Let’s see if I can clear up some confusion.

Hardly any Lyme patients actually know the true nature of their disease. So I’m going to attempt to write this in a way that even the most compromised patients can understand. This is a touchy subject, people really cling onto ILADS as being our saviors. I’ve been kicked out of all the Lyme groups and told to “stop telling sick people about this! It’s hopeless!”. So I’m writing this for those of who are honest enough with yourselves to know that extended antibiotic treatment hasn’t helped you.

A lot of people end up encountering Kathleen Dickson and her work at some point in their illness. Most people ask her right off the bat “Well then how do we get better? Whats the treatment?” and are then immediately met with an answer that they don’t like. Then they turn away from it, move on and never look back. It’s such a shame because there is no information MORE VITAL than HERS. People give this woman more shit every single day than seems possible, and they have no clue who she even is or what she is trying to do for THEM. For all of us. I’ll leave it at that for now, I just thought it should be addressed as it is a daily issue.

I don’t really know where to start, so I guess I’ll start with how we get diagnosed.

So we all know that ILADS says we don’t test positive because Lyme can muck up our immune systems. We all assume that this isn’t permanent and as soon as we kill enough spirochetes it magically kicks back into gear. This is the first fallacy. Most of us hear about how we need to take antibiotics to “help” our immune systems make some antibodies before we test through igenex. Then we usually don’t hear or talk about our immune systems very much until we start buying thousands of dollars in supplements to “boost immunity”. Until a few short years ago, this was not even true for ILADS; they did not speak of “boosting immunity.”

While we learn about the bad tests and what lab to use, we understand a few bands are left off of most western blots because of a vaccine that used to exist but doesn’t anymore. The most important question we as patients should be asking is about the Lymerix vaccine. We all know the vaccine isn’t available anymore, but hardly anyone has more than a vague idea of why. I’ll tell you why, it was making people sick. The FDA gave the manufacturer an ultimatum to either withdraw it or they would. It had absolutely nothing to do with low sales.

Lymerix gave people the same disease as “chronic Lyme” but it had no spirochetes. How is that possible? Why would some of the proteins from spirochetes make people *just as sick* as having actual spirochetes drilling through tissues?  And what does that say about the disease itself if one does not need spirochetes to get this, IDSA’s own “New Great Imitator”?

Neurologic manifestations of Lyme disease, the new “great imitator”

https://www.ncbi.nlm.nih.gov/pubmed/2682960



(That’s IDSA’s own journal, by the way, calling Lyme a “Neurological Great Imitator,” when we know that now IDSA says Lyme is only a temporary arthritis in a knee. Someone should let us know when joints become nerve tissue.)

The transcripts are still available online here:

https://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf

Okay, this is the single most important piece of information pertaining to Lyme that hardly anyone ever thinks twice about. The lymerix vaccine gave people the same disease, but there were no spirochetes.

The antigens of choice for the vaccine were ospA (band 31, but encoded on the same plasmid with OspB, band 34).  To validate a vaccine all you really need to show is that is causes antibody production and voila!  (BTW, FALSE, the vaccine should prevent the disease).  Just like that you have a viable product that you can inject into humans. These were the antigens of choice to force the vaccine receivers immune system to produce antibodies, hence they wouldn’t get sick from a tick bite.

STRANGELY, the idea behind the Lyme vaccines was that humans, when bitten by a tick, would inject their antibodies into the tick and kill all the spirochetes within the tick. In other words, people were to be turned into walking canisters of tick disinfectant. This was all, it turned out, to be part of the elaborate lie, a lie we have to explain to you because people with MD after their names don’t have the science background to investigate important matters like the number one disabling infectious disease in the United States.

But how and why did they get sick without spirochetes? Because ILADS says if you kill enough spirochetes then you will feel better? But you won’t be cured, and theres always potential to relapse so the goal is remission. Hmmmm…. Strange right?

The problem is that because Borrelia are Relapsing Fever germs they could never have been vaccinated against. Antigenic variation makes it impossible. Antigenic variation is also responsible for the wonky changes in western blot results. I won’t go any deeper than that in this post as the point is to keep this as simple to read as possible.

Okay, perhaps I could say one more simple thing. In 1983, Barbour and Burgdorfer showed the newly acquired plasmids – the small DNA, the antigenic variation (think of it as genes recombining within the small DNA in an unpredictable way) – probably come from bacteriophages:

https://www.ncbi.nlm.nih.gov/pubmed/6853449

In other words, how did the apparently new Borrelia acquire OspA, such that it could stick to the inside of the hard body of a hard bodied tick (“Ix-oh-deez” or Ixodes) and also chitinous tissue? Apparently it was DNA that was shuttled between some other organism in the ticks, such as mycoplasma or Brucella. Brucella is found in ticks and has something like OspA on it. Brucella is also known to cause lameness in animals and was used as an experimental bioweapon by the Japanese at Unit 731 in Manchuria. (Go ahead and Google that.)

This “vaccine”, that wasn’t actually a vaccine. It only allegedly tolerized against arthritis, which is probably what it does when used in animal vaccines. We know it does not prevent spirochetes, and never claimed to.

There are two types of Lyme. Two completely seperate disease outcomes. One is the CDC positive HLA-linked hypersensitivity response, lots of antibodies. Think autoimmune. Only about 15% of patients get this outcome and their only symptom is an arthritic knee. The other 85% of us, the chronic neurologic cases have no antibodies and get immune suppression with lots of symptoms. It suppresses the immune system, but the test is to measure an immune response. Opposite of autoimmune, as Beaux (badlymeattitude.com) says- *subimmune*. They threw the ELISA into the mix as a first step to rule all of *us* out in the first step.

We don’t test positive on the stupid test because it was designed to fail. It was designed to market a vaccine, not diagnose Lyme disease.

As it turns out, all credit to Kathleen Dickson’s background in Chemistry, we learned that  OspA is a triacylated lipoprotein. Or pam3cys. It is a fungal like antigen, managed by TLRs 1/2. Anything managed by TLR 1/2 is fungal. Don’t worry, I know how confused I was when I first encountered all those big words. I’ll explain.

A triacylated lipoprotein is very toxic to humans. Humans just can’t take fungi.
I pulled these pictures off of actionlyme.org and badlymeattitude.com. Notice the ratio of spirochetes to blebs!

Pam3C22

IMAGE ORIGINALLY FROM:


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC182019/pdf/aac00017-0141.pdf

Imagine an immune cell floating around inside of you and it has these little things poking out of it. The poky things are called Toll-like Receptors (TLR) and they all have numbers to differentiate. All the different numbers manage different kinds of antigens. So TLR 1/2 manage the fungal stuff, and thats how we know what OspA really is. So TLR 1 and 2, together, manage the fungal stuff, and that’s how we know what OspA really is. We also know from chemical analysis.

(Radolf, https://www.ncbi.nlm.nih.gov/pubmed/2318538 )

OspA is a triacylated lipoprotein, which is a TLR 1/2 agonist, which is exactly what it sounds like, bad. Without getting too technical, once an immune cell comes along and munches up OspA that little thing (with a BIG job) is toast. It will no longer recognize ANY pathogen and this is why we’ve heard that Lyme effects immunity. This is what cross tolerance is all about.

Here is a cute cartoon to help you get a better visual of how your immune system reacts to pathogens:

So now your immune system is broken, no longer able to fight or recognize germs the way it should. This is called immune tolerance. It eventually gets weak enough that all the latent viruses can (and DO) reactivate. This is EBV (mono, kissing disease) and other herpes, CMV and whatever else. Something like 90% of the population has been exposed to EBV by the time we are 10 years old. EBV is known as the *CANCER* virus. It’s a well known fact that it can give you Lymphomas and Leukemia’s since…. like forever. EBV likes to live inside of B cells. B cells are responsible for making antibodies. So this goes back to not testing positive as well, wonky B cells means wonky antibody response. Wonky antibody response means you can’t effectively fight pathogens.

Paul Durray said this about the CSF of Lyme victims- “These immunoblastoid cells in Bb infections at times resemble those found in Epstein-Barr virus infections..”

Here is the link so you can go and read yourself:
http://www.actionlyme.org/Duray.htm

So Lyme and EBV like to live in your lymph nodes, or germinal centers. Beaux helped me understand why this was important so I’ll just tell you what she told me. B cells are made in your bone marrow and they leave there to travel up to the lymphs to mature. They are still children when they leave the bone marrow, like a high school student. Think of the lymph nodes (germinal centers) as college. They go here to finish growing up and learning how to be adults and do their jobs. But since you have lyme and EBV living in your germinal centers the B cells can’t mature. We don’t know the exact MECHANISM, but we know that the shed blebs also contain DNA as well as Osps (NIH’s Dave Dorward): 
https://www.ncbi.nlm.nih.gov/pubmed/2482525
Cells are supposed to commit suicide when they know they’re infected, and this is why the EBV part is so important to understand.

Look up “EBV immortalized cell”, EBV inhibits aptosis. Aptosis is cell death and it is supposed to happen. Infected cells are supposed to commit suicide to stop the proliferation of germs in your body. EBV is sneaky and doesn’t let this happen. So you have a bunch of wonky B cells floating around that are tolerized and taken over. They can’t work the way they need to to keep you healthy. This is why we say Lyme gives you immune suppression, which leads to an AIDS/cancer like outcome, and antibiotics will NOT help this post sepsis outcome. The same thing happens when the immune cell tried to digest an Osp or a triacyl lipoprotein of any sort, not just from spirochetes. Lyme and LYMErix inhibit apoptosis of infected cells. Now imagine an immune cell in a lymph node is infected with latent (inactive) EBV and then gobbles up some Osps. They then become immortalized and the EBV can have a free for all. This is the main way we know Lyme is a Great Imitator. It unleashes EBV.

So to recap- Borrelia spirochetes bleb off their osp’s, ospA is pam3cys, immune cells munch them up and are then rendered broken. This creates a situation where you have cross tolerance to other pathogens, and that’s why we use the word AIDS to describe it. We know all of this because the Lymerix vaccine was made out of an Osp (A), and it somehow gave people the same disease without spirochetes.

I’ve heard it repeatedly on Facebook- people read that OspA is a fungal-like antigen and they assume they need an anti fungal drug to help them. No! It is a fungal-like antigen because of what TLR manages it. Taking anti-fungals won’t kill Ospa, as its just a protein that came off the spirochete. It’s no longer about killing spirochetes once this happens. There isn’t anything to take to fix this, at least that’s being prescribed by any doctors anywhere at this time. This is post sepsis syndrome. Your body turned off your immune system as a way to cope and survive, if it didn’t then you would’ve died.

It’s a new AIDS, and taking antibiotics and herbs or whatever is only going to kill the opportunistics that you’ve picked up and I believe that this is why patients initially feel better. Antibiotics nor anything else will ever fix this!!  The science says chemotherapy for lymphoma is probably the sanest remedy. Get rid of all the badly cloned B cells, the NIH has recommended PERHAPS stem cells when talking about the treatment for post-sepsis syndrome, and we think anti-virals should be added to keep EBV from coming back during the immunosuppression on Rituximab treatment.

This is all hypothetical.

This is why I have lost faith in ILADS, they don’t tell you how you sick you actually are. They know that lyme does this yet they fail to mention it. Why? Kathleen was the author of the Klempner rebuttal. They deliberately don’t talk about OspA because then they would be out of a job. I still can’t decide who’s worse, the Dearborn criminals or the punks at ILADS who prey on our desperation.

Everyone knew before the Dearborn stunt that Lyme was a permanent brain infection.

In all honesty the first time I encountered Beaux and Kathleen the first thing I asked them was “well how do we get better then?”. I was immediately met with being called selfish, and it took me a few weeks of reading to even begin to understand why I would be called selfish to inquire about how to heal. They seemed so smart and like they had all the answers, but this is the one question that they can’t answer. No one can. The NIH, Yale, Mayo, ILADS…. NO ONE knows how to fix post sepsis syndrome!! Certainly not when the disease mechanism is not even acknowledged. If it was, certain Lyme criminals would be in jail right now for trying to push LYMErix and falsifying the case definition at Dearborn to do it.

Prosecution has to come first, I hope this helped you understand. Otherwise only the rich will be able to get these theoretical treatments.  We have to prosecute the Lyme Cryme criminals if we want a chance to have access to treatments that might actually work.

I’ll write about that next.

 

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4 thoughts on “Let’s see if I can clear up some confusion.

    • A couple reasons. One being that it’s a relapsing fever germ, so it relapses and remits naturally. Another being that they could be in the 15% HLA hypersensitivity type group.

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