Birthdaysuit,
 
I was told all about Lyme, Osp31A, and was told that it would take me years to get better.  Doctors also wanted thousands of dollars for treatment and supplements.  Then I sent a sample to Gordo and he saw nothing in the blood.  I don't really believe in conspiracies.  Why would anyone want to suppress the Lyme epidemic?  Why is there so much confusion over this?
 
Within 2 days Gordo let me know that there was nothing there.  How hard is it for these labs to confirm or deny the presence of Spirochetes in the blood?  What does Western Blot and IGenex have that Gordo doesn't?  Are most tests looking for antibodies and not the spirochetes themselves?  Why is this such a clusterfuck?
 
I was recently (Tuesday of this week) diagnosed with SIBO and put on the antibiotic Xifaxan, 550mg 3x daily.  I feel slightly better after only one day, but I don't want to jump to any conclusions.  The problem with feeling like garbage is it could be a million things, and it seems none of the doctors want to work with us to figure it out.  I'm currently in Boston getting treatment from Beth Israel Medical Center, affiliated with Harvard.  I had this appointment for 6 months and wanted to keep it, even though further workups are being done in Chicago.
 
Endocrinologist also said my blood sugar is going down to low 40s when I'm sleeping.  She can't figure it out, and says she wants me to get more follow-up testing.
Hi, Brainfogboy
The 700+ studies on the peresistence of Borrelia Burgdorferi, many of which were written by the NIH and CDC as well as the current antibiotics in vitro only killing a sml. percentage of viable cells, in the case of doxycycline the most frequently prescribed increasing cytic forms of borrelia 200%, whilst killing less than 35% of viable cells in VITRO, it seems obvious that Borrelia Burgdorferi persists. Keep in mind after dearborn the CDC officals have stated that even if you had Borrelia in serum it would not peresist and your body would clear it. So, there's no evidence that the current IDSA guidelines erradicate Borrelia Burgdorferi, let alone kill all of its forms. Symptoms do improve, and spirochetal load plays a big role in an asymptomatic stage but relapse is all too common. However, the idea that once you finish the IDSA's strict guidelines, despite continuing symptoms, i.e. neurological and CNS problems your free of Borrelia is not rooted in science. Also, Beth Israel Medical Center does not really believe in chronic Lyme.
I had my blood tested twice by my UNI. The first blood test was positive. Spirochetes were clearly visible under darkfield microscopy, the 2nd was negative. I also had a tissue biopsy which discovered spirochetes. This was awhile back so I'm not sure how'd I test now. Considering I've been on antibiotics for awhile including Cell-wall inhibitors, It would most likely be negative in serum. Borrelia is not really a blood infection, although it can causees sepsis due to OspA 31. it uses serum to transport. It is mostly a tissue, bone and joint infection.
So, yes Serum is not really an accurate indicator of Lyme infection, although if you can see spirochetes, you have some sort of spirochetal infection. ELISA does not test as many strains as IgeneX does, nor does it test for band 23 and other speific Lyme bands. Keep in mind there are 100 Strains of borrelia in the US, most of which do not show up on diagnostic testing. Though, if you test for multiple bands on IgeneX western blot, say 41, and 31 as positives and have clnical symptoms of Lyme which isn't so cut and dry, you probably still have an active infection. One should not be testing positive on the IgM with fluctuating biomarkers for bands, if they are negative, especially if they have Lyme like symptoms. The problem is the immunosupression of Lyme which makes it nearly impossible to test positive in the case of a desseminated CNS infection.. Hence, why ELISA and IgeneX Western Blots were never meant for diagnostics testing, rather for surveilance purposes.
People conspire everyday. Conspiracies are an everyday occurance, whether big or small. The emotionally mature and fun thing to do with modern technology is own diseases and then say no one can have them, this is essentially what certain Lyme organizations wanted to do. Why is the Lyme debate so polzarized you might ask, well you have to go back to dearborn case definition. I'll explain it in brief and in terms that make sense. If you want later I can post sudies.
The testing for Lyme disease was falsified to pass off fake vaccines and test kits, sounds crazy right?
There are primarily 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 as “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.
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. That isn't to say that spirochetes do not cause problems, howeve rthis is a multi-dimensional infection.
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.
Study:
"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.“
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.
https://www.ncbi.nlm.../pubmed/1634816
In short Pam3Cys OspA 31 causes immunosuppression. This kind of damage is not fixed by removing the source of exposure. Killing spirochetes that shed or bleb OspA won’t reverse these kinds of changes to germinal centers (lymph nodes). What “Lyme” patients are left with is a B cell AIDS-like outcome and reactivated viruses and a mixed bag of opportunistic pathogens that cause everything the sun from cancer to dementia to that bone crushing fatigue. So too, do these re-activated and secondary viral, fungal and bacterial infections of all kinds take over the show as your immune system can no longer recognize other pathogens. Creating the perfect stealth pathogen producing no antibodies, a Hellstorm known as the "Great Imitator" ALS, MS, parkinsons, dementia, lupus, rheumatoid arthritis, chronic fatigue syndrome, fibromyalgia, stroke, cancer, etc.. Spirochetes themselves are not the only problem, it's the AIDS like outcome where all the secondary infections are wrecking havoc.
As for the Lymerix vaccine and the CDC officers and others who were involved in the commercialization of OspA (ALDF, Mayo Clinic, Yale’s L2 Diagnostics, Corixa, Imugen, SmithKline) knew all of this during (and likely prior to) the phase I and II trials of the OspA “vaccine” patented by Yale University (5,747,294).
CDC officer Barbara Johnson owns five patents with SmithKline, the manufacturer of LYMErix. One of her patents from 1992-93 explains that there are two distinct outcomes of OspA exposure: one being an HLA-linked (genetic) hypersensitivity, or allergic, arthritic knee response (15%), and the other being the post-sepsis immunosuppression response (85%) that patients refer to as “chronic Lyme.”
Allen Steere, in 1992-93, published research in Europe in which he 1) developed fraudulent diagnostic testing that left out OspA and OspB despite those being highly immunogenic, primary diagnostic antigens; and 2) added an ELISA to be used as a “screening” test, to exclude the neurologic, or immunosuppression cases from diagnosis. This was in direct opposition to his own 1986 research which was the basis for the original,1990 case definition, and also stated that only Western blot band 41 (flagellin) was necessary to diagnose Lyme borreliosis.
In 1994 the CDC, led by Barbara Johnson, held a conference in Dearborn, Michigan, in which they changed the disease definition (“case definition”) to include ONLY the 15% arthritis cases who otherwise are not sick. The diagnostic standard was changed from one that reflected the persistence of spirochetes and their variable surface antigens (few, changing antibodies based on Steere’s 1986 report), to one that reflects only the hypersensitivity response, or the production of many antibodies, using Steere’s fraudulent ELISA. The labs that were invited to participate did not agree with the change, and reported an average accuracy rate of 15%. This “two-tier” testing protocol is still the only testing accepted by the CDC, insurance industry and medical societies, despite not meeting FDA standards for method validation (specificity, sensitivity, etc.).
Yale, in addition to owning the LYMErix (OspA “vaccine”) patent, owns the patent for the only VALID test method for diagnosing “Lyme disease” (5,618,533), a flagellin method as previously indicated by Steere as valid. They did not use their own test method to assess the outcomes of the LYMErix trials. Instead, the new, falsified Dearborn method was used, and adverse events (immunosuppression outcomes) were discarded.
Dave Persing (Mayo) owns a patent (6,045,804) for testing based on Steere’s European research in which the OspA-B antigens were left out. The patent is described as a method for distinguishing OspA vaccine recipients from OspA tick bite victims. Once LYMErix was on the market, a strain of borrelia that did not have the vaccine antigens in it would have to be used. Vaccine efficacy is never assessed with the very same antigen as the vaccine antigen. Otherwise, it would not be known if the victim has the actual infection in question, or that the antibody that shows up came from the vaccine. Had LYMErix stayed on the market, this test method would have created a monopoly on Lyme disease testing in North America, with Corixa (Persing) Imugen, and L2 Diagnostics (Yale/Robert Schoen) being the only labs licensed to test for Lyme. These entities were listed with the SEC as formal partners and advertised as such. With all tick-borne disease blood samples being processed through only these three labs, they would have had sole access to whatever other tick-borne pathogens could be identified and then commercialized as additional “vaccines” and test kits.
I'm sorry if this was hard to understand. Duckduckgo, Lymecryme or Lyme crinimal charges sheets. If you have questions just message me.
Edited by birthdaysuit, 15 September 2017 - 05:53 AM.
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