
joint. This disease does not need antibiotic treatment, even though
Allen Steere and Arthur Weinstein treat this autoimmune arthritis
with long term antibiotics, including ceftriaxone which is for brain
diseases, but that violates the "IDSA guidelines," which are
themselves in violation of the American Psychiatric Association's
guidelines on the treatment of diseases that need ceftriaxone.
3) No one is allowed to have
antibodies against OspA ("Lyme Disease") and have a diagnosis of
"Lyme Disease." LYMErix is allegedly specific enough to
prevent Lyme, but not specific enough to detect
Lyme, even though it is 100% specific to Lyme.
4) Bb strain B31 is the
"prototypical American strain," but it expresses no OspC- the brain
invasion antigen. There are no brains in America, and brains are "a
complicating variable," anyway, which should be throw
out, according to Yale's Steven Malawista. All psychiatrists at
Yale agree that the brain can and should be thrown out, as
we will see in later chapters.
Conclusion: "Lyme
disease" is an autoimmune arthritis in a knee caused by the
antibodies that no one is allowed to have. It is not caused by OspA,
B, or C, which are the "primary immunodominant antigens (produce the
most antibodies)." It does not go into the brain or the knee or
anywhere else, since there is no OspC in the prototypical strain and
there is no A or B in the diagnostic standard. Since this is
America and Allen Steere is not locked up and Yale is not shut
down. Yet.
To further prove that "Lyme
Disease" is a non-disease, Mark Klempner said at the 2001 Diseases
of Summer Conference in Rhode Island that CDC does not recognize any
other kind of Lyme except this imaginary kind of Lyme. One of the
biggest problems in the Lyme crime world is that IDSociety.org is
basing their "guidelines" on the very seriously invalid and just
plain stupid
Klempner Chronic Lyme Treatment report
released in July 2001- which is based on the Steere/Dearborn notion
of what "Lyme Disease" is. We now know Steere's Dearborn Lyme was a
hoax. But as regards Mark Klempner, for starters, Klempner pretty
much says, "Only the Imaginary Criteria of Allen Steere Invented in
Europe with high passage strain G39/40 may be called (diagnosed and
therefore treated) 'Lyme Disease'- which is not a real disease, but
the placebo response to antibiotics.'"
The following is an excerpt
of the Question and Answer session that followed the Klempner
Non-Diseases of Summer Conference at South Country Hospital, Rhode
Island, July 2001:
[Never mind exact which
city in Rhode Island, since it doesn't matter. South County is
formally Washington County, but what's the difference if we
talking about a state so small it practically doesn't even need
telephones and the MDs are so stupid they already watched this
conference and applaud the same nonsense year in and year out.
It's always the same conference: "There are no diseases and
Fibromyalgia is for women, but women are for men's penises so
everyone's fine here in Rhode Island thanks and have a nice
day."]
Questioner8: I just have one
more question for Dr. Klempner. Um, being that there are
inadequacies, inaccuracies in the tesing methods, seropositivity,
etc, and the surveillance criteria that you used were just that,
surveillance. And the CDC recognizes that there are so many more
people that have Lyme disease who do not meet the CDC criteria.
What’s your feeling on what percentage of patients who have Lyme
disease because they have not met the criteria for diagnosis?
Klempner: I, um, I think
there are a number of inaccuracies in what you just said. The CDC
does not recognize that there are patients who have, um, that
are seropositive that don’t meet seropositive criteria. What they
say, is that these are the criteria. I think
what, the question, if I could reinterpret the question a little
bit, is are there patients who are out there who had Lyme disease
who continue to have symptoms and um, wouldn’t fall into these
categories. And the question is, how do you define patients who
have had Lyme disease? You’ve gotta, you’ve gotta start with
some agreed upon cohort, so what are the agreed upon criteria?
And what we were trying to do, since we know this was a
controversial topic to start with a group of patients who
no one would doubt had had Lyme disease. And that was really
the point of the study. Are there other patients who fall into
equivocal groups that one could say, it’s difficult to document that
they had Lyme disease? Sure, but remember we were about to do a
study that was very risky. Um, meaning giving people parenteral
antibiotics, doing lumbar punctures, doing huge numbers of studies
on these people. It was very important to start patients
that everybody agreed had had acute Lyme disease. Are there
lots of other people out there who say they have Lyme disease where
the documentation is lacking? You know that better than I do. Of
course, there are lots of people out there who says
they have lots of things that you can’t document.
Questioner8: But, but according to what I’ve read is that not
everyone is going to, number one, see an EM rash, um, so when you’re
are using entry criteria, diagnostic criteria, that you need to have
an EM rash, and physician diagnosed…
Klemper: If you’re’re seronegative
Questioner8: Right, okay, but there are seronegative people that
don’t have the initial EM rash, And if they do, they may not see
it, being on the back…
Klempner: So, then how do you know what they have, that is anybody
who walks in the door who says, “I don’t feel well”, with this set
of symptoms. Um, that is not a group of people that I
would be comfortable putting an intravenous catheter in, an LP on,
doing all this very complex study. I needed to be assured that
those patients had had Lyme disease. You’re describing a group of
patients who cluster by virtue of symptoms. No different from the
symptom complex that was given here [previous (Fibromyalgia)
talk]. This is a very different symptom complex, very different
patient population. Very well documented Lyme disease. And I
just wanted to be sure. Um, that’s where I started my talk, at that
point. That is, there are a lot of people all over this
world that claim to have lots of different things. But for
doing studies, I think it’s very important that we cluster patients
by objective findings, strict criteria.
KRÜCH's
HYPOTHESIS: Whilst performing studies with invalid tests where
the outcome is predetermined, one should start out with the
assumption that the only kind of [fill in the blank disease] is the
imaginary Steere kind. The same thing happens with the "vaccines"
for [fill in the blank].
Follow: No one had the imaginary Steere kind of Lyme, therefore no
Lyme emerged in vaccinated people, therefore the "vaccines" were
"safe" and "effective." (It is a very good thing that Lyme
criminals do not attempt to assist NASA and the world should be
grateful.)
Now, cross
apply the Krüch's Hypothesis. In 1996, there was a RARE DISEASES
conference put on by the NIH wherein we learned there were tons of
Ehlichia out there and that Ehrlichiosis and Borreliosis in
combination could make a person very, very sick. Since it is now
more than 10 years later, and there are no tests out there which
detect all the Ehrlichias, we can assume they are are having trouble
with their fake vaccines.
http://www.lyme.org/conferences/96_abstract.html
Laboratory studies indicate the presence of different human
pathogens in Ixodes scapularis populations and that persons
living in tick-infected areas are sometimes exposed to multiple
tick-borne agents. Ehrlichial or Babesia organisms may occur
concurrently with B. burgdorferi in humans and may complicate
Lyme borreliosis infections. Therefore, clinical diagnoses of
tick-related illnesses should include laboratory testing for
ehrlichiosis, babesiosis, and Lyme borreliosis.-- Lou
Magnarelli.
Naturally, looking for
co-pathogens is not standard operating procedure, nor are all
MDs aware that they should be because, well, there's nobody yet
in the background with a vaccine, ready to profit. You don't
expect KAISER labs to be running any scientifically valid tests
on anyone for anything, do you? Since when, since 1990, when
managed care formally took over American Medicine (CastleConnolly.com),
have we heard a word from the AMA about the ALDF.com's DNA and
RNA
primers shell game, for
instance? The AMA is having a clueless cluck contest and the
reward is the top position at the NIH.
There are three essential reports
that the medcrime sleuth absolutely must obtain: the 1986 original
Steere standard development (adopted by the CDC in 1990, but then
replaced with the Steere/Dearborn method), the
1993
Dressler/Steere or the Dearborn IgG method, and the 1992 Steere in
Europe, Antibodies in Europe report.
1) Steere's "Antigens in Europe"
which of course, were not, but were "high passage" strain G39/40 plus
recombinant OspA and B from the prototypical American strain, B31:
ONLY AVAILABLE
HERE
:
J Infect Dis. 1994 Feb;169(2):313-8.
Links
Antibody responses to the
three genomic groups of Borrelia burgdorferi in European Lyme
borreliosis.
Dressler F,
Ackermann R,
Steere AC.
Division of
Rheumatology/Immunology, New England Medical Center, Tufts
University School of Medicine, Boston, Massachusetts 02111.
The antibody responses to
the three genomic groups of Borrelia burgdorferi (B. burgdorferi
sensu stricto, Borrelia garinii, and Borrelia afzelii) were
determined in 97 German patients with various manifestations of Lyme
borreliosis. The geometric mean antibody titers in each patient
group, determined by ELISA, were similar with each antigen
preparation. By Western blotting, however, patients with
meningopolyneuritis tended to respond to more spirochetal
polypeptides of B. garinii, the group 2 strain, whereas those with
arthritis recognized more antigens of B. afzelii, the group 3 strain
(P < .03), as did those with acrodermatitis. Only 1 patient each
with erythema migrans, arthritis, or acrodermatitis had weak
reactivity with outer surface protein A (OspA), and none responded
to OspB. It is concluded that differences among the three groups of
B. burgdorferi may result in variations in the antibody response in
European Lyme borreliosis. PMID: 8106763 [PubMed - indexed for
MEDLINE]
2) Only available free,
full-text, online,
here on ActionLyme, and in the FDA's
archives from the Jan 31, 2001 LYMErix Hearings:
:
J Infect Dis. 1993 Feb;167(2):392-400.
Links
Comment in:
J Infect Dis. 1993 Oct;168(4):1073.
Western blotting in the
serodiagnosis of Lyme disease.
Dressler F,
Whalen JA,
Reinhardt BN,
Steere AC.
Division of
Rheumatology/Immunology, Tufts University School of Medicine, New
England Medical Center, Boston, Massachusetts 02111.
There are currently no
accepted criteria for positive Western blots in Lyme disease. In a
retrospective analysis of 225 case and control subjects, the best
discriminatory ability of test criteria was obtained by requiring at
least 2 of the 8 most common IgM bands in early disease (18, 21, 28,
37, 41, 45, 58, and 93 kDa) and by requiring at least 5 of the 10
most frequent IgG bands after the first weeks of infection (18, 21,
28, 30, 39, 41, 45, 58, 66, and 93 kDa). When these definitions were
tested in a prospective study of all 237 patients seen in a
diagnostic Lyme disease clinic during a 1-year period and in 74
patients with erythema migrans or summer flu-like illnesses, the IgM
blot in early disease had a sensitivity of 32% and a specificity of
100%; the IgG blot after the first weeks of infection had a
sensitivity of 83% and a specificity of 95%. Among patients with
indeterminate IgG responses by ELISA, 6 of 9 patients with active
Lyme disease had positive blots compared with 2 of 34 patients with
other illnesses (P < .001). Thus, Western blotting can be used to
increase the specificity of serologic testing in Lyme disease. PMID:
8380611 [PubMed - indexed for MEDLINE]
3) Steere's First Observations,
1986:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=3531237
free full text link
:
J Clin Invest. 1986 Oct;78(4):934-9.
Links
Antigens of Borrelia
burgdorferi recognized during Lyme disease. Appearance of a new
immunoglobulin M response and expansion of the immunoglobulin G
response late in the illness.
Craft JE,
Fischer DK,
Shimamoto GT,
Steere AC.
Using immunoblots, we
identified proteins of Borrelia burgdorferi bound by IgM and IgG
antibodies during Lyme disease. In 12 patients with early disease
alone, both the IgM and IgG responses were restricted primarily to a
41-kD antigen. This limited response disappeared within several
months. In contrast, among six patients with prolonged illness, the
IgM response to the 41-kD protein sometimes persisted for months to
years, and late in the illness during arthritis, a new IgM response
sometimes developed to a 34-kD component of the organism. The IgG
response in these patients appeared in a characteristic sequential
pattern over months to years to as many as 11 spirochetal antigens.
The appearance of a new IgM response and the expansion of the IgG
response late in the illness, and the lack of such responses in
patients with early disease alone, suggest that B. burgdorferi
remains alive throughout the illness.
PMID: 3531237 [PubMed -
indexed for MEDLINE]
- - - -
Yet one more final incident
worth mentioning was the June, 1994 FDA Vaccine Meeting (a few
months before Dearborn) where State University of New York, Stony
Brook's (SUNY-SB)
Raymond Dattwyler recommended
performing serial or sequential Western Blots to look for Lyme
infection after vaccination. Since Dattwyler proposed using the
CDC's 1990 or 1986 Steere method, we can surmise that Dattwyler at
that time, was not aware of the problem of reading Western Blots in
LYMErix vaccinated people:

Dattwyler also said:

Which means that Lyme is not a knee-disease, but a very scary permanent
central nervous system infection- which the crooks all knew in 1989,
with the publication of the IDSociety's
REVIEWS OF INFECTIOUS DISEASES
October Supplement 6 on Lyme and Spirochetal Diseases in addition to
their own 20-plus treatment failure reports. Nowadays, nearly 20 years
later, IDSA says there is no such thing as chronic central nervous
system disease, despite their own published reports about the
persistence and especially, persistence in the brain past antibiotic
treatment (CHAPTER 11,
PERSISTENCE in the BRAIN).
Following the scientific fraud in the antibody testing, the Lyme
criminals proceeded to perform a shell game with the DNA and RNA
primers. CHAPTER 5,
PRIMERSHELLGAME
The next chapter deals specifically with what the FDA LYMErix Vaccine
Committee was told and informed of otherwise with the hard evidence:
that Steere's Dearborn method was a hoax and the REAL
outcome of LYMErix.
CHAPTER 4,
WHAT HAPPENED at DEARBORN (the whole 30
pages)
on the FDA's website |