141129; Alright, This issue of WHAT IS THE TREATMENT keeps coming up, despite the number of times I say we are barely approaching what the disease even *is,* already. Note that I am taking all my clues from the NIH.
Allow me to start by reminding you that there is no National Institute of Immunosuppression and Infectious Disease, there is only a National Institute of ALLERGY (the opposite) and Infectious Disease. So, there is no National Institute of Immunosuppression Diseases despite the tens of millions of us with post sepsis, Lyme, CFIDS (4 million in the USA according to the NIH), GWI, vaccine brain damaged children (1:50, no numbers on the total), Fibro (8 million, according to the NIH), etc. I don’t know now many millions that is, but 20% of the population as disabled is fair and conservative guess-o-metrics.
When the country’s institutions fail, the country fails - Winston Churchill ...
"And with the hopes and powers will come dangers out of all proportion to the growth of man's intellect, to the strength of his character and to the efficacy of his institutions. Once more the choice is offered between Blessings and Cursings. Never was the answer that will be given harder to foretell." - Winston Churchill, 1932, Popular Mechanics, which is no longer respectable since they pulled the post-911-non-physics stunt re the collapse of WTC7, cute.
1) We know from the NIH that MS is barely distinguishable from chronic late neurologic Lyme and even CFIDS/ME/Fibro with the multiple bacterial/viral pathogens tolerance and cross-tolerance. And note that the NIH is pretty certain MS-Lyme is EBV, mainly (and similar herpes).
These records are all on my website and here in the Files section (of the OCCUPY the USDOJ Facebook group).
THE LINES ARE BLURRING between CFIDS and MS, according to the NIH
The “20 Reports” showing Post-Lyme (more accurately called post-LYMErix since that allows for people with other fungal exposures to be diagnosed with the same thing and also to pay tribute to Yale for effing up all of Western Medicine for 25 years all for vaccine royalties) and post-sepsis syndrome are the same, as is the mechanism whereby children are acquiring brain damage for life from the vaccines:
AND YOU ALL KNOW ALL ABOUT how there is no mab drug to reverse TLR2-agonist tolerance. That means once your immune system is ruined from the exposure to OspA like antigens, there is no mab drug to target the B cells that no longer detect anything aberrant about TLR2 agonist-bearers,… like *myco*plasma stuck to your red blood cells, inside other cells, hijacking sugar metabolism, mitochondrial machinery, and O2 tranfer across the red cell membrane (call it anemia without the low iron or hemoglobin), causing extreme fatigue... these mycos and similars, and whatever else you have been tolerized to from TLR2-agonist cross tolerance (Medvedev and Harding) will just grow right back. And you know all about how Lyme victims immune systems are just like old people’s
and how no one who is either old or has a weakened immune system should get any live, attenuated vaccines – since everyone says, so, even the flu vaccine manufacturers and the CDC.
[You all know this, since you have heard me say it and saw it all on ActionLyme for the last 10 years, right? It’s part of the fungal-viral synergy dynamic where A) as a result of being auto-vaccinated with LYMErix from spirochete blebbing, we know herpesviruses are reactivated; B) we know we get the same result from the failed fungal vaccines of this type for Tuberculosis (Tb)
, and how those Tb vaccine recipient experimentees ended up physiologically worse, and more susceptible to other infections; C) we have seen in the MMR damaged children - children who are not pre-screened for immune status (although they all are supposed to be according to the CDC)-, and we know all about how these vaccines have Thimerosal in them to prevent this mycoplasma/contamination because… the danger is in the children becoming immune suppressed and getting the viruses that cause brain damage, rather than the protection or the antibodies; D) we have seen the same thing in Gulf War Illness – hypervaccination plus exposure to immune suppressors of any type, and DEFINITELY DEET and nerve agent antidote; http://actionlyme.org/OCCUPY_GWI.htm ; E) and recently wustl dot edu and the NIH, themselves, recognize that post-sepsis patients remain chronically ill with reactivated herpesviruses, are neurologically and cognitively damaged, and have severe PTSD from a sense of “I felt like I was gonna die.” You can’t vaccinate with fungi and you can’t reverse what was done to the immune system as a result of fungi-damage (chronicTLR2/1 agonist damage).
[These are all verifiable facts/conditions, yet ILADS and the LDA do not address them at all. ILADS, being physicians and psychiatrists (which are not physicians, any more than a spirochete is a bacterium – spirochetes are their own phylum), are not analytical chemists and are not chemists at all. They never asked the first question, which was “What is OspA, since it caused the same systemic disease as Chronic Lyme?” And they, ILADS, never formally protested or complained in ANY courts about the falsified Dearborn case definition. FDA Regulations, what “molecular structure/function means” (despite the fact that the whole world knows chemists speak in structures for the very purpose of predicting molecular function), and Clinical Trials Regulations are not the bailiwick of the average physician. In America, the way drugs are regulated is by class action lawsuit. And in America, the Senators have to ORDER the Office of Budget and Management to ORDER the FDA to do their jobs and assure that whoever claims a product or method (in this case, the testing for Lyme disease or the Dearborn Method), especially as re any “guidelines” or products, the testing has to be validated according to the FDA’s own “Guidelines on Bioanalytical Validations.” Dearborn wasn’t. Yale’s flagellin method, US Patent 5,618,533 is the only one that is FDA-valid because it detects most cases, satisfying the ACCURACY criterion, and is the first antibody band to show up, detects late, neurologic and arthritic Lyme, and satisfies the SPECIFIC criterion to Borrelia burgdorferi. Therefore, the way to detect Borreliosis in America is to use recombinant specific flagellins to ALL the Borreliae in America, like hermsii, Barbour’s lonestari, Master’s disease, miyamotoi, pizzapii, gimmeabreakii, timetocuttheshitii and prosecuteyalii.
[And this is all in addition to IDSA only now starting to cave on the fact that spirochetes are permanent brain infections largely because they are the authors of 20 such reports and referenced reports on the viability of the spheroplast forms, all along, and
to avoid the bigger issue of what LYMErix and Dearborn did/were – both criminally chargeable as negligent homicide with no Statute of Limitations. ILADS, IDSA, and the CDC will not be able to tell you how to reverse those 6 similar conditions because they’re either stupid or they’re liars. ONLY the NIH is reasonable on the actual science.]
2) We know from the NIH that in Chronic Lyme, CFIDS, etc., you have a condition of HUMORAL immunosuppression (no antibodies in the blood), but with chronic inflammation in the brain. They SAY, we have a reverse hyperimmunity thing going on: immunosuppression in the blood, with chronic immune activation in the brain, is what the NIH says is the result of exposure to OspA and other Borrelial fungal blebs.
And I am CERTAIN, because youz would never consider asking me this over and over again, despite the number of times I answered it, and even made it into a special report on my homepage now:
“141119; For People Interested in what the NIH thinks about treatments for Chronic Active Lyme/Epstein-Barr Etc/Chronic Fatigue Syndrome, which are all basically reactivated herpesviruses with fungal antigen-induced immunosuppression...:
…that you all actually looked at that data and saw for yourselves what the NIH has said and reviewed and suggested on treatments for chronic active EBV as shown (AGAIN) here, which is why you are not bothering to ask me again:
"Optimal Treatment for Chronic Active Epstein-Barr Virus Disease"
"Epstein-Barr virus (EBV) is a ubiquitous virus that infects...
"Most patients with CAEBV present with fever, liver dysfunction, and splenomegaly. About half of patients have lymphadenopathy, thrombocytopenia, and anemia (3). Other frequent symptoms (occurring in 20–40% of patients) include hypersensitivity to mosquito bites, rash, hemophagocytic syndrome, and coronary artery aneurysms. Less common features are calcification of basal ganglia, oral ulcers, lymphoma, interstitial pneumonia, and central nervous system disease. The presence of thromobocytopenia, onset at age 8 or older, and infection of T cells with EBV was associated with a poorer prognosis (5). Death is frequently due to liver failure, malignant lymphoma, or opportunitistic infections.
"Characterization and treatment of chronic active Epstein-Barr virus disease: a 28-year experience in the United States." NIH AGAIN >> http://www.ncbi.nlm.nih.gov/pubmed/21454450
“Although patients with CAEBV from Japan have normal or increased numbers of NK cells, many of our patients had reduced NK-cell numbers. Although immunosuppressive agents, rituximab, autologous cytotoxic T cells, or cytotoxic chemotherapy often resulted in short-term remissions, they were not curative. Hematopoietic stem cell transplantation was often curative for CAEBV, even in patients with active lymphoproliferative disease that was unresponsive to chemotherapy. These studies are registered at http://www.clinicaltrials.gov as NCT00032513 for CAEBV, NCT00062868 and NCT00058812 for EBV-specific T-cell studies, and NCT00578539 for the hematopoietic stem cell transplantation protocol.”
I am 200% certain that you all read the full text of those 2 reports ^^ above and the other reports linked within that 141119 report on what the NIH thinks about the treatment of chronic active EBV and post-sepsis reactivated herpesviruses. About the stem cells and the EBV-specific drugs and the EBV-specific pharmed T cells and whatnot.
There is more; there is “alemtuzumab plus anti-virals” for post-transplant patients (use Pubmed, you just go there and enter the search terms, seriously, without the quotes, and then hit the search button like this:
and tie your shoes…)
who because of their immunosuppressive drug treatment often have to deal with reactivated herpesviruses. This seems to me to be the first course of action since these drugs already exist- but be careful not to go too far and paradoxically reactive herpes again. However, without a synergy of the DATA – including all of the crooks’ data received via a prosecution on how LYMErix failed and whatever else they’re not publishing which would certainly help give us insight – how do we free everyone to treat anything? Insurance companies being inherently part of the Lyme RICO from the beginning and who work closely with their soon-to-be-former-$500,000-a-year-salaried CDC officer “advisors,” like for Kaiser-Permanente, have a choke hold on progress and science, and the legislators are brainless, which is why we are going to OCCUPY the USDOJ
John J. Connolly, one of the founding “entrepreneurial trio” members of the ALDF.com (the other 3 being Wormser, McSweegan and Durland Fish) invited Kaiser-Permanente into the financially-floundering-under-his-leadership New York Medical College to give tuition kickbacks to Kaiser drones and they have been there ever since, writing physician training protocols. No one in the entire world seems to have any problem with Kaiser-Permanente taking over MD training. Me, I think it would be in Kaiser’s interest to say, “There are no diseases unless there are vaccines for them, and oh, if your child was vaccine injured, we’re calling the CPS since you poisoned them How the hell is CPS going to know? They couldn’t think or even read the map to find their way out of a 3 sided box, ha, ha, ha, we got every base covered…”
Regardless, you know what I mean. Without some controlled clinical trial, everyone would fuss about treating anything. This where we are. We have ONLY the patients protesting over the science, over Dearborn, over LYMErix, over the other mechanisms of disease in the other abused groups, etc., and the NIH who agrees with us. But how would any “physicians” know the NIH agrees with us? They don’t read. They just think up charging schemes: “$1500 per initial office visit, CASH ONLY, $250 for 15 minute appointments thereafter and if you fail to have the coinfections I make up as I go along, I will release you as a patient, thanks and no problem, just get a third mortgage if I’ve already run through your second I love my Mercedes ”
Unless you get a diagnosis of MS. With MS, it’s kind of a free-for all. You can get whatever you want. Stem cells, Rituximab, anti-virals, whatever. And you can get approved for SSD in 6 weeks No hassle, no bullshit, a validation of your chronic illness, and you can tell all your asshole “relatives” and “friends” to kindly eat your shorts, “Oh and wash them all too, and clean the house and walk the dogs and do the shopping…” :)
But there is no mab drug to reverse TLR2-agonist tolerance. You ought to all relapse no matter what you call this disease or what treatments you can get for chronic active EBV.
More on POST West Nile (182 citations) causing chronic long term illness like ours:
Other data on Post-Sepsis Syndrome:
Hospitals Take On Post-ICU Syndrome, Helping Patients Recover
“Especially at Risk Are Those Who Treated for Sepsis and Who Experience 'ICU Delirium'
“Hospitals are doing more to help the growing number of patients who receive treatment for serious illness in the intensive-care unit—only to find their release is the start of a whole new set of problems.
“With medical advances, even the sickest patients now often survive potentially life-threatening conditions after a stay in intensive care. Many experience aftereffects, not only of the illness but also of the very medical care that may have saved their lives.
“Doctors call it "post-intensive care syndrome" and say it is becoming more common. In the ICU, patients may be heavily sedated and hooked up to a ventilator, keeping them immobile, breathing and free of pain. But they can develop a temporary brain injury known as "ICU delirium," that is linked to later problems with memory and thinking. As many as 80% of ICU survivors have some form of cognitive or brain dysfunction, according to the Society of Critical Care Medicine, and some never recover. Many experience post-traumatic stress symptoms, depression, fatigue and prolonged muscle weakness….
2004, jus sayin on this next one – think of all the millions of lives not ruined because we got rid of Yale’s non-vaccine, LYMErix with our campaign from 1999 to 2002 when the FDA issued Yale an ultimatum to remove LYMErix or the FDA would order it off themselves…
The chronic consequences of severe sepsis
“THE CHRONICITY OF SEVERE ACTUE INFLAMMATION AND SUBSEQUENT CLINICAL COMPLICATIONS
“The above clinical data support the view that a number of long-term consequences are associated with surviving severe sepsis. It is interesting that this is not the only clinical example of acute inflammation subsequently interphasing with chronic inflammatory disorders. As shown in Table 1 , there are a number of clinical instances whereby an initial severe acute inflammatory event has been associated with distal chronic complications. Pediatricians who deal with severe acute RSV infections in very young children are clearly mindful of the longer term but ill-understood clinical complications, which these children have in dealing with severe chronic asthma. Transplant surgeons are aware of the problems that place a solid organ transplant at long-term risk if during the initial surgery, the donor organ has severe acute ischemia reperfusion injury. Burn and trauma physicians are cognizant of the patients who recover from the acute and severe inflammatory events of burn injury yet are susceptible to chronic clinical complications later in life. One of the uniting themes of the above clinical examples is that there appears to be a correlation with the severity of the initial acute inflammatory event that caused alterations in the innate and/or acquired immune system, which is manifested for not only months but often years after the initial severe insult. The mechanism(s) that are responsible for the chronic consequences of severe acute inflammation are presently not well understood; however, incriminating factors likely include alterations in the normal levels and activity of chemokines, cytokines, Toll-like receptors (TLRs), and dendritic cells (DCs).”
22 articles cite the one above in pubmed:
Here are 2:
Epigenetic regulation of immune cell functions during post-septic immunosuppression.
“Studies in humans and animal models indicate that profound immunosuppression is one of the chronic consequences of severe sepsis. This immune dysfunction encompasses deficiencies in activation of cells in both the myeloid and lymphoid cell lineages. As a result, survivors of severe sepsis are at risk of succumbing to infections perpetrated by opportunistic pathogens that are normally controlled by a fully functioning immune system. Recent studies have indicated that epigenetic mechanisms may be one driving force behind this immunosuppression, through suppression of proinflammatory gene production and subsequent immune cell activation, proliferation and effector function. A better understanding of epigenetics and post-septic immunosuppression can improve our diagnostic tools and may be an important potential source of novel molecular targets for new therapies. This review will discuss important pathways of immune cell activation affected by severe sepsis, and highlight pathways of epigenetic regulation that may be involved in post-septic immunosuppression.”
Reversal of long-term sepsis-induced immunosuppression by dendritic cells.
“Severe sepsis leads to long-term systemic and local immunosuppression, which is the cause of a number of complications, including pulmonary infection. A therapeutic strategy that reverses this immunosuppression is required, given the ongoing high mortality rate of patients who have survived a severe sepsis. The present study demonstrates that experimental severe sepsis renders the lung susceptible to a normally innocuous Aspergillus fumigatus fungus challenge, due to a dominant lung type 2 cytokine profile. Dendritic cells (DCs) obtained from the lungs of mice subjected to cecal ligation and puncture (CLP) model were skewed toward type 2 cytokine profile, which occurred with exaggerated expression of Toll-like receptor 2 (TLR2). The intrapulmonary transfer of bone marrow-derived DCs (BMDCs) in postseptic mice prevented fatal Aspergillus infection. This therapy reduced the overall inflammatory response and fungal growth in the lung, and promoted the balance of proinflammatory and suppressive cytokines in the lung. Thus, intrapulmonary DC supplementation appears to restore the pulmonary host response in the postseptic lung in our animal model. These data strongly suggest that lung DCs are profoundly affected as a consequence of the systemic impact of severe sepsis, and the identification of mechanisms that restore their function may serve as a key strategy to reverse sepsis-induced immunosuppression.
#### The Yale/ALDF Lyme crooks try to say Lyme is a simple bacterial infection (see the PRIMERS SHELL GAME),
http://actionlyme.org/PRIMERSHELLGAME.htm when it fact it is a fungal-antigen-deploying-spirochete that can survive any condition, you can even get them from cadavers, freeze them for decades, and that it is in its own archaic PHYLUM of organisms. It's a "stealth pathogen." <<< That is a FORMAL definition that comes from the Department of Defense and the Department of Energy at Brookhaven. http://www.actionlyme.org/JohnDunn_Brookhaven.htm
That means *** DON'T EXPECT ANTIBODIES *** ####
3) We know that chronic fatigue from mycoplasma in the blood - for which there will be no antibodies-, is something for which there is no treatment now. That is mainly the fault of Yale for lying about Lyme and LYMErix. They have SAID - and by that I mean SHAPIRO and SIGAL, specifically (PBS Life on Earth Series)
http://web.archive.org/web/20091025073535/http://geocities.com/kmdickson0308/1-4.txt ) -, that you cannot have a disease without classical inflammation (HLA-linked autoimmunity or hypersensitivity with the lots and lots of antibodies and autoreactive T cells).
The CDC also lied about this mycoplasma-in-the-blood-causing-chronic-fatigue by centrifuging all the cells out, to which mycoplasma adhere, in order to falsely claim mycoplasma are not involved in Chronic Fatigue:
LOOK CLOSELY AT THIS REPORT BY THE CDC; They THROW OUT (centrifuge out) the whole blood cells to which the mycoplasma adhere and invade - causing fatigue by changing the osmotic potential of the cell dis-allowing Oxygen to transfer, hijacking energy metabolism, etc., causing systemic fatigue:
Absence of Mycoplasma species DNA in chronic fatigue syndrome
Recently IDSA held a conference for which they had a speaker whose lecture title was: WHY ARE THERE NO VACCINES AGAINST ANY FUNGAL DISEASES? (Welcome to 1999 when we were asking the same thing re the other failed lipoprotein/fungal vaccines like Tb? Why’d Yale pick a lipoprotein, we said – they never worked…)
4) And we know from my recent re-reporting which I am sure you all read, that the NIH proposed this, this summer:
"Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS). Neither the antigenic target(s) nor the cell population(s) responsible for CNS tissue destruction in MS have been fully defined. The objective of this study was to simultaneously determine the antigen (Ag)-specificity and phenotype of un-manipulated intrathecal CD4+ and CD8+ T cells of patients with relapsing-remitting and progressive MS compared to subjects with other inflammatory neurological diseases. We applied a novel Ag-recognition assay based on co-cultures of freshly obtained cerebrospinal fluid T cells and autologous dendritic cells pre-loaded with complex candidate Ag's. We observed comparably low T cell responses to complex auto-Ag's including human myelin, brain homogenate, and cell lysates of apoptotically modified oligodendroglial and neuronal cells in all cohorts and both compartments. Conversely, we detected a strong intrathecal enrichment of Epstein-Barr virus- and human herpes virus 6-specific (but not cytomegalovirus-specific) reactivities of the Th1-phenotype throughout all patients. Qualitatively, the intrathecal enrichment of herpes virus reactivities was more pronounced in MS patients. This enrichment was completely reversed by long-term treatment with the IL-2 modulating antibody daclizumab, which strongly inhibits MS disease activity. Finally, we observed a striking discrepancy between diminished intrathecal T cell proliferation and enhanced cytokine production of herpes virus-specific T cells among progressive MS patients, consistent with the phenotype of terminally differentiated cells. The data suggest that intrathecal administration of novel therapeutic agents targeting immune cells outside of the proliferation cycle may be necessary to effectively eliminate intrathecal inflammation in progressive MS."
(PubMed ID 25148387}
So, what is the NIH saying?
Anti-virals + mabs + something like intrathecal delivery of of the disease-modifying anti-IL-2 mab, stem cells, anti-EBV T cells, etc., while Anthony Fauci in his IL-2 patent, proposes this very amazing thing:
5) "FIELD OF THE INVENTION (5,696,079)
"The present invention pertains to a method for activating the immune system of a patient by intermittently administering interleukin-2 (IL-2) to that patient. Such administration of IL-2 can optionally be combined with other therapies, such as anti-retroviral, anti-bacterial or anti-fungal therapies, suitable for treatment of the patient's condition. This invention also relates to an approach to gene therapy that entails administering IL-2 to a patient so as to facilitate in situ lymphocyte transduction by a retroviral vector also administered to the patient.
"BACKGROUND OF THE INVENTION
"....*** Illustrative of specific disease states in treatment of which the present invention can be applied are HIV infection and other diseases characterized by a decrease of T-cell immunity, for example, mycobacterial infections like tuberculosis and fungal infections such as cryptococcal disease. This method also can be used in the treatment of secondary infections that occur in patients with suppressed immune systems, such as the opportunistic infections that occur in AIDS patients. ...*** "
Fauci says give HUMORAL IL-2 for people with wimpy immune systems or fungal-disease victims, while the NIH's newer article says to deliver anti-IL2 antibodies (mabs) into your spinal fluid to temper the hyper-immune response going on in your CNS.
Nobody knows right?
BTW, what’s ILADS treating? I guess I mean, what are they DOING? Since 2001 when I blew the whistle on Dearborn at the FDA and mentioned this immunosuppression business in that same report, when has ILADS ever protested this bullshit in a formal platform?
N E V E R.
141129, KMDickson, ActionLyme.org