NIH’s own mini-Occam’s Razor, Synergism is well-known to science


I wrote this shorter version of the Occam’s Razor for my friends in the ME/CFS world.  I also added some info on biological synergism so that they can see it is not an uncommon or unusual idea that one infectious microbe “helps” another.  For instance, doctors give babies with colds antibiotics to prevent the secondary bacterial infections that cause otitis.  Everyone knows the famous Lou Ferrigno (The Hulk) became deaf in childhood from this.  “Chronic Lyme” is really called Post Sepsis Syndrome because the shed fungal antigens reactivate latent viruses (like the herpes, such as in ME/CFS and Fibromylgia); they cause cross tolerance to other TLR agonists besides fungal (OspA = TLR2/1 agonist).


Quiz:  Who’s the NIH employee *and* CDC officer (they are called officers because the CDC is a wing of the military and they even have uniforms) and head of the NIH Rocky Mountains Bioweapons Lab who talks about the shed-blebbery, and that spirochetes go into a cyst form in the presence of antibiotics?

Quiz:  Who are the OTHER NIH employees who told us OspA on the shed blebs are responsible for the disease?

An NIH patent, explaining how Lyme causes LYMErix-disease:

“The 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 extracellular membrane vesicles 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 Borrelia spirochetes.”,217,872.PN.&OS=PN/5,217,872&RS=PN/5,217,872

Q: Which NIH employees told us Lyme is probably really about EBV?


2) “When Lyme Disease Lasts and Lasts,” by Jane Brody in the New York Times.
“’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.’”



Q: Which NIH employees are responsible for revealing it is OspA on the she blebs that is responsible for the total immunosupression after a tick bite (no antibodies)?
Q: Which other NIH employee said CFIDS/Lyme, OspA-Sepsis is really about reactivated EBV/other herpes?

“Surviving Sepsis: Detection and Treatment Advances” by Carolyn Beans for the National Institutes of Health, August 18, 2014

“…Some people who survive sepsis can develop secondary infections days or even months later. A research team that included Richard Hotchkiss, Jonathan Green and Gregory Storch of Washington University School of Medicine in St. Louis suspected that this is because sepsis might cause lasting damage to the immune system…The researchers looked for viruses like Epstein-Barr and herpes simplex that are often dormant in healthy people but can reactivate in those with suppressed immune systems.”



NIH (Barbour, blebs), NIH (RML, blebs, Dorward), NIH (OspA causes total immunosuppression, Marques and Martin), NIH (sepsis is really about EBV – Duray, Marques, Martin, Bean)… WTF else do you need to know ??



It means here that one organism enhances the other’s destructiveness.  The first example that should come to your head is this controversy over giving children with cold viruses antibiotics to prevent the well-known, secondary ear bacterial infections.  Or, as in the graphic, where the flu in combination with a bacterial infection results in the likes of say, the Spanish Flu pandemic of 1918, where most of the people who died, died from the secondary lungs infections (not really just the flu).

A second example is all the instances where the CDC and BigPharma have revealed that injecting a live attentuated virus into an immune suppressed child could end up giving the child the very same virus the vaccines are intended to prevent:

Thirdly and probably the most applicable one to the ME/CFS scam is where the CDC’s Suzanne Vernon committed research fraud by throwing out the mycoplasma before allegedly looking for it in Chronic Fatigue patients.

Background on fungal antigens (mycoplasmal, eperythrozoal, mycobacterial, spirochetal) causing immunosuppression, changes to erythrocyte osmotic potential (hypoxic fatigue), and activating vaccine viruses:


“In Swiss mice, animals with high natural resistance to hepatitis virus, the pathogenicity of this agent was markedly enhanced by combined infection with eperythrozoa. Eperythrozoa were maintained throughout 18 successive passages in normal Princeton and Swiss weanlings with intact spleens.The combined infection of Princeton mice with eperythrozoa and the virus component of Gledhill, Dick, and Andrewes, which is nearly inactive when injected alone, resulted in acute hepatitis with fatal outcome.”


[The effect of Eperythrozoon suis infection on the osmotic fragility of erythrocytes]

“Osmotic fragility of erythrocytes was tested in weaned pigs experimentally infected with Eperythrozoon (E.) suis. Acute eperythrozoonosis of splenectomized pigs led to an increase of osmotic fragility. It is supposed that E. suis infection causes a structural change in erythrocyte membrane. Possible mechanisms of this cell membrane injury are discussed.”

FUNGAL-VIRAL SYNERGY, again, more, re Lyme specifically, Baumgarth:
The bacteria initially trigger a strong immune response in an infected animal, but findings from this study indicate that the bacteria soon cause structural abnormalities in “germinal centers” — sites in lymph nodes and other lymph tissues that are key to producing a long-term protective immune response.
For months after infection, those germinal centers fail to produce the specific cells — memory B cells and antibody-producing plasma cells — that are crucial for producing lasting immunity. In effect, the bacteria prevent the animal’s immune system from forming a “memory” of the invading bacteria and launching a protective immune response against future infections.
*** The researchers found that following Borrelia burgdorferi infection, this process even prevented induction of strong immune responses to an influenza infection.***
Funding for the study was provided by grants from National Institutes of Health and National Institute for Allergy and Infectious Diseases.

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