The fake Lyme, Dearborn,Vaccines Scam;
What really happened.
CrymeTrainer; Outline for Indictments
Non-HLA-linked diseases =
Mold-Related illnesses (like LYMErix-Disease, Lyme, CFIDS/FM, and Gulf War
Fauci's Patent for MS Tmt is for
Follow the Scam in the order it
Older data on
the incurability of Relapsing Fever
McSweegan trashes Navy for $$$ for ALDF.com
1988, Dattwyler &
about immune-suppressing, seronegative Lyme
1990, CDC: "Diagnose Lyme as if it was Relapsing Fever."
Allen Steere "NeuroLyme won't
test positive," 1990.
CDC officer Allen Steere falsifies testing in Europe
1992, CDC patents with
SmithKline show 2 kinds of Lyme
Barbour and Fish slam Neurologic Lyme victims.
Compare the 2 kinds of Lyme in the RICO complaint
1994, FDA LYMErix
Dearborn Booklet .pdf
invitation to participate in Dearborn .pdf
Dearborn, Who Said What?
Igenex, Harris, Dearborn .pdf
Evidence Lyme criminals knew
LYMErix produced the same "multisystem disease" as "Chronic Lyme"
LYMErix Damage Coverup (short)
120302 NIH Treatments
1998, CIA Oilmen & Israelis plan to overthrow
Saddam for the oil.
ActionLyme/Kathleen Dickson predicts all of Bushie's outcomes in Oct 2000
predicts Bush will have us worshipping his bombs (Shock and Awe"), in Oct 2000
during the Gore Debates
CHAPTER 5, the RNA and RNA
Primers Shell Game
See also, CENTRAL_LYME_RICO_PATENTS.htm for how Alan Barbour and Gary Wormser tricked Ed Masters out of Lone Stari, a cow Relapsing Fever organism (using the wrong DNA. The wrong DNA is the OspA gene, because flagelin defines the species and there are plenty of RF spirochetes that do not have the synthetic Pam3Cys in it.
PART I; We propose that there are four
reports which show that these Lyme 180s knew they could not assess (unreadable results)
whether or not LYMErix or OspA vaccinations prevented "Lyme Disease" with
Western Blotting, and that therefore they simply lied to the FDA, to the
public, and to the journals that published their ImmuLyme and LYMErix
LYMERIX RESULTS (76% "safe and effective"):
IMMULYME RESULTS (92% "safe and effective"):
(New England Journal, again. They never looked at the standard to
assess whether or not this was a scientifically valid report, as was the
case with the Klempner - no DNA
primers listed in the method - report yikes these Mass Medical
Society people are scary stupid and just plain dangerous.)
Here are those 4 reports:
1) SCHOEN and PERSING, with JOHN ANDERSON,1996:
2) SCHOEN AND PERSING IN THEIR 1996 RICO METHOD PATENT:
The Dave Persing, Mayo Clinic FRAUD Patent-6,045,804
3) PERSING WITH SIGAL EXPLAINING THAT THE WESTERN BLOTS WERE
ROBERT SCHOEN in the 1998
instructing MDs to blow off LYMErix systemically injured people.
We can't imagine what their explanation
will be when asked under oath what was the meaning of all of this.
They could have used a recombinant, specific, FDA-valid flagellin method
which they had already validated and to some extent worked up
(Magnarelli and Fikrig in 1992), or they could have used the correct DNA
and RNA primers to assess spinal fluid and blood products from persons
who claimed to feel ill subsequent to LYMErix vaccination, particularly
those people who had "already had Lyme before," since those were the
people who bubbled to the surface in Southeastern Corrupticut Lyme
Support Groupland, as mentioned in the previous chapter (and to the FDA
PART II - THE PRIMERS SHELL GAME -- The
180s have never used the
correct gene primers to detect Borrelia DNA or RNA in patient treatment or
vaccine outcomes with the exceptions of then Wormser tick-bite treatment efficacy report,
below, and the Steere-Nocton knee-persistence report seen in Chapter 11,
where they both proved with these methods that treatment fails.
Yet, they all know which are the correct primers to use.
should be using species specific RNA intragenic spacer genes, such as 16S or
23S RNA, since there are more copies of them, than, say, the flagellin gene.
The 180s always use the variable DNA encoded on the plasmids (like OspA) in
order to find "NO LYME," when appropriate to their spin protocol. This
changes, since these are the sources of the varying proteins seen on the
surface of the spirochete, which make them relapsing fever organisms that
execute "antigenic variation." Antigenic Variation is the mechanism that causes the relapse or
growth of a new population of organism that don't make the surface proteins
against which any vaccine or antibodies would do any good. It's
The following reports show that these criminals know which are the
correct primers to have been using all along to detect Borreliosis either
after treatment or for vaccines assessments:
1) Yale (Schoen and Persing are the authors of this report)
and all the Lyme 180s know how to
detect any kind of borreliosis and they have known since the early 1990s: Use
Borreliae-specific RNA or DNA primers encoded on the chromosome (and don't use
any varying plasmid DNA). This happens to be the same RICO report that
went with the RICO patent.
report was reported after the RICO patent was applied for, by the way,
yet they are basically the same report:.
In this report (above and linked in full
text below) - and this is the RICO report associated with the RICO patent -
Yale demonstrates that they know how to diagnose any kind of Lyme or
borreliosis anywhere in the USA by using Borrelia burgdorferi-specific
23S RNA primers. These primers have never been used to assess
treatment (antibiotics) outcomes in humans (except Gary Wormser on tick
bite, and Steere-Nocton with knees, as mentioned).
Yale demonstrates that they know how to diagnose any kind of Lyme or
borreliosis anywhere in the USA by using 23S RNA primers.
2) The 1992
report where he uses the correct RNA primers to assess erythema migrans rashes
(this is the only report where they use the correct primers to assess any kind
of treatment outcome, and in this case, this is where they found that 2/9
people who were treated with antibiotics for tick bite still had spirochetal
RNA in their skin samples at follow up skin puncture biopsy):
The associated full text .pdf file (use this link for your website):
shows exactly what Gary Wormser did and why:
3) Wormser in 1999 using the correct primers to look for all sorts of borrelia-
primers not used to assess any recent human treatment outcomes.
Genetic diversity of Borrelia
burgdorferi in lyme disease patients as determined by culture versus direct
PCR with clinical specimens.
Biochemistry and Molecular Biology, New York Medical College, Valhalla, New
York 10595, USA.
Two hundred seventeen
isolates of Borrelia burgdorferi originally cultured from skin biopsy samples
or blood of early Lyme disease patients were genetically characterized by PCR-restriction
fragment length polymorphism (RFLP) typing of the 16S-23S ribosomal DNA
intergenic spacer. Three major RFLP types were observed. Of the cultured
isolates, 63 of 217 (29.0%) were type 1, 85 of 217 (39.2%) were type 2, and 58
of 217 (26.7%) were type 3; mixtures of two RFLP types were obtained in 6.0%
(13 of 217) of the cultures. Comparison of typing of B. burgdorferi performed
directly on 51 patient skin specimens with typing of cultures originally
isolated from the same tissue revealed that a much larger proportion of direct
tissue samples had mixtures of RFLP types (43.1% by direct typing versus 5.9%
by culture [P < 0.001). In addition, identical RFLP types were observed in
only 35.5% (11 of 31) of the paired samples. RFLP type 3 organisms were
recovered from blood at a significantly lower rate than were either type 1 or
type 2 strains. These studies demonstrate that the genetic diversity of B.
burgdorferi patient isolates as determined by cultivation differs from that
assessed by PCR performed directly on patient tissue.
PMID: 9986813 [PubMed - indexed
4) Yale's Durland
Fish, in 2001, using the correct primers whenever he wants to find spirochetes in
ticks. These primers have never been used to assess human treatment
outcomes (except for Wormser on tick bite in 1992 and Nocton-Steere on knees
Visualization of Borrelia
burgdorferi sensu lato by fluorescence in situ hybridization (FISH)
on whole-body sections of Ixodes ricinus ticks and gerbil skin biopsies
Annette Moter1, Olaf Kahl2,
Gerd Alberti3 and Ulf B. Göbel1
Institut für Mikrobiologie und Hygiene, Universitätsklinikum Charité,
Humboldt-Universität zu Berlin, Dorotheenstraße 96, D-10117 Berlin, Germany1
Institut für Biologie, Angewandte Zoologie/Ökologie der Tiere, Freie
Universität Berlin, Haderslebener Straße 9, D-12163 Berlin, Germany2
Zoologisches Institut und Museum, Ernst-Moritz-Arndt-Universität, J.-S.-Bachstraße
11/12, D-17487 Greifswald, Germany3
Author for correspondence: Bettina Hammer.
Tel: +49 30 450 524074. Fax: +49 30 450 524902. e-mail: firstname.lastname@example.org
5) Dattwyler and Luft using the correct DNA primers- ones encoded on the
chromosome and not on any varying DNA plasmids (non-varying, species-specific, heat shock protein
6) 1992, Yves
Lobet of SmithKline, Belgium, using the correct (non-varying DNA) primers to
assess for spirochetes in ticks. Never used in human treatment vaccines outcomes:
Evaluation of genetic divergence
among Borrelia burgdorferi isolates by use of OspA, fla, HSP60, and HSP70
German Cancer Research
In order to assess the
genetic variation of immunologically relevant structures among isolates of
the Lyme disease spirochete, Borrelia burgdorferi, three chromosomal genes
encoding flagellin (fla) and the heat shock proteins HSP60 and HSP70, as
well as the plasmid gene encoding outer surface protein A (OspA), from 55
different European and North American strains obtained from ticks and mammal
hosts have been investigated by restriction fragment length polymorphisms (RFLPs).
RFLPs of fla and the HSP60 and HSP70 genes revealed two distinct banding
patterns (A and B) for each of the three genes and allowed the definition of
four genomic groups [AAA, BBB, BBA, and B(A/B)A] for the three chromosomal
genes. On the other hand, RFLPs of the OspA gene revealed six distinct
banding patterns (types I to VI) making up six independent genomic groups
for the plasmid-encoded gene. Furthermore, we have sequenced the chromosomal
HSP60 gene from B. burgdorferi ZS7 and the plasmid-encoded OspA gene from
two strains, ZQ1 and 19857. Alignment of the deduced HSP60 amino acid
sequence from B. burgdorferi ZS7 (genomic group AAA) to a previously
published HSP60 sequence derived from strain ACA-1, which according to the
proposed classification is in a different genomic group (BBA), revealed a
sequence identity of > 99%. Similar alignments of the OspA sequence of
strain ZQ1 to those of other isolates that were published previously
revealed sequence identities of between 70 and 94% among strains of distinct
OspA genomic groups. These data indicate the existence of a restricted
number of species-specific subgroups and clearly show that genotypic
variation is much more pronounced for the OspA gene than for fla and the
HSP60 and HSP70 genes. A phylogenetic tree constructed on the basis of
distance matrix analyses of 12 OspA sequences supports the proposed
classification of genomic groups of B. burgdorferi.
PMID: 1356932 [PubMed -
indexed for MEDLINE]
They wanted to make "Lyme Disease" all about
OspA and they even pulled the wool over the eyes of Edwin Masters and basically
stole his "Southern Lyme Disease" or "Master's Disease" from him and renamed it
There is no test available for
but the way, as if that would surprise you. Barbour owns barbouri
and no one is allowed to have it. Sound familiar?
To this day we are not sure Edwin Masters
understands the Shell Game. All MDs should take a close look at the NIH
NLM Taxonomy database and look at the references the taxonomizers use for
determination of relatedness between these Borreliae spirochetes:
Click on Borrelia, the main heading name:
Comments and References:
- Skerman VBD et al. (1980)
- Skerman, V.B.D., McGowan, V., and Sneath, P.H.A. (editors). "Approved
lists of bacterial names." Int. J. Syst. Bacteriol. (1980) 30:225-420.
[No PubMed record available.]
M et al. (1996b)
- Fukunaga, M., Okada, K., Nakao, M., Konishi, T., and Sato, Y.
"Phylogenetic analysis of Borrelia species based on flagellin gene
sequences and its application for molecular typing of Lyme disease
borreliae." Int. J. Syst. Bacteriol. (1996) 46:898-905.
NM et al. (1996)
- Ras, N.M., Lascola, B., Postic, D., Cutler, S.J., Rodhain, F., Baranton,
G., Raoult, D. "Phylogenesis of relapsing fever Borrelia spp." Int. J.
Syst. Bacteriol. (1996) 46:859-865.
They are organized by differences in flagellin.
Then, the point is to look for all Borreliae in a sick person by using all
recombinant specific flagellins or species-specific RNA spacer genes from ALL
American Relapsing Fever species in America, and likewise for Europe and
everywhere else - because those genes don't undergo antigen variation.
This was all already determined in the early 1990s.
The 180s never mention this, and worse,
Mark Klempner never
reported which DNA primers he used in his fake long term treatment study.
Worse still, the 180s all know these Borreliae are not "clonal," if all the
plasmids undergo antigenic variation, that all the spirochetes "host adapt," and
that one can "select for mutants" (are all Relapsing Fever organisms) simply by
vaccinating or exposing the bugs to antibodies.
Here are those proofs:
1992, CDC "officer" Alan Barbour, discussing "selecting mutants:"
1995, Yale's Erol Fikrig and Richard Flavell, on how LYMErix vaccination
failed but would also "select mutants":
2001, CDC Officer Alan Barbour on "Antigenic
Variation in Vector-Borne Pathogens:"
We like this report very much because it
exposes the fact that due to antigenic variation, not only can there never
be vaccine for them, the Steere diagnostic method is bogus. How can
they say that "due to antigenic variations vaccines would do no good,"
but also claim that we have to have 5 of 10 of the Dressler/Steere bands in
order to have a case of Lyme Disease? If you can't make a vaccine out
of Relapsing Fever relapsing antigens, then it is also true that all we can
do is test for these Relapsing FEver infections with antigens that DON'T
CHANGE, like flagellin.
1990, Andrew Pachner on Borrelial plasmids
in the brain:
"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. "
Recall that the
180s claim that there
is no such thing as Lyme as a brain disease. Mark Klempner
published in 2003 that there was no such thing as brain signs in
"post-treatment chronic Lyme disease."
To which we respond, "That's fine,
Mark, because there is no such entity as 'Lyme Disease,' or Steere's
'receiver operating characteristics,' or an autoimmune, hypersensitivity
knee disease that requires the meningitis drug ceftriaxone (as Steere
proposes and practices), or even a vaccine for this non-disease.
We assert that it was your 'neuroborreliosis' patients who had the
matrix-metalloproteinases or nerve and brain degrading enzymes in their
spinal fluid, and as you mentioned in that same report, the destruction
of glial cells (energy providing cells for the brain). We agree,
Mark. There are no disease signs for Steere's imaginary disease.
Why should there be?"
Cognitive function in
post-treatment Lyme disease: do additional antibiotics help?
Connecticut School of Medicine, Farmington, USA. email@example.com
BACKGROUND: It is
controversial whether additional antibiotic treatment will improve cognitive
function in patients with post-treatment chronic Lyme disease (PTCLD).
OBJECTIVE: To determine whether antibiotic therapy improves cognitive
function in two randomized double-blind placebo-controlled studies of
patients with PTCLD. METHODS: A total of 129 patients with a
physician-documented history of Lyme disease from three study sites in the
northeast United States were studied. Seventy-eight were seropositive for
IgG antibodies against Borrelia burgdorferi, and 51 were seronegative.
Patients in each group were randomly assigned to receive IV ceftriaxone 2 g
daily for 30 days followed by oral doxycycline 200 mg daily for 60 days or
matching IV and oral placebos. Assessments were made at 90 and 180 days
after treatment. Symptom severity was measured from the cognitive
functioning, pain, and role functioning scales of the Medical Outcomes Study
(MOS). Memory, attention, and executive functioning were assessed using
objective tests. Mood was assessed using the Beck Depression Inventory and
Minnesota Multiphasic Personality Inventory. RESULTS: There were no
significant baseline differences between seropositive and seronegative
groups. Both groups reported a high frequency of MOS symptoms, depression,
and somatic complaints but had normal baseline neuropsychological test
scores. The combined groups showed significant decreases in MOS symptoms,
higher objective test scores, and improved mood between baseline and 90
days. However, there were no significant differences between those receiving
antibiotics and placebo. CONCLUSION: Patients with post-treatment chronic
Lyme disease who have symptoms but show no evidence of persisting Borrelia
infection do not show objective evidence of cognitive impairment. Additional
antibiotic therapy was not more beneficial than administering placebo.
We have no idea who these
patients are, who still test positive to the imaginary Steere/Dearborn
method after treatment. If they are knee patients, we don't expect
them to have cognitive signs, as was asserted by Vijay Sikand (East Lyme,
CT) at the 1998 FDA Vaccine Meeting. Sikand said these seropositive
patients were "immune competent," implying they made enough antibodies to
manage the disease and prevent its spread (into neurologic, protected
at Columbia University found 0.5% of all of the patients that he
screened for his Chronic Neurologic Lyme study were still Steere/Dearborn
positive after previous ceftriaxone, intravenous, meningitis treatment.
Mark Klempner in 2001,
found only 78 Steere/Dearborn positive patients out of 1800 (4% accuracy for
the Steere/Dearborn method), but a 2/3 of his victims had not had previous
intravenous ceftriaxone treatment, which was supposedly the stipulation for his long
term re-treatment "study." In the Klempner study, these patients were
offered the standard of care - 30 days of intravenous ceftriaxone for this
permanent central nervous system disease - Relapsing Fever. At that
time, 1997, 30 days of ceftriaxone was the standard of care (arbitrarily
devised), so we have no idea what was the point of proposing a 4.7 million
dollar study to assess the standard of care, since we knew it was inadequate
or not enough treatment, leading to such studies of more or longer
treatment. The Klempner study was yet another hoax.
We say: It is not up
to the patients to determine which drugs should be used for central nervous
system bacterial infection. That was why the Infectious Diseases
Society of America was using intravenous ceftriaxone even at the time of the
1989 IDSA Reviews, where Dattwyler, Luft, Sigal and Steere all said
"treatment fails in more than half the cases," and "we don't know the
ceftriaxone treatment endpoint."
So, now it's a non-disease.
In the 8 months from
September 2007 to May 2008, over billion dollars worth of grants were given
out and this clique got none of it. It's clear that some people in
control of the money - the NIH, the Howard Hughes Foundation, and even a new Rockefeller Foundation neurosciences venture cap group - have
had enough of this nonsense. The Czech Republic basically finished
them off by saying:
Biological aspects of Lyme
disease spirochetes: Unique bacteria of the Borrelia burgdorferi species
Immunology, Faculty of Medicine, Hnevotinska 3, Palacky University,
Olomouc, 775 15, Czech Republic. firstname.lastname@example.org.
burgdorferi sensu lato is a group of at least twelve closely related
species some of which are responsible for Lyme disease, the most
frequent zoonosis in Europe and the USA. Many of the biological features
of Borrelia are unique in prokaryotes and very interesting not only from
the medical viewpoint but also from the view of molecular biology.
Methods: Relevant recent articles were searched using PubMed and Google
search tools. Results and Conclusion: This is a review of the
biological, genetic and physiological features of the spirochete species
group, Borrelia burgdorferi sensu lato. In spite of a lot of recent
articles focused on B. burgdorferi sensu lato, many features of Borrelia
biology remain obscure. It is one of the main reasons for persisting
problems with prevention, diagnosis and therapy of Lyme disease. The
aim of the review is to summarize ongoing current knowledge into a lucid
and comprehensible form.
Lyme research is incomprehensible and stupid. Back to the drawing
board. And where we'll start is the taxonomy database. We're
talking about Borreliae or Relapsing Fever and no more of this 'LYME
.CHAPTER 6, RICO PATENTS
(tell a different story from the public one)
Saint Michael the Archangel,
defend us in battle.
Be our protection against the wickedness and snares of the devil.
May God rebuke him, we humbly pray;
and do Thou, O Prince of the Heavenly Host -
by the Divine Power of God -
cast into hell, satan and all the evil spirits,
who roam throughout the world seeking the ruin of souls.