As many of you Lyme and CFIDS campaigners know, we
lobbied in Washington, DC, June 2017 for a hearing in the Senate regarding
the Lyme disease crimes that we want referred to the Justice Department for
prosecution. On this page,
please find all the information handed out and the presentation we gave the
Congressmen's assistants and legal staff/lawyers.
The presentation primarily had to do with all the previous attempts to have
the Lyme crymes prosecuted such as the 2006 Blumenthal lawsuit, the RICO
complaint filed in 2003, the fake vaccine going down (2002), and the more
recent attempt in 2014 by Senators Durbin, Blumenthal, et al, to force the
FDA to finally do their jobs and look at the falsified case definition for
Lyme we call "Dearborn."
To be perfectly clear: You can't have a vaccine
against a disease known to shed surface antigens that are fungal and known
to cause immunosuppression. Notice there are no vaccines against
Tuberculosis or other fungal diseases. To get around this scientific
dilemma, CDC staff who own patents for vector borne diseases (ALDF.com)
simply declared that only the hypersensitivity or HLA-linked allergy outcome
would be allowed to be a "case" of "Lyme disease" at a fake consensus
conference in Dearborn, Michigan, in 1994.
Contrary to the foolishness of the
non-profits of Lyme and ILADS.org, the CDC is not "endorsing IDSA's
guidelines." IDSA is endorsing CDC staff crime by endorsing CDC's
falsified case definition, from which the IDSA "guidelines" devolved.
It is the CDC, Yale, UConn, NYMC and New Jersey Medical and Dental, mainly,
behind this scam. The State of Connecticut participated in
Yale's/CDC's crimes, particularly as regards the falsified pediatric LYMErix
vaccine trial. The States of Connecticut, New York and New
Jersey will be on the hook for damages, along with Yale. Possibly
even Massachusetts. Consider:
"The New England Journal of Medicine" cant even get this straight.
No one should trust those 3 states (NY, CT, NJ), primarily, with any
more money for "Lyme research." All such statements and requests are
merely stalling tactics. We already know OspA alone caused the
post-sepsis outcome, which is mostly viral (reactivated EBV, CMV, etc.,
tolerance to all sorts of other TLR agonist types besides TLR2/1).
When they claim they need more money, what they want to do is stall
the federal Justice Department prosecution and subsequent class action
lawsuits against them by the other 46-47 states, just like Enron and Madoff.
Everyone should be thinking in
terms of damages, every state government, that is. This is
going to be way bigger than Enron. Connecticut will have
to have a Going Out of Business sale, where all the State's parks
and attractions - along with all of Yale's properties like the
Beinicke Rare Book museum and the Peabody - will have to be sold off
to private entities. Taxes will go through the roof.
... CT in particular because of the fake pediatric LYMErix trial.
This is technically "assault (see the charge sheets on
Stuff you cant make up.
See Allen Steere describe how you can
diagnose Lyme clinically in 1988 (and also says Lyme is like a B cell
This sets up a category of people to sue in a class
action. Importantly, all the slander and libel by the ALDF.com, the
CDC, Yale staff and others, assure this is a RICO charge, which means people
can go after these Lyme criminals for their personal property.
So, not only will they get jail time, but if they ever get out of jail, they
will not have a cent to their names.
Free 200+ page scientific book on the various fraud crimes committed by CDC
and Yale employees. Includes information on how the pediatric vaccines
by giving the children the very brain damage these viruses these vaccines were intended to prevent
(particularly the MMR), according to
IDSA, NYU's Stanley Plotkin, and Johns Hopkins' Paul
Also included are details about how the University of Connecticut
"assaulted" Czech children with a non-vaccine (LYMErix) that they knew
would do those children no good. There was NO chance that
vaccine would have prevented Lyme, not only because OspA is pam3cys, a
triacyl-, fungal lipoprotein which causes immunosuppression, but because
there is none of the USA Borrelia strain B31 OspA in Europe.
We show that Allen Steere published in 1988 that Lyme caused a B cell
mutation (lymphoma-like) that rendered them incompetent and that that's
actually the disease IDSA, the CDC, Yale and UConn deny exists and wrote out
of the "case definition" because that immunosuppression disease was also
caused by LYMErix and they knew this in 1993 - before the Dearborn
stunt (where the CDC falsified the testing for Lyme, 1994).
We show NIAID's "Director" Anthony Fauci even has a patented treatment for
fungal immunosuppression diseases, yet he claimed on national TV (Lou Dobbs)
that "We have a scientifically validated Lyme vaccine, but it's not well
used" - 1.5 years after it was ordered off the market by the FDA via
ultimatum, in February, 2002.
We show that Simon Wessely, et al, while finding that Gulf War Illness was
associated with the vaccines, later claimed the Veterans were just cowardly
airy-fairies and are using "brain magic" (like telekinesis) to fake their
scientifically valid illness signs. (Yes. That is what
"somatoform" technically means.)
The Criminal Charges Sheets - this is
actually a book; you can also find it here:
1. ALDF-CDC "Enterprise" (read
"RICO") Conspires to Defraud USA in
Dearborn-Vaccine Scam; see how next, in the subsequent charge sheet
on patents, the very people who falsified the testing are the ones
who own the patents for the bogus vaccines and test kit products:
Updated -- 2. Lyme Disease
Patents owned by the Dearborn scammers, CDC
officers, Yale in association with Corixa, Mayo Clinic and Imugen.
Leaving OspA and B out of the Dearborn standard was intended to
facilitate a monopoly on post-LYMErix approval on blood testing for
all vectior-borne disease:
3. Lyme Disease
Biomarkers, as compared to scientifically
invalid psychiatric check lists. These biomarkers were identified by
the very people who later said Lyme was not even a disease, and who
are the same people who own the vaccine patents and falsified the
testing at Dearborn:
4. The Primers (DNA, RNA) Shell Game; the very people who own all the
patents and falsified the testing for Lyme in order to falsify the
outcomes of those bogus products, use the wrong DNA to not-find Lyme
or other spirochetes in humans, while using the correct DNA to
patent borrelia-specific DNA; no biofilms.
5.) Occam's Razor
quacks like a duck, it must be Epstein-Barr/post-sepsis syndrome (as the
REAL "Great Imitator"):
6. The Common Mechanisms of Fungal-Viral Damage in CFIDS,
Vaccines-Autism, and "Chronic Lyme"/ New Great Imitator, per the CDC,
NIH and IDSA; This paper reveals the CDC's own data on what Lyme and
CFIDS are, and how immunosuppression-via-fungal contamination also
explains the failed childhood vaccines, giving children the very
viruses the vaccines are intended to prevent (with resultant
7. Simon Wessely and the abuse of Gulf War veterans, Justina
Pelletier and 21st century witch trials; with scientifically valid
evidence for real illness, a vast majority of post-sepsis and
vaccine injured are slandered and libeled with invalid psychiatric
8. The State of Connecticut and Yale
Assaulted Czech Children
with a known fake vaccine (OspA or LYMErix) just to see how serious
would be the adverse events:
All in one pdf,
161219 - Lyme Crooks Wormser and Steere - and even the "CDC
officer" criminal Paul Mead -
admit Late Lyme and LYMErix diseases are immunosuppression outcomes.
'Say the "TLR2/1 agonism" (immunosuppression) is probably the "more
important" driver of the disease outcome.
Abstract (published Dec 15, 2016):
Mario Philipp has long been the guy who says Borrelia and OspA causes
immunosuppression, so look at all of his reports:
Ref 79, above, (Mario Philipp):
anti-inflammatory response to Borrelia burgdorferi, the agent of Lyme
disease: a possible role for suppressors of cytokine signaling 1 and 3.
The crooks report above, saying the more serious disease outcome may be
due to its fungal-ish agonism of TLR2/1, is a little bit of a screwed up way
of saying it, but they, the CDC and the Lyme criminals, finally admitted
their whole Lyme story was a lie.
Notice that ILADS has NEVER said what
Late Chronic Lyme was. They lost
their opportunity to be the ones to bring the truth forward as I had
Steere writes about deformed B cells, later
shown to be an outcome of LYMErix, too:
Remember, OspA is Pam3Cys...
Ann N Y Acad Sci. 1988;539:65-79.
Clinical pathologic correlations of Lyme disease by stage.
Duray PH1, Steere AC.
”....Soon after the onset of ECM, the organism disseminates hematogenously,
with what appears to be random dispersal throughout the body. The immune
response involves virtually all of the organs and structures of the
reticuloendothelial system including the bone marrow, and clinical pain and
discomfort seems to correlate with hyperplasia of lymph nodes and spleen and
bone marrow. Diffuse visceral involvement in this acute stage mimics
infectious mononucleosis or disseminated viral syndromes. These include
conjuctivitis, pharyngitis, pneumonitis with dry cough and mild pleuritic
pain, hepato-splenic tenderness, lymph node swelling of the neck and groin,
and orchitis. There is lymphoid hyperplasia of the lymph nodes and spleen
consisting of prominent germinal centers and numerous perifollicular
lymphocytes, with proliferation of plasma cell precursors and mature plasma
plasma cell precursors are large, appear tumor-like, and can resemble Reed-Sternberg
cells. Others look like typical immunoblasts (FIG. 1). In one example,
cervical lymph nodes show cell degeneration with karyorrhexis and nuclear
debris of lymphoid elements. This patient had repeated high fevers and
marked discomfort of neck nodes. Large atypical immunoblasts can also be
seen in the spleen and bone marrow. The red pulp of the spleen is congested,
not unlike that seen in infectious mononucleosis. Spirochetes can be
demonstrated in the lymph nodes, spleen and bone marrow and liver. There
is a transient hepatitis reflected by elevated liver cell enzymes such as
SGOT, SGPT, and GGT. The liver can vary from a mild lymphocytic portal
triaditis all the way to liver cell derangement that simulates acute viral
hepatitis. The cells at this stage appear swollen with clear cytoplasm and
microvesicles of fat (FIG. 2). Numerous leukocytes are seen in the
sinusoids, and there is Kupffer cell hyperplasia..."
J Immunol. 2005 Jun 1;174(11):6639-47.
Role of TLR in B cell development: signaling through TLR4 promotes B cell
maturation and is inhibited by TLR2.
Hayashi EA1, Akira
AbstractThe role of TLR4 in mature B cell activation is well
characterized. However, little is known about TLR4 role in B cell
development. Here, we analyzed the effects of TLR4 and TLR2 agonists
on B cell development using an in vitro model of B cell maturation. Highly
purified B220(+)IgM(-) B cell precursors from normal C57BL/6 mouse were
cultured for 72 h, and B cell maturation in the presence of the TLR agonists
was evaluated by expression of IgM, IgD, CD23, and AA4. The addition of LPS
or lipid A resulted in a marked increase in the percentage of
CD23(+) B cells, while Pam3Cys had no effect alone, but inhibited the
increase of CD23(+) B cell population induced by lipid A or LPS. The
TLR4-induced expression of CD23 is not accompanied by full activation of the
lymphocyte, as suggested by the absence of activation Ag CD69. Experiments
with TLR2-knockout mice confirmed that the inhibitory effects
of Pam3Cys depend on the expression of TLR2. We
studied the effects of TLR-agonists on early steps of B cell differentiation
by analyzing IL-7 responsiveness and phenotype of early B cell precursors:
we found that both lipid A and Pam3Cys impaired IL-7-dependent
proliferation; however, while lipid A up-regulates B220 surface marker,
consistent with a more mature phenotype of the IgM(-) precursors, Pam3Cys keeps
the precursors on a more immature stage. Taken
together, our results suggest that TLR4 signaling favors B lymphocyte
maturation, whereas TLR2 arrests/retards
that process, ascribing new roles for TLRs in B cell physiology.