I can’t think of a simpler way to explain “what is chronic Lyme disease.”

 

Remember the New England Compounding Center meningitis scandal of 2012? Their injectable steroids were fungally contaminated. They sickened at least 800 people and killed 64. You cannot inject fungi into humans.

 

https://en.m.wikipedia.org/wiki/New_England_Compounding_Center_meningitis_outbreak

“On December 17, federal prosecutors in Boston unsealed a 131-count federal criminal indictment related to the outbreak. It charged 14 former NECC employees, including president Barry Cadden and pharmacist Glenn Chin, with a host of criminal offenses. It alleged that from 2006 to 2012, NECC knowingly sent out drugs that were mislabeled, unsanitary, or contaminated—forming the basis for a massive RICO indictment against six individuals, including Cadden and Chin. The RICO count alleged 68 overt acts—including 25 counts of second-degree murder in seven states against Cadden and Chin. If convicted, Cadden and Chin could potentially get life in prison.[15]”

 

Google this incident. Read about the long-term outcomes. The surviving victims are sick. They are disabled. You could easily mistake their symptoms for chronic Lyme.

 

You cannot inject fungi into humans.

 

When a Lyme-infected tick bites, it injects spirochetes. Spirochetes have a number of outer surface proteins that are shed to avoid attack from the immune system. Outer surface protein A (OspA) is a fungal type antigen because it is managed by the same immune receptors (TLR2/1) as fungi. Essentially, when an infected tick bites, it is injecting organisms that stealth bomb the immune system with something chemically identical to a fungal toxin.

 

Simple, right?

 

The LYMErix “vaccine” (patented by CDC officers) was made with synthetic OspA, so it is obvious why LYMErix recipients in the trials were sickened. They were injected with a fungal type antigen.

 

You cannot inject fungi into humans.

 

LYMErix was pulled off the market when this fact was shown to the FDA. But was anyone prosecuted like with the NECC scandal? Did anyone go to jail for racketeering? Was a fund set up for the victims?

 

Was ANYONE held accountable for the crime of claiming that a fungus was a vaccine and injecting it into people? Was ANYONE held accountable for the blatant crime of changing the case definition of relapsing fever borreliosis so the sickest victims could not be diagnosed?

 

No.

 

If you are a Lyme activist, this is what you should be talking about. Why has justice failed us? Why does justice ignore us? Why has nobody been held accountable for this torture?

 

Are they afraid it might expose the same mechanism at work when children are maimed by fungally contaminated vaccines, thereby kicking down the Pharma house of cards in one swift blow?

 

You cannot inject fungi into humans. It’s the only thing worth talking about, in this month of “awareness.”

 

peace/Beaux

 

———————————————

Here we show you get the same result when the fungal lipoprotein comes from other organisms:

“A deleterious effect on immunity,” “an adverse effect on the protection,” “the immunosuppressive effect,” “diminished protection,” “reduced T cell activation,…”

THEY DON’T WORK; lipoproteins are the opposite of vaccines.

Click to access 2017_All_9_Charge_Sheets.pdf

 

The 3 Tuberculosis vaccine attempts that all failed the same way LYMErix failed, by making people sicker and more susceptible to disease:

Clin Exp Immunol. 2000 May;120(2):274-9.
The 19-kD antigen and protective immunity in a murine model of tuberculosis.
Yeremeev VV1, Lyadova IV, Nikonenko BV, Apt AS, Abou-Zeid C, Inwald J, Young DB.
“The 19-kD antigen is a cell wall-associated lipoprotein present in Mycobacterium tuberculosis and in bacille
Calmette-Guérin (BCG) vaccine strains. Expression of the 19-kD antigen as a recombinant protein in two
saprophytic mycobacteria-M. vaccae and M. smegmatis-resulted in abrogation of their ability to confer
protection against M. tuberculosis in a murine challenge model, and in their ability to prime a DTH response to
cross-reactive mycobacterial antigens. Induction of an immune response to the 19-kD antigen by an alternative
approach of DNA vaccination had no effect on subsequent M. tuberculosis challenge. These results are
consistent with a model in which the presence of the 19-kD protein has a detrimental effect on the efficacy of
vaccination with live mycobacteria. Targeted inactivation of genes encoding selected antigens represents a
potential route towards development of improved vaccine candidates.”
http://www.ncbi.nlm.nih.gov/pubmed/10792376
Infect Immun. 2001 Mar;69(3):1433-9.
Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits Mycobacterium smegmatis-induced cytokine
production by human macrophages in vitro.
Post FA1, Manca C, Neyrolles O, Ryffel B, Young DB, Kaplan G.
“Vaccination of mice with Mycobacterium vaccae or M. smegmatis induces some protection against M.
tuberculosis challenge. The 19-kDa lipoprotein of M. tuberculosis, expressed in M. vaccae or M. smegmatis (M.
smeg19kDa), abrogates this protective immunity. To investigate the mechanism of this suppression of
immunity, human monocyte-derived macrophages (MDM) were infected with M. smeg19kDa. Infection
resulted in reduced production of tumor necrosis factor alpha (TNF-alpha) (P < 0.01), interleukin-12 (IL-12) (P
< 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to infection with M. smegmatis vector (M. smegV).
Infection with M. smeg19kDa and with M. smegV had no differential effect on expression of costimulatory
molecules on MDM, nor did it affect the proliferation of presensitized T cells cocultured with infected MDM.
When MDM were infected with M. smegmatis expressing mutated forms of the 19-kDa lipoprotein, including
non-O-glycosylated (M. smeg19NOG), nonsecreted (M. smeg19NS), and nonacylated (M. smeg19NA) variants,
the reduced production of TNF-alpha or IL-12 was not observed. When the purified 19-kDa lipoprotein was
added directly to cultures of infected monocytes, there was little effect on either induction of cytokine
production or its inhibition. Thus, the immunosuppressive effect is dependent on glycosylated and acylated 19-
kDa lipoprotein present in the phagosome containing the mycobacterium. These results suggest that the
diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis
expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to
reduced induction of T-cell activation.”
http://www.ncbi.nlm.nih.gov/pubmed/11179309

Infect Immun. 2003 Jun;71(6):3146-54.
The Mycobacterium tuberculosis recombinant 27-kilodalton lipoprotein induces a strong Th1-
typeimmune response deleterious to protection.
Hovav AH1, Mullerad J, Davidovitch L, Fishman Y, Bigi F, Cataldi A, Bercovier H.
”Th1 immune response is essential in the protection against mycobacterial intracellular pathogens. Lipoproteins
trigger both humoral and cellular immune responses and may be candidate protective antigens. We studied in
BALB/c mice the immunogenicity and the protection offered by the recombinant 27-kDa Mycobacterium
tuberculosis lipoprotein and the corresponding DNA vaccine. Immunization with the 27-kDa antigen resulted in
high titers of immunoglobulin G1 (IgG1) and IgG2a with a typical Th1 profile and a strong delayed
hypersensitivity response. A strong proliferation response was observed in splenocytes, and significant nitric
oxide production and gamma interferon secretion but not interleukin 10 secretion were measured. Based on
these criteria, the 27-kDa antigen induced a typical Th1-type immune response thought to be necessary for
protection. Surprisingly, in 27-kDa-vaccinated mice (protein or DNA vaccines) challenged by M. tuberculosis
H37Rv or BCG strains, there was a significant increase in the numbers of CFU in the spleen compared to that
for control groups. Furthermore, the protection provided by BCG or other mycobacterial antigens was
completely abolished once the 27-kDa antigen was added to the vaccine preparations. This study indicates that
the 27-kDa antigen has an adverse effect on the protection afforded by recognized vaccines. We are currently studying how the 27-kDa antigen modulates the mouse immune response.”
https://www.ncbi.nlm.nih.gov/pubmed/12761093
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12761093

“A deleterious effect on immunity,” “an adverse effect on the protection,” “the immunosuppressive effect,”
“diminished protection,” “reduced T cell activation,…”
THEY DON’T WORK; lipoproteins are the opposite of vaccines.