Friday, October 23, 2015

LYME the FACTS


How obvious is it that the very definition or type of "Lyme disease" that was EXCLUDED by the Dearborn "two-tiered" case definition is the one caused by the OspA fungus vaccine (Chronic Neurologic)? Lyme was never about arthritis and neither was LYMErix.
NINDS’ MS-Lyme Group, talking about how the TLR2/1 agonists like Pam3Cys or OspA delivered on blebs (shed by the spirochetes) or OspA vaccination inflames the brain while causing humoral immunosuppression:
”The spirochete Borrelia burgdorferi is the agent of Lyme disease, which causes central nervous system manifestations in up to 20% of patients. We investigated the response of human brain microglial cells, glial progenitors, neurons, astrocytes, as well as peripheral blood monocytes to stimulation with B. burgdorferi. We used oligoarrays to detect changes in the expression of genes important for shaping adaptive and innate immune responses. We found that stimulation with B. burgdorferi lysate increased the expression of Toll-like receptors (TLRs) 1 and 2 in all cell types except neurons. However, despite similarities in global gene profiles of monocytes and microglia, only microglial cells responded to the stimulation with a robust increase in HLA-DR, HLA-DQ, and also coexpressed CD11-c, a dendritic cell marker. In contrast, a large number of HLA-related molecules were repressed at both the RNA and the protein levels in stimulated monocytes, whereas secretion of IL-10 and TNF-alpha was strongly induced. These results show that signaling through TLR1/2 in response to B. burgdorferi can elicit opposite immunoregulatory effects in blood and in brain immune cells, which could play a role in the different susceptibility of these compartments to infection.”
http://www.ncbi.nlm.nih.gov/pubmed/16783164
NIH in a patent saying these OspA-ish, TLR2/1 agonist, fungal triacyl lipopeptides like LYMErix are delivered to the brain as blebs or exosomes (just like OspA as a vaccine would):
"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."
http://patft.uspto.gov/netacgi/nph-Parser…

BEN LUFT at the 1998 FDA meeting saying LYMErix causes the same disease as chronic neurologic Lyme:
"The point that I wanted to make in regard to the study is that there is very heavy dependence on serologic confirmation. And when we start thinking about the adverse events, *** it was stated originally when we got the overview of the disease that the disease is really quite protean. And actually the adverse events are very similar to what the disease manifestations are.**** And if you start to, as I think Dr. Hall was eluding to -- if you start to kind of say well how often do you actually become seropositive, you can start to have a different take on when someone has an adverse event or whether it is disease specific or infection specific versus vaccine specific. And I think that that is an important issue that we have to deal with. ..."http://www.fda.gov/ohrms/dockets/ac/98/transcpt/3422t1.rtf

CADAVID on shed blebs with OspA on them travel to the brain to inflame it:
”The current view is that bacteria need to enter the brain to cause inflammation. However, in mice infected with the spirochete Borrelia turicatae, we observed widespread cerebral inflammation despite a paucity of spirochetes in the brain parenchyma at times of high bacteremia. Here we studied the possibility that bacterial lipoproteins may be capable of disseminating from the periphery across the blood-brain barrier to inflame the brain. For this we injected normal and infected mice intraperitoneally with lanthanide-labeled variable outer membrane lipoproteins of B. turicatae and measured their localization in blood, various peripheral organs, and whole and capillary-depleted brain protein extracts at various times. Lanthanide-labeled nonlipidated lipoproteins of B. turicatae and mouse albumin were used as controls. Brain inflammation was measured by TaqMan RT-PCR amplification of genes known to be up-regulated in response to borrelial infection. The results showed that the two lipoproteins we studied, LVsp1 and LVsp2, were capable of inflaming the brain after intraperitoneal injection to different degrees: LVsp1 was better than LVsp2 and Bt1 spirochetes at moving from blood to brain. The dissemination of LVsp1 from the periphery to the brain occurred under normal conditions and significantly increased with infection. In contrast, LVsp2 disseminated better to peripheral organs. We conclude that some bacterial lipoproteins can disseminate from the periphery to inflame the brain.”
http://www.ncbi.nlm.nih.gov/pubmed/20431027
Lyme criminals Dave Persing and Robert Schoen say in their RICO patent that you can’t tell the difference between “multisystem,” “protean” LYMErix outcomes from chronic neurologic Lyme:
"Additional uncertainty may arise if the vaccines are not completely protective; vaccinated patients with multisystem complaints characteristic of later presentations of Lyme disease may be difficult to distinguish from patients with vaccine failure....
http://patft1.uspto.gov/netacgi/nph-Parser…
Latov on how LYMErix causes the same disease as chronic neurologic Lyme:
”Neurological syndromes that follow vaccination or infection are often attributed to autoimmune mechanisms. We report six patients who developed neuropathy or cognitive impairment, within several days to 2 months, following vaccination with the OspA antigen of Borrelia burgdorferi. Two of the patients developed cognitive impairment, one chronic inflammatory demyelinating polyneuropathy (CIDP), one multifocal motor neuropathy, one both cognitive impairment and CIDP, and one cognitive impairment and sensory axonal neuropathy. The patients with cognitive impairment had T2 hyperintense white matter lesions on magnetic resonance imaging. The similarity between the neurological sequelae observed in the OspA-vaccinated patients and those with chronic Lyme disease suggests a possible role for immune mechanisms in some of the manifestations of chronic Lyme disease that are resistant to antibiotic treatment.”
http://www.ncbi.nlm.nih.gov/pubmed/15363064
Marks, one of the OspA trial administrators on how OspA vaccination causes the same disease we know of as chronic neurologic Lyme:
”A wide range of neurological complications have been reported via the medical literature and the VAERS system after vaccination with recombinant outer surface protein A (OspA) of Borrelia. To explore this issue, 24 patients reporting neurological adverse events (AE) after vaccination with Lymerix, out of a group of 94 patients reporting adverse events after Lymerix vaccination, were examined for causation. Five reports of cerebral ischemia, two transient Ischemic attacks, five demyelinating events, two optic neuritis, two reports of transverse myelitis, and one non-specific demyelinating condition are evaluated in this paper. Caution is raised on not actively looking for neurologic AE, and for not considering causation when the incidence rate is too low to raise a calculable difference to natural occurrence.”
http://www.ncbi.nlm.nih.gov/pubmed/21673416
But no "doctor" in America or anyone in the entire hhs.gov knows what Lyme or OspA is. Seriously. Think about it. What is ILADS treating if injecting people with the fungal toxin LYMErix causes the same chronic neurologic disease?
Lyme is a do-over of Tuskegee "Bad Blood." The only "case" you are allowed to have it the one that does not need to be treated: Autoimmune arthritis. This is what is alleged by the CDC and Yale. But in the end all they did was expose the mechanism of the Autism pandemic- fungal antigen induced immunosuppression in the presence of live viruses (or latent ones, in the case of Lyme and CFIDS).
So, a vaccine, they, Yale and the CDC, wanted for a disease that causes no disease. Turns out that was the disease - OspA induced post-sepsis; fungal toxin induced post-sepsis with the reactivated viruses etc of all kinds. Something seen in parallel in so many other circumstances: Burkitt's Lymphoma, Vaccine Autism, the failed Tuberculosis vaccines, CFIDS,... The fact that one infection helps establish another is so well known, doctors give children antibiotics for a cold because that treatment was intended to prevent the secondary bacterial infections that cause otitis.
J Neuropathol Exp Neurol. 2006 Jun;65(6):540-8. Comparative Study; Research Support, N.I.H.,…
NCBI.NLM.NIH.GOV|BY CASSIANI-INGONI R , ET AL.

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