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"It is an indescribable experience knowing that what you are doing will have
an impact on the lives… of millions of people." —Anthony Fauci, 1993
In this guide, we discuss the National Institutes of Health (NIH) model of
Post-Sepsis Syndrome (PSS), a disease of immunosuppression, which parallels
what the Centers for Disease Control (CDC) is calling "fungal meningitis."
We also provide insight into how these agencies think such disease may be
treated. In this PSS/ fungal meningitis model, human TLR2/1 agonists--fungal
antigens--turn off the immune system to prevent death from sepsis. This is
the main reason the mouse model of disease does not parallel human disease.
Mice do not have human TLR2.
Fungal antigens/infections also reactivate herpesviruses, whose chronicity
has been widely proven as leading to cancers and neurological diseases.
Since there are many ways to "acquire" immunosuppression, we will focus on
several well-known outcomes: Lyme borreliosis, Autism, Gulf War Syndrome,
CFS/ME/SEID and Fibromyalgia, to show how they fit the model.
We will begin with Lyme disease, or borreliosis, since it is necessary to
explain what OspA is, to understand how it fits this fungal model.
Borreliosis is a multi-system disease caused by a spirochetal parasite. A
spirochete is a spiral shaped parasite with a unique mechanism for movement
that features a bundle of tail-like “flagella” which resides inside the cell
wall. Borreliosis is transmitted primarily through the bite of an infected
tick, but also can be transmitted in utero to an unborn fetus (according to
Yale), and possibly through insect vectors. If not treated immediately with
antibiotics, the infection can persist for years and cause neurological
diseases such as MS, Lupus, cancer, Chronic Fatigue/ Myalgic
Encephalomyelitis, ALS (Lou Gehrig's Disease) and Alzheimer’s, according to
IDSA and the CDC. Thus, borreliosis is commonly referred to as “The Great
Imitator” or “New Great Imitator.”
In a mechanism commonly known as blebbing, borreliae parasites have the
ability to shed (bleb off) their outer membrane lipoproteins to evade
detection by the immune system, per CDC officer Alan Barbour in (the
probably mis-titled): “Researchers Finding Rewarding Careers As Software
"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 spirochete safe from immunological attack.”
These outer surface lipoproteins, such as OspA (the Lyme "vaccine"-- LYMErix)
are TLR2 agonists (fungal antigens) and also “undergo virtually limitless
antigenic variation, leaving the immune system overwhelmed” says, again, CDC
officer Alan Barbour
essentially, they disable or turn off the immune system.
Fungal antigens shed by Borrelia cause tolerance to other fungal antigens
(TLR2/1-agonists such those borne by mycoplasma and mycbacteria) as well as
tolerance to other antigen types, managed by other TLRs. Tolerance means
that the immune system stops recognizing fungal antigens such as 1)
inhibiting HLA-molecule function and therefore antibodies are no longer
produced (Radolf and Harding,
”Despite the ability of MTB 19-kDa lipoprotein to activate microbicidal and
innate immune functions early in infection, TLR 2-dependent inhibition of
MHC-II expression and Ag processing by MTB 19-kDa lipoprotein during later
phases of macrophage infection may prevent presentation of MTB Ags and
decrease recognition by T cells. This mechanism may allow intracellular MTB
to evade immune surveillance and maintain chronic infection.”
, and 2) exposure to Borrelial fungal antigens causes cross-tolerance to the
TLRs that manage viral infections:
"Because IRAK1 is required forTLR7/9-induced IFN-I production, we propose
that TLR2 signaling induces rapid depletion of IRAK1, which impairs IFN-I
induction by TLR7/9. This novel mechanism, whereby TLR2 inhibits IFN-I
induction by TLR7/9, may shape immune responses to microbes that express
ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus
coinfection." (CV Harding) http://www.ncbi.nlm.nih.gov/pubmed/22227568
This is very important, because often, when you are sick you get blood drawn
to test for antibodies to various pathogens. We are generally led to believe
that the higher the antibodies, the more advanced the infection. As we have
seen, in diseases of immunosuppression, antibodies are not produced. This is
one reason the Lyme Western blot is useless.
At the 1994 Dearborn conference, Steven Dattwyler, MD, agreed:
Dr. O'Brien: "I was concerned about your last slide where you said there was
a poor correlation between serologic response and clinical disease. And as I
heard you say, some people who mount better responses get worse disease. Did
I hear you say that."
Dr. Dattwyler: "No, no, I said the reverse. The better responses tended to
have a better response. And I should clarify where this came from. This is
from antibiotic trials. These are treatment trials of erythema migrans, in
which individuals given an antibiotic regimen which was not optimal--we
didn't know that it was not optimal at the time--the ones that failed to
mount a vigorous immune response tended to do worse, clinically. So, there
was an inverse correlation between the degree of serologic response and the
outcome. So, individuals with a poor immune response tend to have worse
Exposure to shed borrelial lipoproteins causes fungal tolerance in the blood
and the inability to get rid of mycoplasma/eperythrozoons from the blood,
especially from the red blood cells (which causes fatigue). Also, there is
cross-tolerance to TLR4 agonists from constant TLR2-agonism of shed
borrelial antigens like OspA and vice-versa. This creates an environment
where opportunistic infections can thrive and cause chronic, disabling
A well known outcome of immunosuppression, regardless of how this is induced
(e.g., Stelara, Humira, transplant drugs, methotrexate, HIV, etc) is the
reactivation of the latent herpes viruses, particularly Epstein Barr Virus (EBV).
Chronic EBV (or EBV in combination with CMV, HHV-6, or Varicella), is
probably the main driver of all these New Great and Great Imitator diseases.
That is the basic gist of the Post-Sepsis Syndrome model endorsed by the NIH,
as demonstrated in these two studies:
NIH: profound immunosuppression is one of the chronic consequences of severe
Washington University in St. Louis:
Reactivation of multiple viruses in patients with sepsis http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0098819
Borrelial- or OspA-induction of TLR2-antigen tolerance is one example of
-In Autism: fungally contaminated vaccines reactivate the live, attenuated
viruses and suppress the immune system (TLR2/1-agonist tolerance), causing
children to get the disease instead of the protection.
-In Gulf War Syndrome: nerve agent antidote, DEET and hyper-vaccination
[including fungally- (e.g. mycoplasma) contaminated vaccines] all work to
suppress the immune system and reactivate latent herpesviruses.
-In CFS/ME/SEID/Fibromyalgia: chronic mold exposure, OspA (Lyme or LYMErix
vaccine), fungal infections, contaminated vaccines, or a septic event cause
TLR2- agonist tolerance (immunosuppression) and reactivation of latent
herpesviruses. It is well known that mycoplasmas (TLR2/1 agonists) adhere
to, and go inside red blood cells. Mycoplasmas cause permeability issues
with red blood cells in which oxygen cannot cross the cell wall, hence,
fatigue because of low oxygen. Couple that with the reactivation of EBV and
you get double fatigue--fatigue that will not show up in lab tests because
you still have high/ normal red blood cell count, but not anemia.
Finally, everyone should know that the CDC, knowing that fungal antigens
injected directly into the bloodstream cause irreversible immunosuppression
and “immune damage,” later performed research fraud in order to deny that
mycoplasma play any role in the chronic immunesuppression disease or
fatigue--throwing out the red blood cells to which mycoplasma adhere, before
looking for mycoplasma:
Absence of Mycoplasma Species DNA in Chronic Fatigue Syndrome, 2003: “Blood
was collected in sodium citrate Vacutainer tubes (Beckton Dickinson) and
shipped by overnight courier to the Centers for Disease Control (CDC), where
plasma was collected by separation on lymphocyte separation medium (LSM; ICN
Biomedicals). Plasma (1 ml) was concentrated to approximately 250 μl in a
Centricon centrifugal filter unit YM-100 (Millipore). ***Cell-free plasma
DNA was extracted by using a QIAamp DNA Mini kit (Qiagen) according to the
manufacturer's instructions and quantified by using a DyNA Quant 200
fluorometer*** (Amersham Biosciences).”http://jmm.sgmjournals.org/content/52/11/1027.long
It is pretty important that everyone know what the CDC did here. They do not
want anyone to know that mycoplasma are involved in Chronic Fatigue
Syndrome. [Why? Because this is the mechanism behind the Autism pandemic:
NYTimes; Doctors admit Thimerosal is put in vaccines to prevent fungi:
Vaccine Rule Is Said to Hurt Health Efforts (Dec, 2012)
"But a proposal that the ban include thimerosal, which has been used since
the 1930s to prevent bacterial and fungal contamination in multidose vials
of vaccines, has drawn strong criticism from pediatricians.
"They say that the ethyl-mercury compound is critical for vaccine use in the
developing world, where multidose vials are a mainstay.
"'Banning it would require switching to single-dose vials for vaccines,
which would cost far more and require new networks of cold storage
facilities and additional capacity for waste disposal, the authors of the
What is the Treatment?
We have established that tolerance to fungal antigens causes
immunosuppression, reactivation of viruses, (i.e. latent herpesviruses and
live, attenuated viruses in vaccines), susceptibility to other types of
infections, and the "New Great Imitator" diseases, including autism and GWS.
Additionally, herpesviruses are known to lead to cancer.
At this point, the next question is inevitably, "what's the treatment?"
Ask Anthony Fauci. He ought to know.As head of the National Institute of
Allergy and Infectious Diseases (NIAID), he has patented a treatment for the
immune suppression outcomes of chronic Lyme disease--a condition he
simultaneously denies. The CDC calls it "fungal meningitis":
Notice that the CDC's diagnostic criteria there matches exactly the new
Policy Paper by IDSA on using Mass-Spec-PCR to identify DNA pathogens, here: http://ein.idsociety.org/media/publications/papers/2014Blaschke_DMID_14_Unmet_Diagnostic_Needs.pdf
And, the moment we have been waiting for--Fauci's patent for the treatment
of Fungal Meningitis (Chronic Fatigue, Chronic Lyme and LYMErix Disease): http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=/ netahtml/PTO/srchnum.htm&r=1&f=G&l=50&s1=5,696,079.PN.&OS=PN/5,696,079&RS=PN/
"BACKGROUND OF THE INVENTION "....Illustrative of specific disease states in
treatment of which the present invention can be applied are HIV infection
and other diseases characterized by a decrease of T-cell immunity, for
example, mycobacterial infections like tuberculosis and fungal infections
such as cryptococcal disease. This method also can be used in the treatment
of secondary infections that occur in patients with suppressed immune
systems, such as the opportunistic infections that occur in AIDS patients.
So, the next question is, why is this method not being used? Doesn't he want
to experience that feeling of impacting the lives of millions of people? Or
is he satisfied with the impact he already has made?
"It is an indescribable experience knowing that what you are doing will ha