ONLY IN the United States of
you see the likes of the
Edward McSweegan and
Durland Fish, not knowing
spirochetes were their own
phylum (are not regular "bacteria"), are relapsing fever
organisms, that the
nature of the relapse
was antigenic variation (vaccines would do no good), and that the
McSweegan-Fish gang never even asked what
(fungal, TLR2/1 agonist, causes permanent immunosuppression, never could have been a
vaccine). The CDC deployed the stupid
and cowardly Allen Steere who
Rheumatology to avoid VietNam
(there are no old ladies who need aspirin among deployed US combat forces),
probably because he was known to be too stupid to ask any questions about
ticks or spirochetes.
What is the simplest way to explain that the
ALDF dot com / Yale / CDC Lyme cabal
threw out of the Dearborn, "2-tiered" "case definition" the
very same disabling, chronic neurologic, "New
Great Imitator" disease that was caused by the
fungal toxin, Pam3Cys or OspA?
They knew OspA vaccination causes
neurologic, immunosuppression disease before the Oct 1994
Dearborn, Michigan fake consensus conference ever took place (chronology
In order for it to be prosecuted as
criminal case you have to show they knew ahead of time that there was
this problem with their "vaccine" choice and that they CHANGED the
testing definition after that, such as to leave out the chronic
neurologic Lyme definition - the very disease caused by the fungal OspA vaccines.
The current case definition only detects the 15% of cases, only the late-,
HLA-linked- arthritis cases, no early cases, and then
these CDC (vaccine patent holding) criminals say
this late manifestation needs no treatment. The truth is that chronic
neurologic disease is mainly caused by immunosuppression, reactivated
Epstein-Barr and cross tolerance to other infections, or, technically, is
post-sepsis syndrome or a kind of a B cell AIDS (see the
In this criminal case, you have to show to the
DOJ that they
diagnostic criteria from an older one that allowed more people to be
1990 CDC version).
If the DOJ does not respond, clearly this was a bioweapon accident of some
The circumstantial scientific,
epidemiological evidence from
Plum Island as the original outbreak area says so. (Do
the Russians know by now? They knew in 2006. The Chinese, a year
later. Site stats.)
The US press cant handle it, and no
one has ever written about it in any book.
Whoever does not know
what LYMErix-disease is, does not know what Lyme
disease is. This includes ILADS.org and all of the Lyme non-profits.
One has to know what the antigen is, in order to know what it does.
This is basic science.
And it turns out that Lyme and Syphilis as "Great Imitators" are
really Great Detonators of latent viruses and general immunosuppression -
also known as post-sepsis syndrome. It turns out that Pam3Cys (OspA),
a triacyl lipopeptide, is a functional mimic of E. coli's Lipid A, a serious
fungal (TLR2/1-agonist) ENDOTOXIN. Think about that. The CDC
wanted to inject everyone with several blobs of bathroom scum. And
that's what happens with a tick bite, too.
Cadavid on Septic Spirochetes:
"Finally, spirochetal lipoproteins have more prominent
pro-inflammatory effects compared to other bacterial lipoproteins and
synthetic lipopeptides (28)."
says OspA alone is responsible for this sepsis-then-immunosuppression
on how OspA vaccination caused the same disease as chronic Lyme:
Neuropathy and cognitive impairment following vaccination with the OspA protein
of Borrelia burgdorferi.
“Neurological syndromes that follow vaccination or infection are often
attributed to autoimmune mechanisms. We report six patients who
developed neuropathy or cognitive impairment, within several days to 2
months, following vaccination with the OspA antigen of Borrelia
burgdorferi. Two of the patients developed cognitive impairment, one
chronic inflammatory demyelinating polyneuropathy (CIDP), one multifocal
motor neuropathy, one both cognitive impairment and CIDP, and one
cognitive impairment and sensory axonal neuropathy. The patients with
cognitive impairment had T2 hyperintense white matter lesions on
magnetic resonance imaging. The similarity between the neurological
sequelae observed in the OspA-vaccinated patients and those with chronic
Lyme disease suggests a possible role for immune mechanisms in some of
the manifestations of chronic Lyme disease that are resistant to
antibiotic treatment.” http://www.ncbi.nlm.nih.gov/pubmed/15363064
Gary Wormser on OspA causing immunosuppression (which means it was the
opposite of a "vaccine"):
Modulation of lymphocyte proliferative responses by a canine Lyme
disease vaccine of recombinant outer surface protein A (OspA).
After exposure to either the unaltered vaccine preparation or OspA prepared
in saline, normal lymphocyte responses to the mitogens concanavalin A,
phytohemagglutinin-M or pokeweed mitogen, or the antigen BCG were
consistently reduced. Whole cell extracts of B. burgdorferi also
modulated immune responses but required a much greater quantity of
protein than needed for theOspA preparation.
The magnitude of modulation was directly dependent on the quantity of OspA. OspA interferes
with the response of lymphocytes to proliferative stimuli including a
blocking of cell cycle phase progression. Future studies designed to
delete the particular region or component of theOspA molecule
responsible for this effect may lead to improved vaccine preparations.”
Donald H. Marks - an OspA vaccine trial administrator -
on how LYMErix caused the same disease as chronic Lyme:
Neurological complications of vaccination with outer surface protein A (OspA).
wide range of neurological complications have been reported via the
medical literature and the VAERS system after vaccination with
recombinant outer surface protein A (OspA)
of Borrelia. To explore this issue, 24 patients reporting neurological
adverse events (AE) after vaccination with Lymerix, out of a group of 94
patients reporting adverse events after Lymerix vaccination, were
examined for causation. Five reports of cerebral ischemia, two transient
Ischemic attacks, five demyelinating events, two optic neuritis, two
reports of transverse myelitis, and one non-specific demyelinating
condition are evaluated in this paper. Caution is raised on not actively
looking for neurologic AE, and for not considering causation when the
incidence rate is too low to raise a calculable difference to natural
could be that a person has an HLA-linked outcome to one of the secondary
infections like Epstein-Barr or HHV-6, reactivated by the AIDS-like Lyme
and LYMErix. Those people would for instance have the official,
hypersensitivity outcomes of MS or Lupus or whatever. But they are not
also called Incompetent Incantation-ators and they are not mistreated by
the entire universe (family, friends, Social Security, “doctors,”
everyone, including ILADS and the non profits).
It’s not “Autoimmune.” It’s Subimmune. This Subimmunity represents the
entire class of the DSM's VooDoo Somatoformia – as well as cancer. Cancer
is in the Subimmune class, at the other end of the immunity spectrum
from Autoimmunity. This fact or condition completely flips the entire
medical paradigm where you have to have a biomarker that is above-, or
more-than- the normal range. Lyme is not an inflammatory disease.
There are always negative correlations to biomarkers of autoimmunity or
illness or infection except when using sophisticated DNA techniques
using spinal fluid, in particular in these chronic, waste-basket
diseases. Henceforth, Autoimmunity will be an
obsolete word that connotes the previous Medical Establishment where BigPharma is going to “block” something with their drugs. They are
dinosaurs. You can’t block a mechanism that is already permanently
blocked and you can’t unblock it.
Luft at the 1998 FDA Vaccine Meeting on LYMErix:
point that I wanted to make in regard to the study is that there is very
heavy dependence on serologic confirmation. And when we start thinking
about the adverse events, ***
it was stated originally when we got the overview of the disease that
the disease is really quite protean. And actually the adverse events are
very similar to what the disease manifestations are.**** And if you
start to, as I think Dr. Hall was eluding to -- if you start to kind of
say well how often do you actually become seropositive, you can start to
have a different take on when someone has an adverse event or whether it
is disease specific or infection specific versus vaccine specific. And I
think that that is an important issue that we have to deal with. ..." http://www.fda.gov/ohrms/dockets/ac/98/transcpt/3422t1.rtf
5.) Dave Persing who together with Yale’s Robert Schoen
developed this test in 1994 or 1995 says this about the similarities
between Lyme and LYMErix disease:
"Additional uncertainty may arise if the vaccines are not completely
protective; vaccinated patients with multisystem complaints
characteristic of later presentations of Lyme disease may be difficult
to distinguish from patients with vaccine failure....”
Who else says OspA alone is responsible for the immunosuppression with brain inflammation that is characteristic of "Chronic Lyme?"
6.) THE NIH (Martin and Marques):
burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral
blood monocytes but differentially regulates HLA-class II expression
spirochete Borrelia burgdorferi is the agent of Lyme disease, which causes
central nervous system manifestations in up to 20% of patients. We
investigated the response of human brain microglial cells, glial
progenitors, neurons, astrocytes, as well as peripheral blood monocytes to
stimulation with B. burgdorferi. We used oligoarrays to detect changes in
the expression of genes important for shaping adaptive and innate immune
responses. We found that stimulation with B. burgdorferi lysate increased
the expression of Toll-like receptors (TLRs) 1 and 2 in all cell types
except neurons. However, despite similarities in global gene profiles of
monocytes and microglia, only microglial cells responded to the stimulation
with a robust increase in HLA-DR, HLA-DQ, and also coexpressed CD11-c, a
dendritic cell marker. In contrast, a large number of HLA-related
molecules were repressed at both the RNA and the protein levels in
stimulated monocytes, whereas secretion of IL-10 and TNF-alpha was strongly
induced. These results show that signaling through TLR1/2 in response to B.
burgdorferi can elicit opposite immunoregulatory effects in blood and in
brain immune cells, which could play a role in the different susceptibility
of these compartments to infection.
The NIH patent
explaining how Lyme causes LYMErix-disease (“stealth bomber”):
invention relates to novel antigens associated with Borrelia burgdorferi
which are exported
(or shed) in vivo and
whose detection is a means of diagnosing Lyme disease. The antigens are
and other bioproducts including the major extracellular protein antigen.
Another object of the invention is to provide antibodies, monoclonal
and/or polyclonal, labeled and/or unlabeled, that are raised against the
antigens. A further object of the invention is to provide a method of
diagnosing Lyme disease by detecting the antigens in a biological sample
taken from a host using the antibodies in conventional immunoassay
formats. Another object of the invention is to provide kits, for the
diagnosis of Lyme disease, comprising the antibodies and ancillary
reagents. The advantage of the antibodies used in the invention is that
they react with the antigens from geographically diverse strains of
Borrelia burgdorferi, but do not react with antigens from related
The shed blebs (or exosomes
or vesicles) have LYMErix on them (delayed fuse or “time bomb”):
multiprotein complexes of the Borrelia burgdorferi outer membrane
"Although we uncovered the existence of at least 10 distinct OM
complexes harboring several unique subunits, the complexome is dominated
by the frequent occurrence of a limited diversity of membrane proteins,
most notably P13, outer surface protein (Osp) A, -B, -C, and -D
Luft in 1989, in IDSA's own "journal," saying "treatment
fails in half the cases." And the OspA vaccine caused the same
systemic disease, say the crooks, themselves. See the
Occam's Razor report for who says so.
Steere was at this 1994 FDA meeting:
DATTWYLER: "-- the ones that (sic) failed to mount a vigrous immune response tended to do worse. So, there is an inverse correlation between the degree of serologic response and the outcome.
"So, individuals with a poor immune response tend to have worse disease."
1994 FDA Meeting Transcripts where Ray Dattwyler tells the FDA Vaccine Committee that the
patients with low or no antibodies are the sickest: http://www.actionlyme.org/Dattwyler_Luft_DNA_in_CSF.htm
Ray Dattwyler (SUNY-SB) says in 1988 that exposure to Lyme or even just its supernatants (OspA-like molecules) turn off the NK cell activity (or is immunosuppressive):
"Effect of B burgdorferi Culture on Normal PBL
"..when lymphocytes are cultured in the presence of growing Bb there is a marked inhibition ( p < .0005 ) of NK activity on days 3, 5, and 7 when compared to lymphocytes cultured in BSKII media in the absence of spirochetes. This effect is not due to a selective depletion or or toxicity to endogenous NK since viability studies and monoclonal antibodies demonstrate no significant changes after culture with the organism.
"The inhibition is directly attributable to the organism or its supernatants (data not shown)."
From: Modulation of natural killer cell activity by Borrelia
Department of Pathology, State University of New York, Stony
PMID: 3056196 [PubMed - indexed for
Ann N Y Acad Sci. 1988;539:103-11.
Dattwyler on Seronegative Lyme and how that is like fungal diseases:
DOWNLOAD THE FULL TEXT of Dattwyler talking about seronegative, neuroLyme,
Lyme is like Jeopardy! Ask the right question: "Something that
causes a 'multi-system disease' and is
IDSA's own 'New Great Imitator.'"
The answer is, "What is OspA?"
UCSF says Lyme and LYMErix-Disease are a diseases of
immunosuppression, and they say that half the Lyme/tick bite victims
remain ill and are not cured with antibiotics
Feb 12, 2016:
“Early Lyme disease prior to antibiotic therapy was characterized by marked
upregulation of Toll-like receptor signaling but lack of activation of
the inflammatory T-cell apoptotic and B-cell developmental pathways seen in
other acute infectious syndromes,” wrote the study’s authors. “Six
months after completion of therapy, Lyme disease patients were found to have
31 to 60% of their pathways in common with three different immune-mediated
chronic diseases. No differential gene expression signature was observed
between Lyme disease patients with resolved illness to those with persistent
symptoms at six months post-treatment.”
See more below from UC Davis, and in the
Occam's Razor report. The Great
Imitator is EBV, the Great Initiator is the fungal antigen OspA, shed by
spirochetes - their own phylum, and not regular "bacteria" -
on blebs, says the NIH.
America is a really stupid country, when you consider that nearly every
disease is an outcome of the first immune disordered step - inhibition of
apoptosis of infected B cells.
Look at the experience of Lewis Bull, East Lyme, CT,
back in the OspA "vaccines" trials days (late 1990s) to see exactly what
these evil bastards of the CDC (Barbour, Johnson, Steere) had planned from
the beginning to do with LYMErix - "multisystem
(read: "sepsis")," Chronic Fatigue Syndrome-like - outcomes.
'Says it all.
University of California, Davis, says the
Steere, Gary Wormser, Edward McSweegan, et al
must be lying their faces off:
and LYMErix cause permanent immunosuppression or is like a B cell AIDS.
Lyme is not an "inflammatory," "autoimmune disease," it is the
Great Initiator of latent viruses, as
a fungal antigen shedder, SPIROCHETE (its own phylum). Fungal antigens
like triacyl lipopeptides (OspA) have always been known to cause
immunosuppression. The complete opposite of an "autoimmune" or
"inflammatory" disease. The only
will be signs of nerve and brain degradation in the cerebral spinal fluid;
no antibodies in the blood.
exactly is OspA?
“I did not get the vaccine so this does not concern me.” Oh,
yes, you got the vaccine. Everyone with Lyme got LYMErix. Here is what
LYMErix is, and how this "vaccine-was-the-disease" works:
This is image is of Pam3Cys
or OspA. What is variable is the protein end "("peptide"), but what is
immunogenic (seen as an invader to the immune system) are the fatty acids or
acyl groups and the very electronegative cysteine core:
Pam3Cys is a triacylated lipoprotein, the degree of acylation is
equated with its toxicity. So what is acylation? It’s the zig-zaggy
lines that mean Carbon-Carbon-Carbon, yes, hydrocarbons, like margarine
or octane. Exactly, the name just refers to the number of carbons in
each carboxyl or acyl group. Palmitic (the Pam in Pam3Cys) has X number
of carbons, gasoline, 8, linoleic acids, like 14. Look up what are
alkanes then add a COOH group and you have one of these fatty acids.
Something highly acylated like this (3 or more fatty acids hanging off)
are managed by Toll-like Receptor (TLR) 2 and TLR1, together.
Therefore a “TLR2/1-agonist” is another term that generally refers to
lipoproteins like those from Borrelia, mycoplasma, mycobacteria, and
others like Brucella. (But they can manage other compounds.)
This thing, Pam3Cys and fungal lipid molecules like it, is shed with the
blebs. In other words, like this:
likes of OspA is on these blebs. They go to the brain, inflame it, get
eaten up by immune cells - which renders them incompetent-, they go to
the kidneys (LUAT), etc. You will find this to be so in an NIH-owned
patent (5,217,872) and elsewhere.
So, the fungal antigens are on the shed blebs and they go everywhere and
they render the immune cells incompetent, resulting in an AIDS-like
disease. Everyone who has Lyme disease also has LYMErix disease.
Cadavid and the NIH say these shed
vesicles or blebs go to the brain and
In other words, the NIH is saying that thanks to exposure to shed blebs
with TLR2/1 agonists like OspA on them, the HLA molecules will be
downregulated and that you will make no antibodies. This
mechanism is mimicked elsewhere, in other fungal diseases models. It
is also CALLED endotoxin tolerance.
Endotoxin Tolerance Inhibits
Lyn and c-Src Phosphorylation and Association with Toll-Like Receptor 4
but Increases Expression and Activity of Protein Phosphatases.
“Endotoxin tolerance protects
the host by limiting excessive 'cytokine storm' during sepsis, but
compromises the ability to counteract infections in septic shock
It reprograms Toll-like receptor (TLR) 4 responses by attenuating the
expression of proinflammatory cytokines without suppressing
anti-inflammatory and antimicrobial mediators, but the mechanisms of
reprogramming remain unclear. In this study, we demonstrate that the
induction of endotoxin tolerance in
human monocytes, THP-1 and MonoMac-6 cells inhibited lipopolysaccharide
(LPS)-mediated phosphorylation of Lyn, c-Src and their recruitment to
TLR4, but increased total protein phosphatase (PP) activity and the
expression of protein tyrosine phosphatase (PTP) 1B, PP2A, PTP
nonreceptor type (PTPN) 22 and mitogen-activated protein kinase
phosphatase (MKP)-1. Chemical PP inhibitors, okadaic acid, dephostatin
and cantharidic acid markedly decreased or completely abolished LPS tolerance,
indicating the importance of phosphatases in endotoxin tolerization.
Overexpression of PTPN22 decreased LPS-mediated nuclear factor
(NF)-x03BA;B activation, p38 phosphorylation and CXCL8 gene expression,
while PTPN22 ablation upregulated LPS-induced p65 NF-x03BA;B and p38
phosphorylation and the expression of TNF-α and pro-IL-1β mRNA,
indicating PTPN22 as an inhibitor of TLR4 signaling. Thus, LPS tolerance interferes
with TLR4 signaling by inhibiting Lyn and c-Src phosphorylation and
their recruitment to TLR4, while increasing the phosphatase activity and
expression of PP2A, PTPN22, PTP1B and MKP1.
See more at: