Ethics and Science in Lyme Disease; Who is Lying about the fact that there are two distinct outcomes and WHY.

They say a picture is worth a thousand words, so here it is:


There are two distinct disease outcomes in Lyme disease.  Right now only one type is allowed to exist and we refer to that outcome as “bad-knee Lyme” and the other is “tick bite induced post sepsis syndrome”.  Bad knee only accounts for 15% of total cases, the other 85% of us are the chronic neurological cases.  Today, Lyme disease means that you have an HLA-linked hypersensitivity response to spirochetes with high antibody production.  These are the CDC positive positive people (with the exception of about 1.2% of cases who have both says Fallon) are not very sick and typically only have an arthritic “bad-knee”.

The rest of us are extremely disabled with several neurologic diseases all at the same time.  The 85% of us who are VERY sick and disabled were purposely cut out of the diagnostic standard and case definition in 1994 at the Consensus Conference in Dearborn, Michigan.  The reason being that patent holders like Allen Steere, Barbara Johnson and members of the fake non-profit propaganda firm the ALDF wanted to sell a vaccine called LYMErix that was actually an endotoxin and gave people the same disease we know as “Chronic Lyme”.  If this form of the disease didn’t exist, the disabling kind, they could say that their vaccine was at least 85% effective.  That’s the crime.  The crime is the disease itself.

Dearborn scam

Borrelia lipoproteins are endotoxins and that’s how spirochetes cause disease.  If only it was a spirochete that drilled through tissues that you could eventually kill enough off of to reach a state of remission..  I wish that’s all it was.  But it’s not.  We know from the LYMErix vaccine that this is true.  The victims got the same disease but there were NO spirochetes injected into them.


Yes, spirochetes do persist.  We have known that Relapsing Fever germs persist for 106 years.  What is more troubling about this disease is the anti-inflammatory effects.  Spirochetes stealth bomb the host with toxic lipoproteins that cause permanent immunosuppression.  If the host didn’t down-regulate after initial cytokine storm then the host would die, it’s a survival mechanism.  That is why we call this post sepsis syndrome which is ultimately a B cells AIDS-like disease with reactivated neurotropic viruses and a mixed bag of opportunistic pathogens.

steere wormser 2016 anti-inflam effects

The report in the graphic above is Wormser and he’s saying “the anti-inflammatory effects might be the more important function of TLR signaling” which basically just means that this is indeed a disease of immunosuppression.  This next one is extremely interesting (as well as damning to the criminals position that lyme is just a bad-knee):

“Bacteria that are able to persist in hosts to cause long term infections are, by definition, able to evade host immune defenses. While establishment of persistent infection can benefit the bacteria, in certain cases where the bacteria itself causes little damage, allowing the establishment of prolonged infection may be more beneficial to the host than continued attack by the immune system. Borrelia burgdorferi, the causative agent of Lyme disease, produces no toxins or other virulence factors thought to damage the host. Instead, most of the manifestations of Lyme disease are thought to be the result of the immune response to the organism. In its natural Peromyscus mouse host, little or no reaction to the organism is typically seen despite the fact that, once infected, the organism persists for the life of the animal. In humans and inbred mice (which do develop immune responses to the organism), inflammation is thought to be initiated by receptors of the innate immune system. In vitro, loss of receptors of the innate immune system that recognize B. burgdorferi such as toll-like receptor 2 (TLR2) or Nod2 results in a decrease inflammatory response. However, in vivo studies of animals deficient in these receptors or their adaptor molecules have not reduced inflammation and in many cases, have actually resulted in increased inflammation. We hypothesize that the host has evolved methods for dampening the immune response over time and that during the course of prolonged exposure, these receptors play a more important role in triggering innate immune tolerance, rather than activating acute inflammatory pathways. In preliminary studies, we have shown that exposure of macrophages to B. burgdorferi can reduce release of inflammatory cytokines and increase release of anti-inflammatory cytokines upon re-exposure to the organism. In this proposal, we will first identify pathways and mechanisms involved in mediating innate immune tolerance to B. burgdorferi. We will study both pathways that have been identified in playing a role in tolerance to other agents (e.g. lipopolysaccharide) as well as perform unbiased studies to identify new mechanisms. In Aim 2, we will develop animal models to study the importance of innate immune tolerance in Lyme disease. We will test both ex vivo and in vivo systems for isolating the role of different pathways during B. burgdorferi infection. Successful completion of these experiments will provide proof of principle for a new strategy of host defense (mutualism or “benign neglect”) against organisms that are considered pathogens and establish a rationale for the existence of innate immune tolerance.


I have to ask the question even though it makes me unpopular- why isn’t ILADS talking about this?  They should be very interested in this considering they are constantly trying to find out why patients don’t get better from killing bugs.  This is why.  This is EXACTLY why.  The treatment fails in at least half the cases no matter what they do to treat.  Patients relapse and remit to and fro between differing levels of disability it seems no matter what they try to do or how much money they spend or how long they set off the equivalent to an atomic bomb of antibiotics into their bodies.

We know everything we need to know about why these patients don’t get better.  We know that spirochetes deploy TLR 2/1 agonists that permanently suppress the immune system, we know that in the presence of antibiotics spirochetes just casually morph into cysts, we know that they are intracellular.  So why to seemingly everyone is this treated like some extraordinary mystery?  It’s not.  It’s really not.

klempner fibroblasts

Remember Klempner and his fraudulent re-treatment study?  Yeah, before he went and lied to the world he was writing about stuff like this- fibroblasts protecting spirochetes and the infection resisting eradication.  Another really curious thing about all of these idiots is that they recommend ceftriaxone as the treatment for “Lyme disease”, which is a CNS acting drug.  But I thought this disease was just a bad knee?  Hmm..

Shapiro on TV show

This is not just a chronic bacterial infection.  It never was and it never will be.  It’s also not about inflammation which is the only way that doctors know how to diagnose disease.  “They” have always known that there are two completely separate outcomes.  We all know this because “they”, the criminals, said it themselves multiple times.  How hilarious is that?  They are such blatant liars the only thing left to do really is to laugh.  Don’t fear these stupid assholes, because they are STUPID assholes.  They are freaking out right now because they know that we are reaching critical mass in the kind of awareness that actually matters- the things that TruthCures is bringing to the surface.  We all have a duty to know this stuff and spread the word so that we can end this once and for all.  We have plenty of evidence proving without a shadow of a doubt that this is a crime and the only thing left to do is prosecute it.

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…………maybe this is why no one wants to admit that there are two types of Lyme.  Plus, admitting it at this point would mean severe sentences… like potentially the death penalty for a cryme such as this.  Look up RICO charges 😉



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