Archive for the ‘research’ Category

Vaccine-Induced Thrombocytopenia With Severe Headache – Why Lyme/MSIDS Patients Should Care

https://www.nejm.org/doi/full/10.1056/NEJMc2112974?

Vaccine-Induced Thrombocytopenia with Severe Headache

To the Editor:

Vaccine-induced immune thrombotic thrombocytopenia (VITT), a serious adverse event after vaccination with ChAdOx1 nCoV-19 (AstraZeneca) or Ad26.COV2.S (Johnson & Johnson–Janssen), is caused by platelet factor 4 (PF4)–dependent, platelet-activating antibodies.1-3 High-dose immune globulins and anticoagulation are the main treatments.4,5 In this report, we present evidence that vaccine-induced thrombocytopenia (VIT) without associated cerebral venous sinus thrombosis (CVST) or other thromboses and with severe headache as the heraldic symptom may precede VITT (“pre-VITT syndrome”).

Eleven patients presented with severe headache in the absence of CVST 5 to 18 days after ChAdOx1 nCoV-19 vaccination.

  • All the patients had thrombocytopenia (low platelets in the blood which can cause hemorrhaging)
  • high d-dimer levels (a test to detect blood clots – a high level indicates clot formation and breakdown in the body)
  • high levels of anti–PF4–heparin IgG antibodies
  • during follow-up, intracranial hemorrhage occurred in three patients (Patients 1, 2, and 3), with radiologic evidence of new CVST in Patients 2 and 3 (Figure 1, and Table S1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org).
  • Only two patients (Patients 2 and 4) were initially admitted with conditions that met the criteria for VITT; both patients had pulmonary embolism, and additional splanchnic vein thrombosis was present in Patient 2.

In Patient 2, anticoagulation treatment had been initiated several days earlier for pulmonary embolism (without diagnosis of VITT) but was stopped after the onset of headache, shortly before CVST developed.

  • In two patients (Patients 1 and 3), peripheral thromboses were eventually identified during follow-up.

Thrombotic complications did not develop in seven of the patients (Patients 5 through 11); all but one of these patients received high-dose immune globulin, glucocorticoids, or therapeutic-dose anticoagulation within 5 days after headache onset. In contrast, in all four patients with subsequent thrombosis (Patients 1 through 4), therapeutic-dose anticoagulation either was not started until 6 to 9 days after headache onset or was stopped prematurely before the development of CVST.

Although the combination of thrombocytopenia and severe headache due to CVST has been recognized as the typical presentation of VITT,1,2 the experience with these 11 patients suggests that VIT with severe headache, elevated d-dimer levels, and strongly positive results on anti–PF4–heparin IgG enzyme-linked immunosorbent assay may precede VITT.

Our findings have immediate implications for clinical practice: in this pre-VITT syndrome, severe headache may not develop as a symptom secondary to CVST but instead may precede CVST by several days, potentially in association with microthrombosis in smaller cortical veins.

Consequently, patients who present with severe headache 5 to 20 days after adenovirus vector vaccination against coronavirus disease 2019 should undergo immediate testing for thrombocytopenia and d-dimer levels and, if available, testing for anti–PF4–heparin IgG antibodies.

When these antibodies are present at high titers, patients are at imminent risk for CVST, and it is likely that this condition can be prevented with immediate treatment, such as with intravenous immune globulin. The decision to initiate therapeutic-dose anticoagulation is a difficult one; the risk of emerging thrombosis, including CVST, has to be balanced against the risk of intracranial hemorrhage on an individual basis (e.g., with consideration of platelet count and fibrinogen levels).

Farid Salih, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Linda Schönborn, M.D.
Universitätsmedizin Greifswald, Greifswald, Germany

Siegfried Kohler, M.D., Christiana Franke, M.D., Martin Möckel, M.D., Thomas Dörner, M.D., Hans C. Bauknecht, M.D., Christian Pille, M.D., Jan A. Graw, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Angelika Alonso, M.D.
University Hospital of Mannheim, Mannheim, Germany

Johann Pelz, M.D.
University Hospital of Leipzig, Leipzig, Germany

Hauke Schneider, M.D., Antonios Bayas, M.D., Monika Christ, M.D.
University Hospital of Augsburg, Augsburg, Germany

Joji B. Kuramatsu, M.D.
University Hospital of Erlangen, Erlangen, Germany

Thomas Thiele, M.D., Andreas Greinacher, M.D.
Universitätsmedizin Greifswald, Greifswald, Germany

Matthias Endres, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Supported by Deutsche Forschungsgemeinschaft project number 374031971–TRR 240 (to Prof. Greinacher) and EXC-2049–390688087 NeuroCure under the German Excellence Strategy (to Prof. Endres) and by the Domagk-Programm of the Universitätsmedizin Greifswald (to Dr. Schönborn).

Disclosure forms provided by the authors are available with the full text of this letter at NEJM.org.

This letter was published on September 15, 2021, at NEJM.org.

Profs. Greinacher and Endres contributed equally to this letter.

___________________

**Comment**

Both Thrombocytopenia and severe headaches are common with Lyme/MSIDS patients.

Therapy for thrombocytopenia requires treatment or removal of the underlying infection, in addition to maintenance of platelet counts and hemostatic function.

Hopefully it’s clear that a Lyme/MSIDS patient getting a COVID shot could be diagnosed with thrombocytopenia that either already exists or worsens after the injection.  Treating the underlying infection is imperative but won’t be considered by mainstream medicine.

For more:

Go here for the latest VAERS data and the mounting list of adverse reactions and deaths.

Category:

Heart Issues, Inflammation, research, vaccines

New Study: Half of Hospitalized COVID Patients Have Mild Case, Are Asymptomatic, or in Hospital for Another Reason

https://thenewamerican.com/new-study-half-of-hospitalized-covid-patients-have-mild-case-are-asymptomatic-or-in-hospital-for-another-reason/

New Study: Half of Hospitalized COVID Patients Have Mild Case, Are Asymptomatic, or in Hospital for Another Reason

by R. Cort Kirkwood
New Study: Half of Hospitalized COVID Patients Have Mild Case, Are Asymptomatic, or in Hospital for Another Reason
Hispanolistic/E+/Getty Images

About three million people in the United States with the China Virus have been admitted to hospitals in the past year, data from the Centers for Disease Controls show.

Yet not all of those hospitalized with the virus were hospitalized because of the virus. Instead, the Atlantic reported on September 13, they went into the hospital for another reason, but tested positive after they were there.

That means the data on hospitalizations with the virus might not tell us what we think it does.

(See link for article)

_______________________
**Comment**
Once again, data is being twisted to provoke fear for a bigger agenda.

The important issue here is how the “virus” is affecting any given individual.

Due to vast testing being done at hospitals, they are recording incidental COVID cases that never would have been recorded otherwise. The past CDC director has admitted that hospitals have a monetary incentive to over count COVID deaths.  This has occurred in Wisconsin and in every state.  It’s notoriously been done in nursing homes.  Remember that even the CDC has withdrawn EUA for the PCR test as it can’t distinguish between COVID and the flu.  Further, the CDC stopped counting the flu to purposely pad COVID cases.

Important quotes:

Let’s read that again: About 50 percent of COVID-positive VA patients in the hospital were there for another reason or had a mild case of the disease.

Of vaccinated patients, 57 percent presented with mild or asymptomatic disease, and “unvaccinated patients have also been showing up with less severe symptoms, on average, than earlier in the pandemic,” the Atlantic reported:

While the authors want to give credit to the “vaccines”, historically it is known that viruses weaken over time.

The most logical conclusion is to refine the definition of hospitalization.

 “Those patients who are there with rather than from COVID don’t belong in the metric.”

I’m not downplaying the fact people can become very ill from COVID.  I was one such case.  What is despicable; however, is the fact our corrupt public health ‘authorities’ are censoring and denying cheap, effective, successful treatments that is killing thousands upon thousands as well as continues to push a narrative that our only hope is a fast-tracked, experimental gene therapy injection that is literally maiming and killing thousands more.

Category:

research, Viruses

Controversy Continues: “True Chronic Lyme Disease” Rather Than “Post-treatment Lyme Disease Syndrome”

Although written in 2018, it’s a perfect example how the debate continues on the issue of pathogen persistence due to thousands of patients who continue to have severe symptoms of Lyme/MSIDS despite years of treatment.  Similarly to the censorship and maligning of ivermectin, HCQ, and other effective treatments for COVID, doctors treating Lyme/MSIDS are afraid to treat patients long-term as the same bullying has occurred.

**********************

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6100330/

2018 Jul-Sep; 10(3): 170–171.
doi: 10.4103/jgid.jgid_152_17
PMCID: PMC6100330
PMID: 30166820

The Persistent Lyme Disease: “True Chronic Lyme Disease” rather than “Post-treatment Lyme Disease Syndrome”

Alexis Lacout, Mostafa El Hajjam,1 Pierre-Yves Marcy,2 and Christian Perronne3
Author information Copyright and License information Disclaimer
 

Sir,

A controversy continues regarding the reality of a chronic form of Lyme disease. Chronic Lyme disease can present as a “post-Lyme syndrome” explained by inflammatory and immunological phenomena, or as a genuine “chronic form” attributable to the persistence of the bacteria despite proper antibiotic therapy as per the current guidelines. The current guidelines however may not be so appropriate in the latter case.

The case referenced is of a 40-year-old patient, a hunting gard, regularly suffering from multiple tick bites. He began experiencing a lack of energy with diffuse palate of pains (cramps, stiffness, and neuropathic burning pain), tremor and fluctuating migrating arthralgia that evolved over a 3-month period. A first Lyme serology proved positive in Western blot. A second Lyme serology, performed a few months later, was negative but showed the presence of IgM antibodies below the threshold of of positivity: OspCBss(0,6), OspCBaf (0, 7), OspCBag (0, 5) and OspCBspp (0, 6).

A 21-day treatment of ceftriaxone (2 g/day) resulted in a spectacular improvement in his overall state of health. Yet, despite the improvement, there remained persistent bouts of moderate asthenia with episodes of arthralgia. Consequentially, two new antibiotic treatments were administered: ceftriaxone (2 g/day) for 15 days and doxycycline (100 mg twice a day) for 1 month. His symptoms disappeared almost completely. However, his symptoms gradually reappeared. A new approach with antibiotics was initiated: ceftriaxone (2 g/day for 1 month) followed by doxycycline (200 mg twice a day) associated with hydroxychloroquine 200 (once a day). Two months later, after a quick improvement, the patient exhibited no symptoms. Five months later, while the treatment was continued, the patient was still asymptomatic.

The clinical improvements and setbacks corresponding strictly to the administration and interruption of antibiotics, and the final remission are in favor of a chronic persistence of Borrelia. Interestingly, the persistence of Borrelia infection, despite a proper antibiotherapy, has been well described in literature.[] It would be due to the existence of the cystic shapes of Borrelia resisting to antibiotics and the creation of extracellular (matrices) biofilms protecting the bacteria.[] Bacteria that grow as a biofilms are indeed protected from killing by antibiotics.

In patients presenting with a chronic form, the interferon-gamma response is not followed by an increase in IL-4, thus suggesting both a persistent Th1 response and a deficiency in the Th2 response.[] Borreliosis may thus induce immunosuppression with a lack of humoral response and long-term immunity.[] False-negative serological results could be attributed to a deficiency of antibody production. As a matter of fact, Leeflang et al. reported a poor sensitivity of the enzyme immunoassay/immunoblot of 0.77 (95% confidence interval: 0.67–0.85) in the diagnosis of neuroborreliosis.[] A meta-analysis of test accuracy reported a sensitivity of only 59.5%, varying from 30.6%–86.2%.[] Antibiotic testing is necessary to reach Lyme disease final diagnosis, namely in patients presenting with negative tests and a suggestive clinical presentation.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

REFERENCES

  1. Miklossy J, Kasas S, Zurn AD, McCall S, Yu S, McGeer PL, et al. Persisting atypical and cystic forms of borrelia burgdorferi and local inflammation in lyme neuroborreliosis. J Neuroinflammation. 2008;5:40. [PMC free article] [PubMed] []
  2. Widhe M, Jarefors S, Ekerfelt C, Vrethem M, Bergstrom S, Forsberg P, et al. Borrelia-specific interferon-gamma and interleukin-4 secretion in cerebrospinal fluid and blood during lyme borreliosis in humans: Association with clinical outcome. J Infect Dis. 2004;189:1881–91. [PubMed] []
  3. Elsner RA, Hastey CJ, Olsen KJ, Baumgarth N. Suppression of long-lived humoral immunity following borrelia burgdorferi infection. PLoS Pathog. 2015;11:e1004976. [PMC free article] [PubMed] []
  4. Leeflang MM, Ang CW, Berkhout J, Bijlmer HA, Van Bortel W, Brandenburg AH, et al. The diagnostic accuracy of serological tests for lyme borreliosis in europe: A systematic review and meta-analysis. BMC Infect Dis. 2016;16:140. [PMC free article] [PubMed] []
  5. Cook MJ, Puri BK. Commercial test kits for detection of lyme borreliosis: A meta-analysis of test accuracy. Int J Gen Med. 2016;9:427–40. [PMC free article] [PubMed] []

Please see Microbiologist Tom Greer’s Important paper on “The Complexities of Lyme Disease”:

https://mail.google.com/mail/u/0/#inbox/FMfcgzGljlpcXbHDNVSpLsZWzfHRfWQV?projector=1&messagePartId=0.1

For more:

Similarly to what’s occurring with effective COVID treatments, treatments for Lyme/MSIDS have been attacked as well.

 

Category:

Lyme, research, Testing, Treatment

Cellular Blueprint of MS Lesions

https://www.nih.gov/news-events/news-releases/nih-scientists-build-cellular-blueprint-multiple-sclerosis-lesions

Friday, September 10, 2021

NIH scientists build a cellular blueprint of multiple sclerosis lesions

Study lays the groundwork for potential new therapies for progressive multiple sclerosis.
An MRI scan of a human brain with multiple sclerosis Mapping multiple sclerosis lesions. Researchers used single-cell RNA sequencing to map the cells found at the edges of chronic MS lesions.Reich lab, NIH/NINDS.

Chronic lesions with inflamed rims, or “smoldering” plaques, in the brains of people with multiple sclerosis (MS) have been linked to more aggressive and disabling forms of the disease. Using brain tissue from humans, researchers at the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS) built a detailed cellular map of chronic MS lesions, identifying genes that play a critical role in lesion repair and revealing potential new therapeutic targets for progressive MS. The study was published in Nature.

“We identified a set of cells that appear to be driving some of the chronic inflammation seen in progressive MS,” said Daniel Reich, M.D., Ph.D., senior investigator at NINDS. “These results give us a way to test new therapies that might speed up the brain’s healing process and prevent brain damage that occurs over time.”

Chronic active lesions are characterized by a slow, expanding rim of immune cells called microglia. Microglia normally help protect the brain, but in MS and other neurodegenerative diseases, they can become overactive and secrete toxic molecules that damage nerve cells. Other cells found at the edge of the lesions, such as astrocytes and lymphocytes, may also contribute to ongoing tissue damage. Prior studies suggest that microglia are the main culprits behind lesion expansion, but the exact types of cells found near lesions and their biological mechanisms are elusive.

To better understand MS lesions, Dr. Reich and his colleagues used single-cell RNA sequencing, a powerful technique which enables researchers to catalog gene activity patterns in individual cells, to examine post-mortem brain tissue of five MS patients and three healthy controls. Samples were provided by the Netherlands Brain Bank, Netherlands Institute for Neuroscience, Amsterdam, the Netherlands, and the NINDS Neuroimmunology Clinic.

“Single-cell RNA sequencing technology allows us to do a much deeper dive into the types of cells present in MS lesions,” said Dr. Reich.

By analyzing the gene activity profiles of over 66,000 cells from human brain tissue, researchers created the first comprehensive map of cell types involved in chronic lesions, as well as their gene expression patterns and interactions.

Dr. Reich’s team found a great diversity of cell types in the tissue surrounding chronic active lesions compared to normal tissue, and a high proportion of immune cells and astrocytes at the active edges of those lesions. Microglia comprised 25% of all immune cells present at the lesion edges.

“Our dataset is very rich. The beauty of having such a detailed map is that now we have a better understanding of the entire network of cells involved in smoldering inflammation,” said Martina Absinta, M.D., Ph.D., a former post-doctoral fellow in Dr. Reich’s lab and current adjunct assistant professor at Johns Hopkins University, Baltimore, who led the study.

More detailed analyses revealed that the gene for complement component 1q (C1q), an important and evolutionarily ancient protein of the immune system, was expressed mainly by a subgroup of microglia responsible for driving inflammation, suggesting that it may contribute to lesion progression.

To determine the function of C1q, researchers knocked out the gene in the microglia of mouse models of MS and examined the brain tissue for signs of neuroinflammation. In mice lacking microglial C1q, they found significantly decreased tissue inflammation compared to control animals. Additionally, in another group of animals, blocking C1q reduced iron-containing microglia, revealing a potential new therapeutic avenue to treat chronic brain inflammation in MS and related neurodegenerative diseases.

According to the authors, it’s possible that targeting C1q in human microglia could halt MS lesions in their tracks.

In MS, the immune system attacks myelin, a protective layer that forms around nerve cells in the brain and spinal cord, leading to vision loss, muscle weakness, problems with balance and coordination, fatigue, numbness, and other debilitating symptoms. A subset of people develop progressive MS, resulting in extensive brain tissue damage and disability. Anti-inflammatory medications help patients manage their symptoms by dampening the responses of immune cells in the blood and lymph nodes. But treatments are not as effective for patients with chronic lesions who experience ongoing brain tissue inflammation.

“We have terrific therapies that block new inflammation but nothing to stop the inflammation that’s already there,” said Dr. Reich. “In order to make strides in developing new therapies for progressive MS, we’re going to need to pick apart the cellular and molecular mechanisms one by one.”

In 2019, Dr. Reich and his team reported that damaging, chronic active lesions may be a hallmark of progressive MS. The current study identifies microglia and C1q as promising targets for progressive MS and supports the use of chronically inflamed rim lesions as an MRI biomarker for disease progression.

There is no cure for MS, and no therapies that directly treat chronic active lesions. By gaining a deeper understanding of lesion features, this study may help pave the way toward early clinical trials to test new therapies for this aspect of the disease.

This study was supported in part by the Intramural Research Program at the NINDS.

NINDS is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH…Turning Discovery Into Health®

Article

Absinta et al. A lymphocyte-microglia-astrocyte axis in chronic active multiple sclerosis. Nature, September 8, 2021 DOI: 10.1038/s41586-021-03892-7(link is external)

__________________

For more:

Category:

Inflammation, Lyme, research

Open Letter to Governors and Congressmen in Lyme Endemic Areas

https://www.change.org/p/the-us-senate-calling-for-a-congressional-investigation-of-the-cdc-idsa-and-aldf

Open letter to Governors and Congressmen in Lyme endemic areas

Carl Tuttle

Hudson, NH, United States

Sep 9, 2021 — 

Please see the latest email below sent to the Chair of the NH Lyme Disease Study Commission…

———- Original Message ———-

From: CARL TUTTLE runagain@comcast.net
To: Leah Cushman <Leah.Cushman@leg.state.nh.us>, Jerry Knirk Jerry.Knirk@leg.state.nh.us
Cc: All members of the NH Lyme Disease Study Commission
Date: 09/08/2021 9:10 AM
Subject: Dr. Paul H. Duray Pathology Fellowship; Open letter to  Governors and Congressmen in Lyme endemic areas

To Members of the Lyme Disease Study Commission,Autopsy results are painting an entirely different picture of disease from what our public health officials have been propagating; “hard to catch and easily treated”

This deception, (for the sake of a vaccine) has caused untold pain and suffering as persistent infection after extensive antibiotic treatment has been denied for three decades. A chronic relapsing seronegative disease did not fit the vaccine model.

Please see the following Open Letter from Tom Grier, Pathology Study Coordinator from the Dr. Paul H. Duray Pathology Fellowship:

A copy of this letter can be downloaded from my personal Dropbox storage area:
https://www.dropbox.com/s/gre4ej07f2p3jd5/congress4pageLTR.pdf?dl=0

_______________________________________

Dr. Paul H. Duray Pathology Fellowship
Thomas M. Grier MS (Pathology Study Coordinator)
902 Grand View Ave
Duluth MN 55812-1146
218-216-5670
donatebrain@gmail.com

Open letter to  Governors and Congressmen in Lyme endemic areas

Why Lyme disease is so confusing, and what the medical experts got wrong

  • Today’s medical perspective of Lyme disease is entirely based on serology (blood tests) and not pathology. (*Pathology includes brain and heart autopsies, culturing, and tissue staining – see photo section.)
  • Lyme disease (LD) blood-tests are fundamentally flawed. *(explanation follows)
  • The authorities that support current diagnostic and treatment guidelines for Lyme disease often have financial conflicts of interests.
  • Since 1975, many so called “FACTS” about Lyme disease have been proven wrong, but medical institutions won’t ever admit their mistakes.
Untrue facts that the public and doctors were told by the IDSA, CDC, NIH, Yale, Harvard, SUNY, and Mayo Clinic that were never true and proven wrong by many studies, and never publicly corrected.
  • Only one tick species (Ixodes damminii) transmits Lyme disease
  • Lyme disease does not cross from infected mother to fetus
  • Lyme disease is not an intracellular disease (can invade inside human cells)
  • Lyme disease stays in the blood and does not enter the human brain.
  • The Lyme disease ELISA tests ate 99% accurate
  • Lyme disease does not persist after 28 days of antibiotic treatment
  • Lyme disease is mainly and arthritic disease
  • Lyme disease is mainly found in the NE USA
  • Lymerix Lyme vaccine had no side effects and was pulled because of anti-vax hysteria.

All these so called “Lyme-Facts” are wrong. They were never true. These published  untruths are a result of major medical institutions relying almost entirely on their own Lyme-Disease-Blood-Tests to determine both diagnosis, and successful treatment. Our own medical experts have continually ignored  overwhelming pathology evidence that proves their assumptions and observations about Lyme have been fundamentally flawed. Their reputations mean more than patient’s lives!

What’s wrong with the Lyme disease blood Tests?

The LD tests that we have used for 35 years are made with B-31 lab-strain of Borrelia burgdorferi . B-31 Lab-strain is not found in ticks, humans or animal reservoirs. It is a manmade analog of a strain found in nature stripped of two chromosomes. The proteins expressed on B-31 Lab Strain Borrelia, never change in culture. In nature these bacterial surface proteins that our immune system attack are constantly changing. B-31 Lab Strain is a cheap way to make consistently bad Lyme-disease blood-tests.

In independent comparison testing: B-31 tests, overall even under the best conditions, are  only 50 % accurate: So, Lyme disease testing has always been like  flipping a coin.

To be blunt, the LD blood-tests using B-31 strain are flawed by design.

  • LD blood tests at best, can only detect one species of Lyme (There are 11 pathogenic species) The blood tests only detect the first isolate of Lyme disease from 1982. The original isolate is a Genus-species we named Borrelia burgdorferi. But since 1982 we have discovered a dozen new Borrelia species that cause human disease. (*See partial table)

Borreilia burgdorferi lato species table
https://www.dropbox.com/s/zgl2pxl1qcl2lwc/Bb%20species.png?dl=0

-The Deer-Ticks also carry Borrelia myamotoi , a Tick-Born Relapsing Fever (TBRFs) that is transmitted from the Deer-Tick in just 20 minutes. So, continuing to tell patients that a deer-tick must be attached for 24-48 hours is irresponsible

Borrelia myamotoi has an affinity for the human brain. The Borrelia myamotoi pathogen is a serious threat in the America.  It is carried by the same ticks as Lyme disease, it has the ability to enter the human brain undetected until brain autopsies are performed. Lyme disease blood tests cannot detect this species of Borrelia.

(See the Borrelia  myamotoi biofilms found embedded in Alzheimer’s amyloid plaques)

-Borrelia species including burgdorferi and B. myamotoi penetrate blood vessels quickly and easily. They are highly motile so within hours of a tick bite, the bacteria can enter any human organ, including the brain and the heart.

Once the Lyme spirochete has entered a blood vessel wall, an organ or has gone inside a human cell: it is harder to detect.

Our tax-dollars pays for the creation of CDC Lyme-disease blood tests. These tests are patented, but the patents are put in the names of CDC officers.

I will show that these tests were never better than 50 % accurate.

The CDC is now funding a new group of Lyme tests. I am asking: Who will own those fresh patents?

Borrelia spirochetes inside hippocampal neurons in Alzheimer’s disease
https://www.dropbox.com/s/5gyqcjn3wp9s93g/Nerve%20Cell.jpg?dl=0

Please stop listening to the Lyme disease experts that misled us since 1975 and start looking at the pathology evidence that proves them wrong.

  • Request human brain pathology studies without CDC or previously mentioned institutions involvement.
  • Create an independent panel of researchers to review the accuracy of Lyme disease IDSA facts
  • Allow doctors to treat beyond the IDSA guideline without harassment or loss of their medical license.
  • Support the investigation to look into the weaponization of Ticks and Tick-Borne-Diseases

Thank You,

100+ References and 100+ Photos available proving persistence post antibiotic treatment.

Sincerely,

Thomas M. Grier
(Director of pathology studies at the Dr. Paul H. Duray Pathology Fellowship)

Brain Autopsy Neuroborreliosis Patient from MN
https://www.dropbox.com/s/qsx6eni1icq4n0w/Brain%20Autopsy%20Neuroborreliosis%20Patient%20from%20MN.png?dl=0

_________________________________________________

WHAT IS PATHOLOGY?
https://www.mcgill.ca/pathology/about/definition

“Pathology is a branch of medical science that involves the study and diagnosis of disease through the examination of surgically removed organs, tissues (biopsy samples), bodily fluids, and in some cases the whole body (autopsy).”

Carl Tuttle
Hudson, NH

Cc:
-Pistis LLC, Hired by HHS
-Bennett Nemser, Senior Program Officer, the Cohen Lyme and Tickborne Disease Initiative
-Holiday Goodreau and Linden Hu, M.D. Co-chairs of the Tick-borne Disease Working Group
-Governor Chris Sununu

Category:

Activism, Lyme, research, Testing