See the Big Picture (Autism vaccines = kids getting the viruses, says the CDC and Big Pharma)

The brain damage epidemic of Autism has to do with the babies actually GETTING those brain-damaging, neurotropic viruses.  SEE THE BIG PICTURE!!!

THERE IS *NO* NIIID, there is only the opposite, ALLERGY:



THIS IS PAUL AUWAERTER, the one who trashes Lyme victims as psychiatric, and who lists on his website that his expertise is in Lyme and Epstein-Barr. Here is is talking about pediatric vaccines given to children who are immunosuppressed and how that results in reactivated vaccine viruses. So, the theory we had, that GWI, ME/CFS, and Lyme victims are trashed because the mechanism of illness betrays the AUTISM PANDEMIC is correct.
And BTW the stupid rich Lyme activists of Greenwich give all kinds of money to Johns Hopkins to continue to calls us psychiatric.

(Also, one has to ask if Lyme reactivates our vaccine viruses, too, since there is also more data on that too, when you study reversion to wild type data – they’re saying everyone basically has a mild form of the vaccine viruses-“disease”.)

“To understand the molecular determinants of measles virus (MV) virulence, we have used the SCID-hu thymus/liver xenograft model (SCID-hu thy/liv) in which in vivo MV virulence phenotypes are faithfully duplicated. Stromal epithelial and monocytic cells are infected by MV in thymus implants, and virulent strains induce massive thymocyte apoptosis, although thymocytes are not infected. To determine whether passage of an avirulent vaccine strain in human tissue increases virulence, we studied a virus isolated from thymic tissue 90 days after infection with the vaccine strain Moraten (pMor-1) and a virus isolated from an immunodeficient child with progressive vaccine-induced disease (Hu2). These viruses were compared to a minimally passaged wild-type Edmonston strain (Ed-wt) and the vaccine strain Moraten. pMor-1, Hu2, and Ed-wt displayed virulent phenotypes in thymic implants, with high levels of virus being detected by 3 days after infection (105.2, 102.8, and 103.4, respectively) and maximal levels being detected between 7 and 14 days after infection. In contrast, Moraten required over 14 days to grow to detectable levels. pMor-1 produced the highest levels of virus throughout infection, suggesting thymic adaptation of this strain. Similar to other virulent strains, Ed-wt, Hu2, and pMor-1 caused a decrease in the number of viable thymocytes as assessed by trypan blue exclusion and fluorescence-activated cell sorter analysis. Thymic architecture was also disrupted by these strains. Sequence analysis of the hemagglutinin (H) and matrix (M) genes showed no common changes in Hu2 and pMor-1. M sequences were identical in pMor-1 and Mor and varied in H at amino acid 469 (threonine to alanine), a position near the base of propeller 4 in the propeller blade/stem model of H structure. Further study will provide insights into the determinants of virulence.”

However, fatal infections have been documented in immunodeficient children vaccinated with these strains (1, 12, 14, 15). The symptoms of infection occur many months after immunization, and the viruses isolated are similar to the original LA vaccine (1, 15), suggesting that in the absence of an effective host immune response, persistent infection with the vaccine strain can lead to fatal disease. Viruses isolated from these children could potentially represent virulent revertants of the original LA vaccine.



2)  “Vaccination with mumps measles and rubella (MMR) vaccine containing the live attenuated mumps strain, Urabe AM9, is associated with an increased incidence of meningitis. The isolation of mumps virus from CSF and subsequent identification as Urabe AM9-like by sequence analysis confirmed the causative role of Urabe AM9 vaccine in meningitis.”
3)  The Infectious Diseases Society of America says:

“Amanda Jezek, the vice president of Public Policy and Government Relations at the Infectious Diseases Society of America (IDSA), in Arlington, Va., said there is concern that this push to recommend a vaccine before the ACIP has reviewed the evidence would completely “jeopardize the integrity of ACIP’s recommendations.”
“Most of the vaccinations given in this country are received by those younger than 2 years of age, so assuring the safety and efficacy of vaccines is paramount. Every year, more than 40 million vaccines are given to children younger than 1 year of age, usually between 2 and 6 months of age, Dr. Temte said. At this age, infants are at greatest risk for certain serious medical adverse events, including high fevers, seizures and sudden infant death syndrome, according to the U.S. Vaccine Adverse Event Reporting System. Therefore, it is important for the ACIP to consider carefully the risks versus the benefits before making a recommendation rather than be on a forced schedule that suits the manufacturer as opposed to the patient.”


4) The MMR vaccine safety and efficacy studies did not look for these post-“meningitis” events we call Autism, and only followed the children 14-21 days at most.
See for yourselves:


Do “doctors” know this?  No.  They never check immune status prior to vaccination.  They’re total idiots.
5) See the MMR-II monograph for “Contraindications.”  It says not to vaccinate an immunosuppressed kid (like with a cold?) and the MMR contains no mercury to kill the fungi that cause the immunosuppression from the fungi:


It says ^^^ this results in the “live, attenuated viruses” becoming reactivated.  There are absolutely NO properly studies on brain damage adverse events – at least published 😉

6)  Except where they refer to the Borna virus as the model of the “neurodevelopmental brain damage” we call Autism FROM VACCINES >>


7)  “Subclinical infection is not uncommon after all three vaccines…”



8)  See the Wikipedia page on “attenuated vaccine.”  You will see the exact same claims as above – the dangers are that the vaccines will fail and those children will GET those brain damaging viruses:



Now, see the CDC and BigPharma actually admitting the children are GETTING these brain damaging viruses, and see the same phenomenon happening in parallel  (dual or multiple infections causing sepsis and the reactivation of latent viruses of all kinds) below this extra explainer by the NIH and the Einsteiner:

“Some people who survive sepsis can develop secondary infections days or even months later. A research team that included Richard Hotchkiss, Jonathan Green and Gregory Storch of Washington University School of Medicine in St. Louis suspected that this is because sepsis might cause lasting damage to the immune system. To test this hypothesis, the scientists compared viral activation in people with sepsis, other critically ill people and healthy individuals. The researchers looked for viruses like Epstein-Barr and herpes simplex that are often dormant in healthy people but can reactivate in those with suppressed immune systems. [Sepsis Has Long-Term Impact for Older Adults, Study Finds]




The NIH is apparently fearful of funding research that reveals common mechanisms across immunosuppression diseases such as the ones below because they simultaneously reveal the primary source of the Autism pandemic. WHY???

Look at the Big Picture – these are all conditions and diseases you know about and hear about and see about every day, even on the television commercials:

  1.  Transplant patients (and reactivated EBV from immune suppressing meds)
  2.  Humira, Stelara, and Lymphoma (risk of EBV from too much suppression)
  3.  Autommunity (are really EBV, et al, from sepsis, see Fauci’s patent)
  4.  Negative Autoimmunity: Fibro, CLD, ME/CFS is really: non-HLA linked post-sepsis, the opposite of Autoimmunity (see Fauci’s patent)
  5.  Four Failed Fungal Vaccines types, all failed via immunosuppression
  6.  Failed Childhood (“Autism”) vaccines from viruses reactivating, says the CDC
  7.  Astronauts and Med Students can have a real disease, everyone else is “psychiatric”
  8.  Failed Animal Vaccines: CDC says result in humans getting that vaccine virus
  9.  Flumonia: It’s not the flu that’s deadly, but the fungal opportunistics
  10.  Gulf War Illness: VA/Pentagon says due to vaccines, hires Wessely to trash them
  11.  Burkitt’s Lymphoma is due to EBV and Malaria (synergism otherwise denied but every “doctor” has heard of it)
  12.  Immunosenescence,” old people’s immunity is called this. which is identical to post-sepsis syndrome, ME/CFS, Lyme, etc., or acquired/adaptive immune deficiency.
  13.  CDC: “Lyme and LYMErix do cause immunosuppression,” Dec 2016: Steere, Wormser, and Paul Mead report that the “more important” driver of chronic, neurologic Lyme, is immunosuppression.
  14.  ALS or Lou Gehrig’s Disease: McSweegan says Lyme does not cause ALS, after the IDSA/ALDF said it was associated; see the secondary opportunistics (fits the model) from the initial sepsis/immunosuppression.
  15.  “Mental Formation” – Why cant some people “see” a goal for activism? This is nearly the same reason “doctors” cant see what is right in front of them.

There is no NIIID – National Institute of Immunosuppression and Infectious Diseases -, yet here are ~12 IN YOUR FACE obvious examples of what a NIIID should be about:

Transplants, Humira/Stelara, Autism vaccines, other failed fungal-antigen vaccines beside Lyme, astronauts with chronic fatigue, Gulf War Illness and vaccines, Fauci’s patent for fungal-related immunosuppression-and- Autoimmune diseases associated with the opposite of what Fauci explained in his patent,

Burkitt’s Lymphoma, humans getting animal vaccine diseases, Flu-monia and old people’s failed immune systems, the Lyme cabal’s chronic histrionics because they failed in their attempts to narrow the definition of Lyme, thanks to their bogus OspA vaccines…??

Why isn’t this all obvious?   Why since 2001-2002 when the FDA finally ordered LYMErix off the market via ultimatum, hasn’t there been any coherent activism to bring all this forward? What is the nature of this mental disorganization?
Here is the data/evidence:

1) ** Lymphoma and leukemia in TRANSPLANT recipients (from reactivated EBV, et al, from the immmunosuppression drugs they must take)
2) ** HUMIRA or STELARA (and the like) patients are warned that due to this immunosuppression medication, they may have a reactivation of EBV, CMV, and the like (“lymphoma”).
These patients are warned against being “exposed to FUNGAL DISEASES” because it is well known that fungal diseases cause immunosuppression, so that would increase their risk of lymphoma or reactivated EBV, et al.

3) ** Secondary Opportunistics from Sepsis causing the dysimmunity we call “AUTOIMMUNITY” that are HLA-linked or hypersensitivity or ALLERGY responses, such as Rheumatoid Arthritis, Multiple Sclerosis, Lupus, etc.,

The NIH does not acknowledge that sepsis or a polymicrobial infection event preceded this outcome, most of which are EBV-linked,

yet ANTHONY FAUCI has a patent exactly describing that outcome:


“….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.*** …”,696,079.PN.&OS=PN/5,696,079&RS=PN/5,696,079


4) ** the Secondary Opportunistics of post-sepsis immunosuppression outcomes causing illness *WITHOUT* classic “autoimmune inflammation;” we know of these as the “somatoform” diseases such as Chronic Fatigue, Fibromyalgia and Chronic Lyme as shown above in FAUCI’s patent.

And see the bottom right of this chart, that people with Chronic Fatigue syndrome have immunosuppression, and it’s not an “inflammatory” or “autoimmune” disease:


There basically are no markers of immunosuppression and no labs actually test for it.

However, the CDC and IDSA published documents explaining how to test for immunosuppression *INFECTIONS or DISEASES* that get into the CNS from a weakened blood brain barrier due to sepsis, by assaying cerebral spinal fluid (CSF) using Mass Spec ToF PCR.  This methods is said to be 7 times faster than culture or other DNA methods, and much much cheaper. See Number XIII here:

“Virological diagnosis of central nervous system infections by use of PCR coupled with mass spectrometry analysis of cerebrospinal fluid samples.”

“Viruses are the leading cause of central nervous system (CNS) infections, ahead of bacteria, parasites, and fungal agents. A rapid and comprehensive virologic diagnostic testing method is needed to improve the therapeutic management of hospitalized pediatric or adult patients. In this study, we assessed the clinical performance of PCR amplification coupled with electrospray ionization-time of flight mass spectrometry analysis (PCR-MS) for the diagnosis of viral CNS infections. Three hundred twenty-seven cerebrospinal fluid (CSF) samples prospectively tested by routine PCR assays between 2004 and 2012 in two university hospital centers (Toulouse and Reims, France) were retrospectively analyzed by PCR-MS analysis using primers targeted to adenovirus, human herpesviruses 1 to 8 (HHV-1 to -8), polyomaviruses BK and JC, parvovirus B19, and enteroviruses (EV). PCR-MS detected single or multiple virus infections in 190 (83%) of the 229 samples that tested positive by routine PCR analysis and in 10 (10.2%) of the 98 samples that tested negative. The PCR-MS results correlated well with herpes simplex virus 1 (HSV-1), varicella-zoster virus (VZV), and EV detection by routine PCR assays (kappa values [95% confidence intervals], 0.80 [0.69 to 0.92], 0.85 [0.71 to 0.98], and 0.84 [0.78 to 0.90], respectively), whereas a weak correlation was observed with Epstein-Barr virus (EBV) (0.34 [0.10 to 0.58]). Twenty-six coinfections and 16 instances of uncommon neurotropic viruses (HHV-7 [n = 13], parvovirus B19 [n = 2], and adenovirus [n = 1]) were identified by the PCR-MS analysis, whereas only 4 coinfections had been prospectively evidenced using routine PCR assays (P < 0.01). In conclusion, our results demonstrated that PCR-MS analysis is a valuable tool to identify common neurotropic viruses in CSF (with, however, limitations that were identified regarding EBV and EV detection) and may be of major interest in better understanding the clinical impact of multiple or neglected viral neurological infections.”

“Unmet diagnostic needs in infectious disease”

“1. Introduction
The importance of diagnostic testing in the management of infectious diseases (ID) was recently highlighted in the report of the Infectious Diseases Society of America’s (IDSA) Diagnostics Task Force report: “Better Tests: Better Care: Improved Diagnostics for Infectious
Diseases” (Caliendo et al., 2013). Similar sentiments are expressed in the report on Antibiotic Resistance Threats in the United States Centers for Disease Control (2013) from the Centers for Disease Control and Prevention (CDC).
****A number of new diagnostic technologies for ID are rapidly emerging: e.g., broad-range PCR, next-generation sequencing, and matrix-assisted laser desorption/ionization time of flight mass spectrometry.*** The reports from the IDSA and the CDC highlight deficiencies in current diagnostic methods and call for approval and access to methods that are rapid and available at the point of care, use directfrom-specimen analysis, and demonstrate high levels of sensitivity and specificity across a wide range of disease syndromes. The importance of syndrome-based panels (e.g., for central nervous system, bloodstream and respiratory tract infections) is highlighted in the IDSA report (Caliendo et al., 2013). Both the IDSA and CDC emphasize the critical need for culture-independent testing for specific pathogens and their pattern of susceptibility to antimicrobial agents….”

Better Tests, Better Care: Improved Diagnostics for Infectious Diseases 
Angela M. Caliendo,1 David N. Gilbert,2,3 Christine C. Ginocchio,4,5,6 Kimberly E. H…


5) ** the Failures of 4 types of vaccines, the
A) TUBERCULOSIS (fungal lipoproteins) and
B) BORRELIA lipoprotein vaccines or experiments injecting into mammals which all failed in the same way as other TLR2/1 agonists (mimics post-ICU-sepsis syndrome); a third example is where the
C) Brucella antigen OMP19 is also a lipoprotein an also suppresses the immune system as Borrelia OspA or PamCys as shown here:

Brucella abortus Inhibits Major Histocompatibility Complex Class II Expression and Antigen Processing through Interleukin-6 Secretion via Toll-Like Receptor 2
The strategies that allow Brucella abortus to survive inside macrophages for prolonged periods and to avoid the immunological surveillance of major histocompatibility complex class II (MHC-II)-restricted gamma interferon (IFN-γ)-producing CD4+ T lymphocytes are poorly understood. We report here that infection of THP-1 cells with B. abortus inhibited expression of MHC-II molecules and antigen (Ag) processing. Heat-killed B. abortus (HKBA) also induced both these phenomena, indicating the independence of bacterial viability and involvement of a structural component of the bacterium. Accordingly, outer membrane protein 19 (Omp19), a prototypical B. abortus lipoprotein, inhibited both MHC-II expression and Ag processing to the same extent as HKBA. Moreover, a synthetic lipohexapeptide that mimics the structure of the protein lipid moiety also inhibited MHC-II expression, indicating that any Brucella lipoprotein could down-modulate MHC-II expression and Ag processing. Inhibition of MHC-II expression and Ag processing by either HKBA or lipidated Omp19 (L-Omp19) depended on Toll-like receptor 2 and was mediated by interleukin-6. HKBA or L-Omp19 also inhibited MHC-II expression and Ag processing of human monocytes. In addition, exposure to the synthetic lipohexapeptide inhibited Ag-specific T-cell proliferation and IFN-γ production of peripheral blood mononuclear cells from Brucella-infected patients. Together, these results indicate that there is a mechanism by which B. abortus may prevent recognition by T cells to evade host immunity and establish a chronic infection.


A1) The 19-kD antigen and protective immunity in a murine model of tuberculosis.
“The 19-kD antigen is a cell wall-associated lipoprotein present in Mycobacterium tuberculosis and in bacille Calmette-Guérin (BCG) vaccine strains. Expression of the 19-kD antigen as a recombinant protein in two saprophytic mycobacteria-M. vaccae and M. smegmatis-resulted in abrogation of their ability to confer protection against M. tuberculosis in a murine challenge model, and in their ability to prime a DTH response to cross-reactive mycobacterial antigens. Induction of an immune response to the 19-kD antigen by an alternative approach of DNA vaccination had no effect on subsequent M. tuberculosis challenge. These results are consistent with a model in which the presence of the 19-kD protein has a detrimental effect on the efficacy of vaccination with live mycobacteria. Targeted inactivation of genes encoding selected antigens represents a potential route towards development of improved vaccine candidates.”

A2) Mycobacterium tuberculosis 19-kilodalton lipoprotein inhibits Mycobacterium smegmatis-induced cytokine production by human macrophages in vitro.
“Vaccination of mice with Mycobacterium vaccae or M. smegmatis induces some protection against M. tuberculosis challenge. The 19-kDa lipoprotein of M. tuberculosis, expressed in M. vaccae or M. smegmatis (M. smeg19kDa), abrogates this protective immunity. To investigate the mechanism of this suppression of immunity, human monocyte-derived macrophages (MDM) were infected with M. smeg19kDa. Infection resulted in reduced production of tumor necrosis factor alpha (TNF-alpha) (P < 0.01), interleukin-12 (IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to infection with M. smegmatis vector (M. smegV). Infection with M. smeg19kDa and with M. smegV had no differential effect on expression of costimulatory molecules on MDM, nor did it affect the proliferation of presensitized T cells cocultured with infected MDM. When MDM were infected with M. smegmatis expressing mutated forms of the 19-kDa lipoprotein, including non-O-glycosylated (M. smeg19NOG), nonsecreted (M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced production of TNF-alpha or IL-12 was not observed. When the purified 19-kDa lipoprotein was added directly to cultures of infected monocytes, there was little effect on either induction of cytokine production or its inhibition. Thus, the immunosuppressive effect is dependent on glycosylated and acylated 19-kDa lipoprotein present in the phagosome containing the mycobacterium. These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to reduced induction of T-cell activation.”

A3) The Mycobacterium tuberculosis recombinant 27-kilodalton lipoprotein induces a strong Th1-type immune response deleterious to protection.
Th1 immune response is essential in the protection against mycobacterial intracellular pathogens. Lipoproteins trigger both humoral and cellular immune responses and may be candidate protective antigens. We studied in BALB/c mice the immunogenicity and the protection offered by the recombinant 27-kDa Mycobacterium tuberculosis lipoprotein and the corresponding DNA vaccine. Immunization with the 27-kDa antigen resulted in high titers of immunoglobulin G1 (IgG1) and IgG2a with a typical Th1 profile and a strong delayed hypersensitivity response. A strong proliferation response was observed in splenocytes, and significant nitric oxide production and gamma interferon secretion but not interleukin 10 secretion were measured. Based on these criteria, the 27-kDa antigen induced a typical Th1-type immune response thought to be necessary for protection. Surprisingly, in 27-kDa-vaccinated mice (protein or DNA vaccines) challenged by M. tuberculosis H37Rv or BCG strains, there was a significant increase in the numbers of CFU in the spleen compared to that for control groups. Furthermore, the protection provided by BCG or other mycobacterial antigens was completely abolished once the 27-kDa antigen was added to the vaccine preparations. This study indicates that the 27-kDa antigen has an adverse effect on the protection afforded by recognized vaccines. We are currently studying how the 27-kDa antigen modulates the mouse immune response.”

That’s 6 attempts to use TLR2/1 agonist lipoproteins as potential vaccines and they all failed in the same way:
3 of Tuberculosis,
2 of Borrelia (OspA),
1 of Brucella;  they all caused immunosuppression and an increased susceptibility to disease.

One more:
“In Swiss mice, animals with high natural resistance to hepatitis virus, the pathogenicity of this agent was markedly enhanced by combined infection with eperythrozoa. Eperythrozoa were maintained throughout 18 successive passages in normal Princeton and Swiss weanlings with intact spleens. The combined infection of Princeton mice with eperythrozoa and the virus component of Gledhill, Dick, and Andrewes, which is nearly inactive when injected alone, resulted in acute hepatitis with fatal outcome.”
Mycoplasma = Eperythrozoa
That’s Brucella, Mycoplasma, Mycobacteria, and Borrelia vaccines or experimentally co-injected, and all failed in the same way.  All caused immunosuppression.

So what we are doing is showing this model or mechanism in PARALLEL, or show it occurs in other disease models.  OspA or Borrelial lipoproteins that are TLR2/1 agonists were never and could never have been “vaccines,” which means the criminal CDC needs to be prosecuted for maintaining their stance that OspA was a vaccine and that the Dearborn method was a valid way to diagnose Lyme.

Thimerosal was put in vaccines to prevent LYMErix.  This is a fact:

Vaccine Rule Is Said to Hurt Health Efforts 
“But a proposal that the ban include thimerosal, which has been used since the 1930s to prevent bacterial and fungal contamination in multidose vials of vaccines, has drawn strong criticism from pediatricians…. They say that the ethyl-mercury compound is critical for vaccine use in the developing world, where multidose vials are a mainstay…Banning it would require switching to single-dose vials for vaccines, which would cost far more and require new networks of cold storage facilities and additional capacity for waste disposal, the authors of the articles said.'”     



6) ** the Reversion of pediatric viruses in vaccine vials to “WILD TYPE” which is code language for the fact that children are getting the very, active viruses these vaccines are intended to prevent – many of which are neurotropic – as a result of some immunosuppression event, such as a simultaneous infection at the time of vaccination or vaccination with a contaminated vaccine vial,

CDC’s Patent, US # 7,632,510,
Methods of inducing flavivirus immune responses through the administration of recombinant flaviviruses comprising an engineered japanese encephalitis virus signal sequence

“Finally, there is the risk that the virus may not be fully or completely inactivated or attenuated and thus, the vaccine may actually cause disease.”,632,510.PN.&OS=PN/7,632,510&RS=PN/7,632,510

B) CDC SAYS,…Measles, Mumps, and Rubella — Vaccine Use and Strategies for Elimination of Measles, Rubella, and Congenital Rubella Syndrome and Control of Mumps: Recommendations of the Advisory Committee on Immunization Practices (ACIP)

“Updated information on adverse events and contraindications, particularly for persons with severe HIV infection, persons with a egg allergy or gelatin allergy, persons with a history of thrombocytopenia, and persons receiving steroid therapy [are immunosuppressed – KMD].”


“To determine whether passage of an avirulent vaccine strain in human tissue increases virulence, we studied a virus isolated from thymic tissue 90 days after infection with the vaccine strain Moraten (pMor-1) and ***a virus isolated from an immunodeficient child with progressive vaccine-induced disease (Hu2). ***”


7) ** Astronauts and Medical School students whose stress or CORTISOL activates latent viral infections like Epstein-Barr is at least acknowledged as such (“chronic active Epstein-Barr or mono”),


Fatigue in Medical Residents Leads to Reactivation of Herpes Virus Latency



8) ** the NIH prefers not to tie in conditions ANIMAL DISEASE VACCINES are transferred to humans because of immunosuppression in the animal, leading to the viruses being fully reactivated and contagious,

A) “Human Illness Associated with Use of Veterinary Vaccines”

Currently, veterinary facilities do not routinely warn pet owners when they are administering live aerosol vaccines in close proximity to the owners, and the risk among immunocompromised pet owners of acquiring an infection with a vaccine strain directly from the vaccine or fromshedding of the vaccine strainis unknown.

B) CDC SAYS:Human Exposure to Brucella abortus Strain RB51 — Kansas, 1997
In the above, an immunosuppressed pregnant cow was given a Brucella (LYMErix-like) “live attenuated” vaccine and the baby cow ended up with the disease, which then was transferred to the humans handling the cow and her dead baby. This parallels what is happening to children who are vaccinated while immunosuppressed, or who receive mycoplasmally (LYMErix-like) contaminated vaccines -KMD.



9) ** [“FLU-MONIA”] the NIH does not formally demonstrate that Influenza primarily becomes deadly due to the secondary opportunistic pneumonia – they do not like to mention this synergy openly.

But here again is NIAID’s Chief Anthony Fauci on the ‘monia part of 1918 Spanish Flumonia® being what causes people to choke to death — it was inflammatory response in the lungs to the fungal-ish pneumonia:
J Infect Dis. 2008 Oct 1;198(7):962-70. doi: 10.1086/591708.

Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemicinfluenza preparedness.

”Despite the availability of published data on 4 pandemics that have occurred over the past 120 years, there is little modern information on the causes of death associated with influenza pandemics.


We examined relevant information from the most recent influenza pandemic that occurred during the era prior to the use of antibiotics, the 1918-1919 “Spanish flu” pandemic. We examined lung tissue sections obtained during 58 autopsies and reviewed pathologic and bacteriologic data from 109 published autopsy series that described 8398 individual autopsy investigations.


The postmortem samples we examined from people who died of influenza during 1918-1919 uniformly exhibited severe changes indicative of bacterial pneumonia. Bacteriologic and histopathologic results from published autopsy series clearly and consistently implicated secondary bacterial pneumonia caused by common upper respiratory-tract bacteria in most influenza fatalities.


The majority of deaths in the 1918-1919 influenza pandemic likely resulted directly from secondary bacterial pneumonia caused by common upper respiratory-tract bacteria. Less substantial data from the subsequent 1957 and 1968 pandemics are consistent with these findings. If severe pandemic influenza is largely a problem of viral-bacterial copathogenesis, pandemic planning needs to go beyond addressing the viral cause alone (e.g., influenza vaccines and antiviral drugs). Prevention, diagnosis, prophylaxis, and treatment of secondary bacterial pneumonia, as well as stockpiling of antibiotics and bacterial vaccines, should also be high priorities for pandemic planning.



10) ** in GULF WAR ILLNESS victims, the Pentagon found a link between this illness and vaccinations,

BMJ. 2000 May 20;320(7246):1363-7.

Role of vaccinations as risk factors for ill health in veterans of the Gulf war: cross sectional study.

“Among veterans of the Gulf war there is a specific relation between multiple vaccinations given during deployment and later ill health. Multiple vaccinations in themselves do not seem to be harmful but combined with the “stress” of deployment they may be associated with adverse health outcomes. These results imply that every effort should be made to maintain routine vaccines during peacetime.”

But the Pentagon or VA deployed the same Simon Wessely to *not* examine the role immune-suppressors such as DEET and nerve agent antidote, which in combination with the hypervaccination could be troublesome, in that, these, if “live attenuated” viruses in a vial could be reactivated via IMMUNOSUPPRESSION – not just from STRESS, but DEET or other immune suppressing exposures -, then why must the victims be blamed and this called “psychiatric?”

WESSELY SAID:  “One way of doing that is through neuro-imaging, but we didn’t get the money to do that, so instead we have used sophisticated neuro-psychological testing,”…  — [NOT SCIENTIFICALLY VALID-SASH].

“Those tablets, the NAPS tablets, it’s just not possible to study. Pesticides, we don’t find evidence. [The antidotes to nerve agents given to veterans are a problem- SASH]  Chemical weapons, well, we don’t think that for the British armed forces that was a big issue. But we do think there is a relationship between a particular pattern of protection [long for “cowardice”- SASH] and what happened later.”—[NOT SCIENTIFICALLY VALID-SASH]

Yet here is the truth:
2004 — Pyridostigmine bromide (PYR) alters immunefunction in B6C3F1 mice.

“Pyridostigmine bromide (PYR) is an anticholinesterase drug indicated for the treatment of myasthenia gravis and neuromuscular blockade reversal. It acts as a reversible cholinesterase inhibitor and was used as a pretreatment for soldiers during Operation Desert Storm to protect against possible nerve gas attacks. Since that time, PYR has been implicated as a possible causative agent contributing to Gulf War Illness. PYR’s mechanism of action has been well-delineated with regards to its effects on the nervoussystem, yet little is known regarding potential effects on immunological function. To evaluate the effects of PYR on immunological function, adult female B6C3F1 mice were gavaged daily for 14 days with PYR (0, 1, 5, 10, or 20mg/kg/day). Immune parameters assessed were lymphoproliferation, natural killer cell activity, the SRBC-specific antibody plaque-forming cell (PFC) response, thymus and spleen weight and cellularity, and thymic and splenic CD4/CD8lymphocyte subpopulations. Exposure to PYR did not alter splenic and thymus weight or splenic cellularity. However, 20 mg PYR/kg/day decreased thymic cellularity with decreases in both CD4+/CD8+ (20 mg/kg/day) and CD4-/CD8- (10and 20 mg/kg/day) cell types. Functional immune assays indicated that lymphocyte proliferative responses and natural killer cell activity were normal; whereas exposure to PYR significantly decreased primary IgM antibody responses to a T-cell dependent antigen at the 1, 5, 10 and 20 mg/kg treatment levels for 14 daysThis is the first study to examine the immunotoxicological effects of PYR and demonstrate that this compound selectively suppresses humoral antibody responses.”

DEET and Immunosuppression:

N,N,-diethyl-m-toluamide (DEET) suppresses humoral immunologicalfunction in B6C3F1 mice.

DEET and Immunosuppression, especially combined with Nerve Agent Antidote:

Evaluation of immunotoxicity induced by single or concurrent exposure to N,N-diethyl-m-toluamide (DEET), pyridostigmine bromide (PYR), and JP-8 jet fuel.

So, while Wessely knew there was an association between vaccines and Gulf War Illness, he later discounted – by saying he did not have the money to study it – the scientifically valid signs of immunosuppression due to other Gulf War Veterans’ exposures and declared these soldiers mental cases to deny them any care or compensation.

11)  “Doctors” are supposed to know this basic medical science – the synergy where Malaria activated Epstein-Barr and caused BURKITT’S LYMPHOMA due to the immunosuppression:
“It was found that intact erythrocytes infected with P. yoelii do not induce maturation of DC unless they are lysed, suggesting that accessibility of parasite inflammatory molecules to their receptors is a key issue in the activation of DC by P. yoelii. This activation is independent of MyD88. It was also observed that pre-incubation of DC with intact P. yoelii-infected erythrocytes inhibits the maturation response of DC to other TLR stimuli. The inhibition of maturation of DC is reversible, parasite-specific and increases with the stage of parasite development, with complete inhibition induced by schizonts (mature infected erythrocytes). Plasmodium yoelii-infected erythrocytes induce a broad inhibitory effect rendering DC non-responsive to ligands for TLR2, TLR3, TLR4, TLR5, TLR7 and TLR9.”

“The Epstein–Barr virus was named after Michael Anthony Epstein (born 18 May 1921), now a professor emeritus at the University of Bristol, and Yvonne Barr (born 1932), a 1966 Ph.D graduate from the University of London, who together discovered[36] and, in 1964, published on the existence of the virus.[37] In 1961, Epstein, a pathologist and expert electron microscopist, attended a lecture on “The Commonest Children’s Cancer in Tropical Africa—A Hitherto Unrecognised Syndrome.” This lecture, by Denis Parsons Burkitt, a surgeon practicing in Uganda, was the description of the “endemic variant” (pediatric form) of the disease that bears his name. In 1963, a specimen was sent from Uganda to Middlesex Hospital to be cultured. Virus particles were identified in the cultured cells, and the results were published in The Lancet in 1964 by Epstein, Bert Achong, and Barr. Cell lines were sent to Werner and Gertrude Henle at the Children’s Hospital of Philadelphia who developed serological markers. In 1967, a technician in their laboratory developed mononucleosis and they were able to compare a stored serum sample, showing that antibodies to the virus developed.[38][39][40] In 1968, they discovered that EBV can directly immortalize B cells after infection, mimicking some forms of EBV-related infections,[41] and confirmed the link between the virus and infectious mononucleosis.[42]



12)  If you have Lyme or CFIDS, what you actually physically have is this, this “Old Age Immunity,” called immunosenescence (or post-sepsis or endotoxin tolerance and cross-tolerance or immune-paralyis, etc). We say “there is no NIIID” and “no one talks about his whole class of people (data in the Occam’s Razor),” but when they do, they are also referring to the known immunology of the aged.


“The low blood pressure and inflammation patients experience during sepsis may lead to brain damage that causes cognitive problems. Sepsis patients also frequently become delirious, a state known to be associated with Alzheimer’s disease.

“Inflammation and infection can attack the muscles, and lack of proper physical therapy during sepsis might also contribute to the patients’ later disability, Iwashyna said.

“Older patients should get their flu and pneumonia vaccines to reduce the risk of infections that can lead to sepsis. New treatments are also needed to prevent the cognitive and physical consequences of the condition, Iwashyna said.

“The results will be published tomorrow (Oct. 27) in the Journal of the American Medical Association.

“Study: Disease, Not Old Age, Causes Forgetfulness

The NIH and HHS dot gov do not care to tie all these separate events and illnesses in and reveal that these mechanisms and outcomes are all very similar, and that the majority of the sick and the vaccine-damaged people in this country have experienced these common mechanisms and have common outcomes.

We call these outcomes an “Occam’s Razor” because there seems to be no other outcome to immunosuppression events but that latent vaccine viruses, other viruses, and non-viral opportunistics take over.

Some people have the genetic background to fight off these infections, and we call that HLA-linked hypersensitivity or autoimmunity (too many antibodies), but the vast majority of the disabled do not have these genes.

This is a form of racism or genetic discrimination, and we wonder to whom is the National Institutes really beholden?

The NIH and CDC do not want to admit that CHILDREN could be getting the live, attenuated VACCINE viruses – reactivated – and most of which are neurotropic. This is why they abuse these other groups.

Secondarily, BIOWEAPONS work in the same way “overwhelming the immune system”
such that they, by their type, inhalation or other inhalation fungi, for instance, cause immunosuppression and the reactivation of other viruses to which a person may previously had been exposed. There is no other “covert” or hidden way a bioweapon works.

You can find the scientific, published data – even by the CDC and BigPharma regarding vaccines that fail and give children the very neurotropic, brain damaging viruses they are intended to prevent -, for the above claims here in the criminal charge sheets:

The diagnostic codes for post-sepsis syndrome or Chronic Fatigue/ME, Lyme, Fibro:

You can see there is one (diagnostioc code for post-sepsis due to an infection) due to Brucella, which I showed you earlier and you can see below, has an antigen like OspA (fungal):


Brucella abortus inhibits major histocompatibility complex class II expression and antigen processing through interleukin-6 secretion via Toll-like receptor




Pam3Cys as an analog of Brucellar triacyl lipoprotein Omp19 inhibited MHC class II expression exactly the same as LYMErix or recombinant OspA did.



13) Steere, Wormser and CDC’s Mead, report on Dec 15, 2016 that…


Abstract (published Dec 15, 2016):

Full Text:

Of course that is what we have been claiming for the last 17 years, since we say that LYMErix was causing the same disease we know of as chronic, neurologic Lyme, and was the same outcome written out of the case definition by Allen Steere in 1993-1994 when he and his cabal defrauded the Government to see their fake vaccines and test kids for Vector Borne Diseases (VBDs).

We’re guessing the criminals deployed the truth here in a backhanded sort of way so as to have a Get Out of Jail Free card, when the indictments come down.


You remember AG and now Senator Richard Blumenthal sued these characters for racketeering over 10 years ago.  Blumenthal was a former DOJ prosecutor.



14)  Edward McSweegan, happy about ALS not being “only a bad knee.”



Arch Neurol. 1990 May;47(5):586-94.

Immunologic reactivity against Borrelia burgdorferi in patients with motor neuron disease.

Halperin JJ1, Kaplan GPBrazinsky STsai TFCheng TIronside AWu PDelfiner JGolightly MBrown RH, et al.

Author information


“Of 19 unselected patients with the diagnosis of amyotrophic lateral sclerosis (ALS) living in Suffolk County, New York (an area of high Lyme disease prevalence), 9 had serologic evidence of exposure to Borrelia burgdorferi; 4 of 38 matched controls were seropositive. Eight of 9 seropositive patients were male (8 of 12 male patients vs 2 of 24 controls). Rates of seropositivity were lower among patients with ALS from nonendemic areas. All patients had typical ALS; none had typical Lyme disease. Cerebrospinal fluid was examined in 24 ALS patients–3 (all with severe bulbar involvement) appeared to have intrathecal synthesis of anti-B burgdorferi antibody. Following therapy with antibiotics, 3 patients with predominantly lower motor neuron abnormalities appeared to improve, 3 with severe bulbar dysfunction deteriorated rapidly, and all others appeared unaffected. There appears to be a statistically significant association between ALS and immunoreactivity to B burgdorferi, at least among men living in hyperendemic areas.”

ALS after Lyme might not be due to Lyme/spirochetes, but the secondary opportunistics due to the fungal antigen tolerance and cross-tolerance, as is the case with everything. Use PubMed.





15)  “Formation” – the idea that you can mold minds in such a way as to be more perceptive of the big picture, and means training, or education, but also, morally.
The difficulty we have in the Western Culture is that around the late 1950s and early 60s there emerged various philosophies about human motivation, which, in an attempt to be scientific, were assessed by taking polls.
For instance, there were all the sex question (Kinsey Reports) surveys that concluded that “due to the frequency debauched behavior,” that made it “normal” or “common” or “everybody does it.”  You know the “S” in DSM stands for statistics.  Some people think they can reduce human beings to a set of traits, yet they exclude the first observation (how self-centered are they?), because they told themselves self-centeredness or ego was “normal.”
Yet, here, scientifically, we can see that selfishness or self-centeredness is not “normal” because the statistics show people know it when they’re being selfish or hypocritical:

Deep Down, We Can’t Fool Even Ourselves – The New York Times


“… Politicians are hypocritical for the same reason the rest of us are: to gain the social benefits of appearing virtuous without incurring the personal costs of virtuous behavior. If you can deceive even yourself into believing that you’re acting for the common good, you’ll have more energy and confidence to further your own interests — and your self-halo can persuade others to help you along.

“But as useful as hypocrisy can be, it’s apparently not quite as basic as the human instinct to do unto others as you would have them do unto you. Your mind can justify double standards, it seems, but in your heart you know you’re wrong.”

The science, as you have just seen, says selfish behavior is actually assholish and that we all know it when we do it.  We’re just deceiving ourselves to say, “No one should pay attention to the truth of the Lyme crymes because it is HARSH,” because clearly that person would have some other motivation than to have others know they are actually crime victims and deserve compensation, as well as scientific validation for what they suffer.

So, again, take the idea of “Lyme activism” where the purveyors of false stories, such as: “It is more important to talk about how miserable you are, than to end the misery” – which is what all of the Lyme non-profits claim.

This is an example of a mental MAL-FORMATION or a hypocritical tale, because what they are really trying to say is, “I want you to talk about how miserable you are – and I will provide you the platform for this endless drama -, instead of doing anything about your misery, because to be a real activist and have the crime prosecuted, means I cant sell you my ‘services’ any more. You wont be thinking about me, and I want you to be thinking about me, and giving me all your attention, and I will pretend to ‘care.'”

This is the old “Love Does Not Mean ‘Do,'” routine, where all you have to do is run your mouth and never actually lend anyone a physical hand when they are distressed or in need of physical help, as in the case of the chronic ill/abuse of Lyme and ME/CFS.

[“Love’s not a verb, it’s not an ActionMan, hero.  It’s something we spend 4 dollars on and says ‘Hallmark’ on it.”]

Cognitive or emotional mal-formation such as this is only allowed to take wing in a society so perverted by Me-isms (ego as God, or “defense mechanisms,” such as violence or verbal violence), that they can no longer see the big picture of how a 100% self-centered society does not scale up.

No one asks the question, “Well, what exactly is a society, after all, if we are to throw out all true service and cohesiveness?  What’s next?  What’s next on this downward spiral away from the idea of an inter-dependent society that depends on each person playing a role towards an end game of stability…. towards everyone saying, instead, ‘I’m not playing unless this is All About Me?”

They no longer “SEE” how foolish and underdeveloped they are as human beings.  And we are at the point where if someone calls them out over their bogus platform that “we should NOT work together to end our abuse,” that person is called the bad guy.


It’s become totally perverse, and most people buy into it.


The people have become unable to think for themselves.  The me-centrism actually KILLS independent thought, the very objection they have over being denied the validity of their illness – the very thing they prefer to fuss over and tell personal stories.

Beaux said it best in the Lyme Cryme movie:  These people in these online support groups are “just talking in circles.”

They’re so mentally malformed that they don’t know they should have a direction or a goal for the community.  They don’t know they’re part of a society, and furiously reject the notion that, “Um, no, actually you are just a cog.  We’re all cogs.”

Adult Formation says:  “Put those cogs on a wheel and go somewhere.”

Mal-formation says: “No, I want everyone to know I am the biggest cog. That’s the most important thing.

“Who’s the biggest cog.

“Who’s the biggest knob.


“Lyme,” in the end, is about incompetence on our own side- the”LLMDs,”  who are clearly carpet baggers and charlatans,…  and “activism” by fairies who say it is more important to whine about how miserable we are than to put the crooks in jail.

This after Sen Blumenthal – a former DOJ prosecutor – sued for Antitrust under CT civil law (lacks power to grab all the criminals’ evidence) 10 years ago.

Blumenthal’s findings include the following:

  • The IDSA failed to conduct a conflicts of interest review for any of the panelists prior to their appointment to the 2006 Lyme disease guideline panel;
  • Subsequent disclosures demonstrate that several of the 2006 Lyme disease panelists had conflicts of interest;
  • The IDSA failed to follow its own procedures for appointing the 2006 panel chairman and members, enabling the chairman, who held a bias regarding the existence of chronic Lyme, to handpick a likeminded panel without scrutiny by or formal approval of the IDSA’s oversight committee;
  • The IDSA’s 2000 and 2006 Lyme disease panels refused to accept or meaningfully consider information regarding the existence of chronic Lyme disease, once removing a panelist from the 2000 panel who dissented from the group’s position on chronic Lyme disease to achieve “consensus”;
  • The IDSA blocked appointment of scientists and physicians with divergent views on chronic Lyme who sought to serve on the 2006 guidelines panel by informing them that the panel was fully staffed, even though it was later expanded;
  • The IDSA portrayed another medical association’s Lyme disease guidelines as corroborating its own when it knew that the two panels shared several authors, including the chairmen of both groups, and were working on guidelines at the same time. In allowing its panelists to serve on both groups at the same time, IDSA violated its own conflicts of interest policy.


The LDA wants to give the crooks a seat at the table – same strategy they had in the late 1990s.

‘As if nothing has happened in between including the FDA ordering LYMErix off the market and the Blumenthal racketeering charge.


“But a four-month investigation by United Press International found a pattern of serious problems linked to vaccines recommended by the CDC — and a web of close ties between the agency and the companies that make vaccines.

“Critics say those ties are an unholy alliance in a war against disease where vaccine side effects have damaged, hurt or killed people, mostly children.

“The CDC is a disgrace. It is a corrupt organization,” said Stephen A. Sheller, a Philadelphia attorney who has sued vaccine makers for what he says were bad vaccines. “The drug companies have them on their payroll.”


That was 2003.

Good one.

What happened to everyone’s balls?

It looks like psychiatry with all their sex-adorations and perversions and endorsing self-idolatries and their Me-Centric culture,…  shrunk everyone’s balls.

Sixty years on, since Kinsey and the Psych-Pervert Gang,… and America has no balls.















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