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1988 Steere says Lyme is like a B cell leukemia
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Chapter 3
of Cryme
Disease-
What did Allen Steere do in Europe to falsify the diagnostic standard for Dearborn ??
There were 2 reports and not one- not just Desssler/Steere, that were involved in falsifying the antibody panel for the current, CDC diagnostic standard. The most significant one was not included in the CDC's Dearborn booklet - this one: STEERE_IN_EUROPE.htm
This was how Allen Steere left OspA and B out of the antibody panel to set up the RICO which included Imugen, Yale's L2 Diagnostics and Corixa as formal business "partners":
“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 [21]. The group 2 strain, FRG
[Federal Republic of Germany], was isolated from Ixodes ricinus near
Cologne [22]. 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 -"
-- illegal,
plasmid-dropping, antigen-and-antibody dropping, “high passage
strains” and OspA and B with no lipids attached (not likely to produce
antibodies), resulting in the new, 1994, Centers for Disease Control
(CDC), “case definition” of “Lyme Disease (8,
9)."
BACKGROUND, EXTRA INFO:
Allen Steere is the author of both CDC standards,
the 1990 standard and the 1994
Dearborn standard. For the fake standard - the current CDC Dearborn standard - Allen Steere
went to Europe alone in 1992 with bogus high-passage strains and recombinant OspA-B with no lipid
attached and therefore little
immunogenicity (means, "produces antibodies") to leave OspA and B
out of the standard. Osp A in
the diagnostic test, when the antigen is also the vaccine, invalidates
the test. One never tests for vaccine
efficacy with the same antigen as the vaccine.
Steere also falsely claimed that his pool of
Dressler/Steere neurologic
Lyme patients must have proteins
or cells in the CSF, when it was known that at least half of neurologic
Lyme victims do not have antibodies in their CSF or is an "aseptic
meningitis." So, all of Dressler/Steere was deliberate scientific
fraud. Steere had previously proposed that we perform sequential
Western Blots to diagnose Lyme.
FAIRY-ALERT!!
"The Non-Stalking of Allen Steere - the TRUE story of my interview
with David Grann of the NYT Magazine."
NINDS' MS Group
Leader, Roland Martin, went back home to Germany after not exactly
discovering that autoimmune T cells are the result of Lyme infection:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17060473
Studies of Lyme arthritis and chronic
neuroborreliosis suggest that spirochete-specific T cells cross-reacting
with self-antigens may be at least partly responsible for autoimmune
mechanisms possibly leading to chronic disease manifestations (8,
12,
25).
Cross-recognition of
self-antigens by B.
burgdorferi-specific CD4+ T cells has been
implicated in the pathogenesis of chronic manifestations of the
disease. Patients with treatment-resistant Lyme arthritis, but not
other forms of arthritis, expressing the rheumatoid
arthritis-associated MHC allele HLA-DRB1*0401
[STEERE's DEARBORN HAPLOTYPE]
generated clonal responses to both the immunodominant borrelial
outer surface protein A and the human leukocyte function-associated
antigen 1, which was tested as a candidate autoantigen (8).
In a patient with chronic NB expressing the MS-associated HLA-DRB1*1501
[MARTIN's "LYME RESULTS
IN MS" HAPLOTYPE] allele, we previously showed that a
single TCC preferentially recognizes different borrelial peptides
but also responds to human autoantigenic mimics (12).
Our data clearly indicate that degenerate antigen recognition that
includes pathogen-derived and self-epitopes is not restricted to
chronic and treatment-resistant manifestations of the disease.
Molecular mimicry alone is thus not sufficient to induce chronic
Lyme disease, and other genetic, environmental, and infectious
factors must be involved. Probably the best risk-conferring
candidate is the HLA haplotype, since both of the aforementioned
studies were performed with patients who expressed HLA class II
alleles associated with autoimmunity in the affected organ
compartment. However, studies investigating the association between
HLA haplotypes and chronic Lyme disease have up until now been
lacking, and a clear association between certain HLA alleles and
organ involvement other than the joints, e.g., the brain and/or
spinal cord, has not yet been documented.
Apparently, NINDS' Roland Martin did
not hear about the other, secret, Mark Klempner's, MS haplotype
(HLA-DQB1*0602):
http://www.youtube.com/watch?v=yPn_T9qy4C0&mode=related&search=
Or maybe he did, and that's the reason
he went home to Germany.
I point out that brains are somewhat
more significant than knees except to Yale staff, who have suggested
(literally) that
the brain
should be thrown out.
Comparison between the Western Blots of 1) people who have Steere's haplotypes
or a genetic link to having a hypersensitivity or allergy reaction to
Borrelial antigens (Lyme arthritis or acrodermatitis) and 2) normal people.
You have to actually look at this graphic, and then the whole
cryme will be clear to you.
http://alpha1.mpk.med.uni-muenchen.de/bak/nrz-borrelia/miq-lyme/Frame-MiQ-microbiological53.html
Introduction-
Ya wanna go to the USDOJ "reading room" (although
there not be evidence that the US Attorney's read anything other than Woman's Day, or
People, or Soap Opera Digest, due to the
influence of eunuch-fication of the DOJ by the likes of the fairy-ass,
girly-man-gossip and evil twerp, Karl Rove) and read about what is the
nature of a "false claim" against the United States, because that's what
"Lyme Disease" is, as will be shown in this chapter.
[Allen Steere's Strains Shenanigans in Europe to
create the bogus Lyme Disease diagnostic standard; Lyme is simply part
of the Relapsing Fever Group. "To know Relapsing Fever is to know
medicine."]
Title 18, United States Code, section 287--the false
claims statute--provides in part:
Whoever makes or presents to any person or
officer in the civil, military or naval service of the United
States, or to any department or agency thereof, any claim
upon or against the United States, or any department or agency
thereof, knowing such claim to be false, fictitious, or
fraudulent, shall be imprisoned not more than five years . .
. .
See Project, Tenth
Annual Survey of White Collar Crime, 32 Am. Crim. L. Rev. 137,
309-32 (1995)(discussing § 287). There is also a companion conspiracy
statute, 18 U.S.C. § 286.
In 1863 Congress enacted a false claims and
statements statute "in the wake of a spate of frauds upon the
government." United States v. Bramblett, 348 U.S. 503, 504
(1955). As originally enacted the statute penalized presentment "for
payment or approval" of false claims upon or against the Government. .
." (Bramblett, 348 U.S. at 504) as well as false statements made
"for the purpose of obtaining, or aiding in obtaining, the approval
or payment of such claim." On June 25, 1948, the statute was divided
into 18 U.S.C. § 287 and 18 U.S.C. § 1001, respectively. 62 Stat. 749.
The Section 287 statute is designed to "protect the
government against
those who
would cheat or mislead it in the administration of its programs" (United
States v. White, 27 F.3d 1531, 1535 (11th Cir. 1994)), and it has
been employed to combat fraudulent claims filed under numerous Federal
programs, including Medicare and Medicaid. White (Medicare claims
by a chiropractor); United States v. Hooshmand, 931 F.2d 725, 733
(11th Cir. 1991)(Medicare claims for tests); see also United States v. Abud-Sanchez, 973 F.2d 835, 836 (10th Cir.
1992)(Medicare and Medicaid claims); United States v. Siddiqi,
959 F.2d 1167, 1171-72 (2d Cir. 1992)(physician submitted Medicare
claims for a period when he was out of the country); United States v.
Nazon, 940 F.2d 255, 258, 261 (7th Cir. 1991)(Medicaid claims for
lab work not done); United States v. Beasley, 550 F.2d 261,
263-64 (5th Cir.), cert. denied, 434 U.S. 863 (1977)(claims for
costs of clinics never built).
=========================================
Recent Slam-o-Grams to the Steere cabal:
Chapter 3
of Cryme
Disease ;
Chapter 3, The Scientific Fraud Crime
Committed by Allen Steere in Europe
to facilitate the
bogus definition of "Lyme Disease" as an autoimmune bad knee (whoring for
BigPharma), needing no intravenous IV treatment (whoring for
Kaiser-Permanente, et al).
Previous Chp 2,
McSweegan and Goldwater
Subsequent Chp 4, What happed at the Jan 2001 LYMErix Hearing
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
perpetrators 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 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-related 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
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================
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."
This is Steere's first, 1986,
standard/observation of serology set
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 Allen 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 Vijay 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 or TOLERANT TO or CAN'T FIGHT OFF 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.
.
http://www.cdc.gov/ncidod/eid/vol3no1/baseman.htm mycoplasma associated
with arthritis and immune suppression outcomes.
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; CDC Officer Alan Barbour
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 OspA is/does:
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
compound 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 sort of 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
~OspA stuck on an HIV vaccine:
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=525594&blobtype=pdf
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?
http://www.cdc.gov/ncidod/eid/vol3no1/baseman.htm (Tully,
bioweaponeer on mycoplasmas and immune suppression.)
==========
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
incompetent MDs..
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 Diagnostics
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 already 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 of 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 Big
Tobacco
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.
Click to enlarge and then click again to enlarge further.
"Medications for
psychiatric disorders can be both the cause of delirium and
exacerbate or contribute to delirium from other causes."- The
American Psychiatric Association.
The above means Ely
Lilly certainly knew they were committing a crime (malpractice) by
recommending Zyprexa for dementia patients (or CNS depressants for the
CNS depressed as demonstrated by
scientifically valid relapsing and remitting brain
SPECT scans in response to the IV drug ceftriaxone), since
the American Psychiatric Association's own guidelines say central
nervous system depressants make the delirium or dementia worse.
Lyme is an organic delirium as shown by
diminished perfusion or blood flow
to the brain in brain SPECT scan imaging and
Brian Fallon's Relapsing Fever,
Relapsing brain disease 4.7 million dollar research study
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 testing 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…
Klempner: If you’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 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 medical crime 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
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