Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."
 


18 May 2017


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PDFs
CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
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BarbourFish, 1993
Dearborn, 1994
BarbourFishpdf.pdf
 

Pathogenic Fungi

Predicting all of GW Bush's warcrimes, Oct 2000

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Borreliosis Basics – Version 3

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 an internal bundle of flagella (think of it as an internal bungie). Borrelia and Treponema (close cousins) have never been known to be curable with antibiotics “or even arsenic (Jay Sanford, U.S. Uniformed Services Hospital, 1975, and Andrew Balfour, U.K. Wellcome Research, BMJ, April 1911). They typically reside in the brain/nervous system and are found in the brains of Alzheimer’s victims at nearly a universal rate as compared to controls or non-Alzheimer’s victims. (Riviere, Oregon Health and Sciences University, 2002).

Borreliosis is transmitted primarily through the bite of an infected tick, but also may be transmitted by insect vectors and transplacentally to an unborn fetus, according to Yale and the NIH (Paul H. Duray). 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), Cancer, and Alzheimer’s, according to IDSA and the CDC. Thus, borreliosis is commonly referred to as “The Great Imitator” or “New Great Imitator.” As you will later see, it would be more correct to call Lyme and Syphilis, the Great Detonators.

Borreliae parasites have the ability to shed (bleb off) their outer membrane lipoproteins to both evade detection by –, and disable- the immune system. They modify their numerous different surface proteins in a mechanism commonly known as antigenic variation. These lipoproteins are called “outer surface proteins” (Osps, rhymes with wasps) and “variable major proteins” (Vmps, rhymes with wimps). The blebbing, or shedding, of OspA and similar antigens by the spirochete sends the immune system after the sloughed-off or pinched off antigens like OspA (much like flak confuses radar), allowing the spirochete to hide from immune attack and persist in the host (Barbour and Barthold, The Scientist, 1996). This mechanism renders antibodies useless (note: no vaccines can therefore be made against these surface antigens).

These outer surface lipoproteins, such as OspA (the Lyme "vaccine"), are TLR-2 agonists or fungal antigens, meaning they essentially disable the immune system
. They are very similar to toxins in this regard (see post-sepsis or post-septic shock survivors, Washington University, St, Louis, 2014). They do this by way of tolerance to other fungal antigens (TLR2s) as well as tolerance to other antigen types, managed by other TLRs, such as viruses (TLR7/9) and other bacterial TLR4-agonists (“cross-tolerance”). [(Clifford Harding, Case Western Reserve): "Because IRAK1 is required for TLR7/9-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." http://www.ncbi.nlm.nih.gov/pubmed/22227568 ]

Tolerance means the immune system will stop responding to the antigen. Cross tolerance means spreading or expanding normal disease-combating insufficiency to other antigen types such as TLR4 agonists or TLR7/9 agonists (viruses). Exposure to shed borrelial lipoproteins causes fungal tolerance in the blood and the inability to get rid of mycoplasma/eperythrozoons (also bearers of fungal antigens like OspA) from the blood, especially from the red blood cells. It is well known that fungi infections in the blood, particularly these blood parasites, the eperythrozoa or mycoplasma, causes fatigue, because they, by attaching to the surfaces of- and within- red blood cells hijack sugar metabolism and change the osmotic potential of the red cell membrane, rendering Oxygen unable to cross the red cell membrane, starving the body cells of Oxygen.

This generalized immunosuppression as a result of exposure to borreliae and their shed varying surface antigens creates an environment where common opportunistic infections are reactivated, such as latent Epstein-Barr, and cause chronic disabling disease. We know Lupus and MS are generally accepted as being caused by the herpesviruses (Epstein-Barr, HHV-6, or Cytomegalovirus, etc., or some combination of them). We have called chronic Lyme and LYMErix Disease: Tick-, or Lyme-, or LYMErix-Acquired Immune Deficiency (TAIDS or LAIDS).

Since we knew Lyme was formerly called the New Great Imitator because it caused Lupus, MS, etc, it now appears that the TLR2-agonists shed by these spirochetes cause the tolerance and cross-tolerance that reactivates latent herpes viruses, particularly Epstein Barr Virus (EBV). This came to light because the OspA vaccines caused the same systemic, “multi-system” (Dave Persing, Mayo), “protean” (Ben Luft, SUNY-SB) disease in those victims. Reactivation occurs thru IL-10, the inhibition of apoptosis of OspA or EBV infected cells, the mechanism shown above re TLR2-signaling and the inhibition of IFN-I, and apparently generalized immune activation or common cytokines. One group of researchers simply reported:
“Certain cytokines, particularly TGF -beta, can also induce lytic viral infection in a subset of Burkitt lymphoma lines in vitro, and could potentially reactivate EBV in vivo (Fahmi et al., 2000; Adler et al., 2002). The interaction between CD 4 T cells and EBV -infected B cells has also been reported to induce lytic infection (Fu and Cannon, 2000). Finally, there is increasing evidence that severe host cell stress in response to many different toxic stimuli (including chemotherapy and irradiation) can induce lytic EBV infection (Feng et al.,2002a, 2004; Westphal et al., 2000; Roychowdhury et al., 2003).” – Kenney, 2007, from the book, Human Herpesviruses, Biology, Therapy, Immunoprophylaxis, chp 25.

Recently, it was reported in the New York Times by Jane Brody quoting the National Institutes of Health’s Adrianna Marques, who now manages the Lyme-MS Division of NINDS (her boss, Roland Martin, quit the NIH and returned home to Germany once he found out OspA was responsible for the MS outcome of Lyme), "Complicating the picture is the fact that some people with PTLDS symptoms apparently never had Lyme disease in the first place, Dr. Marques said in an interview. There are other infectious organisms — Epstein-Barr virus, for example — that can produce similar symptoms and may be the real culprits." - When Lyme Disease Lasts and Lasts, July, 2013.

Chronic EBV is probably the main driver of all these New Great and Great Imitator diseases. Inasmuch as the Infectious Diseases Society of America, Yale, the CDC and related participants in the OspA vaccine fiasco vehemently oppose antibiotic treatment for Lyme for whatever [false] reason, the truth is that they worry antibiotic resistance will be acquired by the OTHER infections such as the fungal types, such as mycobacteria and mycoplasma for which we now have become carriers.

--- USDOJ OCCUPY, All Abused Groups, Summer, 2014