Case Report: Multifocal Necrotizing Encephalitis and Myocarditis after COVID Shot

June 30, 2022

https://www.preprints.org/manuscript/202206.0308/v1

A Case Report: Multifocal Necrotizing Encephalitis and Myocarditis after BNT162b2 mRNA Vaccination against Covid-19

Michael Mörz
Version 1 : Received: 21 June 2022 / Approved: 22 June 2022 / Online: 22 June 2022 (07:53:57 CEST)

How to cite: Mörz, M. A Case Report: Multifocal Necrotizing Encephalitis and Myocarditis after BNT162b2 mRNA Vaccination against Covid-19. Preprints 2022, 2022060308 (doi: 10.20944/preprints202206.0308.v1). Mörz, M. A Case Report: Multifocal Necrotizing Encephalitis and Myocarditis after BNT162b2 mRNA Vaccination against Covid-19. Preprints 2022, 2022060308 (doi: 10.20944/preprints202206.0308.v1).

Abstract

The current report represents a case of a 77-year-old man with Parkinson’s disease who died three weeks after receiving his third COVID-19 vaccination in January 2022. The patient was first vaccinated in May 2021 with the ChAdOx1 nCov- 19 vector vaccine, followed by two more doses with the BNT162b2 mRNA vaccine in July and December 2021. The family of the deceased requested an autopsy due to the ambivalent clinical features noted before death. The underlying illness (Parkinson’s disease) was confirmed by autopsy. However, no sign of a florid COVID-19 was discovered. Meanwhile, the immunohistochemical staining of the brain and heart revealed previously undiagnosed conditions. The brain, in distinctive, revealed multifocal necrotizing encephalitis with massive inflammatory lymphocyte infiltrates. In addition, the heart showed signs of serious myocarditis. Finally, immunohistochemical staining revealed that the SARS-CoV-2 spike protein was evident in the tissues investigated. Based on these immunohistochemical findings, it appears that the inflammatory changes in the patient’s brain tissues are most likely the result of immunological processes. Concurrently, the absence of SARS-CoV-2 nucleocapsid-protein was evidenced, indicating that the detected spike-protein is unrelated to a SARS-CoV-2 infection. If such an infection was the cause of the spike protein, the SARS-CoV-2 nucleocapsid protein would also be detectable. As a consequence, the confirmed presence of the spike protein had to be attributed to the previous vaccination with the BNT162b2 mRNA vaccine that the deceased patient had received.
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**Comment**
Finally autopsies are being done, despite Fauci telling everyone NOT do autopsies.
This case report is important for  the following reasons:
  1. there is Lyme-associated Parkinsonism
  2. necrotizing encephalitis is also related to tick-borne infections, both viral and bacterial
  3. Inflammation is common with tick-borne illness
  4. Myocarditis is also associated with tick-borne illness
  5. Finding the spike protein in the tissues investigated puts to rest the fact it goes systemically into the body, and not only the injected arm.  This was admitted by a vaccine researcher over a year ago but is still denied/ignored by ‘the powers that be’
    1. It accumulates in ovaries, the liver, spleen, bone marrow, and adrenal glands
    2. It can bind to receptors that are on our platelets & the cells that line our blood vessels
    3. It can cause platelets to clump, leading to clotting, or bleeding which explains the many reports of heart issues after these injections
    4. It crosses the blood, brain barrier and can cause neurological damage
  6. Not having the nucleocapsid-protein ruled COVID infection out, leaving the only reason for the presence of the toxic protein to be due to the injection which led directly to this man’s death

Category:

Heart Issues, research, vaccines, Viruses

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Infectious Agents and Alzheimer’s Disease

https://www.imrpress.com/journal/JIN/21/2/10.31083/j.jin2102073

Infectious agents and Alzheimer’s disease

Thomas Piekut1, Mikołaj Hurła1, Natalia Banaszek1, Paulina Szejn1, Jolanta Dorszewska1,*, Wojciech Kozubski2, Michał Prendecki1
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*Correspondence: dorszewskaj@yahoo.com; jolanta.dorszewska@ump.edu.pl (Jolanta Dorszewska)
Academic Editor: Rafael Franco
J. Integr. Neurosci. 2022, 21(2), 73; https://doi.org/10.31083/j.jin2102073
 
Submitted: 8 March 2021 | Revised: 25 March 2021 | Accepted: 29 April 2021 | Published: 28 March 2022
 
Abstract

Alzheimer’s disease (AD) is the leading cause of dementia worldwide. Individuals affected by the disease gradually lose their capacity for abstract thinking, understanding, communication and memory. As populations age, declining cognitive abilities will represent an increasing global health concern. While AD was first described over a century ago, its pathogenesis remains to be fully elucidated. It is believed that cognitive decline in AD is caused by a progressive loss of neurons and synapses that lead to reduced neural plasticity. AD is a multifactorial disease affected by genetic and environmental factors. The molecular hallmarks of AD include formation of extracellular amyloid (A) aggregates, neurofibrillary tangles of hyperphosphorylated tau protein, excessive oxidative damage, an imbalance of biothiols, dysregulated methylation, and a disproportionate inflammatory response.

Recent reports have shown that viruses (e.g., Herpes simplex type 1, 2, 6A/B; human cytomegalovirus, Epstein-Barr virus, hepatitis C virus, influenza virus, and severe acute respiratory syndrome coronavirus 2, SARS-CoV-2), bacteria (e.g., Treponema pallidum, Borrelia burgdorferi, Chlamydia pneumoniae, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Fusobacterium nucleatum, Aggregatibacter actinomycetemcmitans, Eikenella corrodens, Treponema denticola, and Helicobacter pylori), as well as eukaryotic unicellular parasites (e.g., Toxoplasma gondii) may factor into cognitive decline within the context of AD. Microorganisms may trigger pathological changes in the brain that resemble and/or induce accumulation of Apeptides and promote tau hyperphosphorylation. Further, the mere presence of infectious agents is suspected to induce both local and systemic inflammatory responses promoting cellular damage and neuronal loss.

Here we review the influence of infectious agents on the development of AD to inspire new research in dementia based on these pathogens.

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For more:

Category:

Alzheimer's, Lyme, Parasites, research, Viruses

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Bb Persistence in Lyme and PTLDS

https://journals.asm.org/doi/10.1128/mbio.03440-21

Borreliella burgdorferi Antimicrobial-Tolerant Persistence in Lyme Disease and Posttreatment Lyme Disease Syndromes

Authors: Felipe C. Cabello https://orcid.org/0000-0001-8496-8147 cabello@nymc.edu, Monica E. Embers https://orcid.org/0000-0003-4051-7592, Stuart A. Newman https://orcid.org/0000-0002-3569-6429, Henry P. Godfrey https://orcid.org/0000-0002-7195-6363Authors Info & Affiliations
DOI: https://doi.org/10.1128/mbio.03440-21
Full TextPDF/EPUB
Volume 13, Number 3

28 June 2022
ABSTRACT
The annual incidence of Lyme disease, caused by tick-transmitted Borreliella burgdorferi, is estimated to be at least 476,000 cases in the United States and many more worldwide. Ten to 20% of antimicrobial-treated Lyme disease patients display posttreatment Lyme disease syndrome (PTLDS), a clinical complication whose etiology and pathogenesis remain uncertain. Autoimmunity, cross-reactivity, molecular mimicry, coinfections, and borrelial tolerance to antimicrobials/persistence have been hypothesized and studied as potential causes of PTLDS. Studies of borrelial tolerance/persistence in vitro in response to antimicrobials and experimental studies in mice and nonhuman primates, taken together with clinical reports, have revealed that B. burgdorferi becomes tolerant to antimicrobials and may sometimes persist in animals and humans after the currently recommended antimicrobial treatment. Moreover, B. burgdorferi is pleomorphic and can generate viable-but-nonculturable bacteria, states also involved in antimicrobial tolerance. The multiple regulatory pathways and structural genes involved in mediating this tolerance to antimicrobials and environmental stressors by persistence might include the stringent (rel and dksA) and host adaptation (rpoS) responses, sugar metabolism (glpD), and polypeptide transporters (opp). Application of this recently reported knowledge to clinical studies can be expected to clarify the potential role of bacterial antibacterial tolerance/persistence in Lyme disease and PTLDS.
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**Comment**
What’s truly sad is none of this is new.  This 2017 study talks about the stringent response, and this 2016 presentation by Dr. Zhang discusses the importance of persisters, or the dormant form borrelia takes when it feels threatened.  And this 2017 study also points out that Bb mutates (changes form) as previously described by Barbour and Hays way back in 1986.  I’m sure there are many more older studies presenting all of this.
Why is this simple fact still not believed and accepted?

What is not discussed in this article is the fact most Lyme/MSIDS patients are infected with multiple infections simultaneously, further complicating their cases, and requiring different medications.  This article shows that higher doses of antibiotics are required to eliminate a bacterial infection when other microbes are present, yet corrupt public health ‘authorities’ continue to push a faulty one pathogen, one drug paradigm based on faulty testing that misses 70-86% of cases!

What is also not discussed in this article is the larger subset of patients (30-40%) that are diagnosed and treated late – thereby not even making the PTLDS group, and therefore never studied in research.  This is a huge chunk of people are often seronegative in testing and don’t have the EM rash.  This is me, and everyone I work with.  There is ZERO data on us.  ZERO.

The PTLDS moniker is confusing at best and misleading at worse.  The whole ball of wax is based on faulty premises and faulty research.  Time for a do-over.

For more:

Similarly to polarization on COVID treatment, it’s not a scientific debate. It’s a political one.

Category:

Lyme, research, Uncategorized

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Heroic Mom Exposes Junk COVID Shot Data

June 29, 2022

https://thehighwire.com/videos/mom-exposes-bunk-covid-vax-data/  Video Here (Approx. 8 Min)

June, 28, 2022

Heroic Mom Fact Checks CDC, ACIP, Researchers and Media

Del BigTree and Jeffrey Jaxen break down a mom’s astute work showing that COVID is NOT the “leading cause of death” in children as well as dismantles fraudulent trial data being used by corrupt public health ‘authorities’ to push gene-therapy shots on children.

The following deceitful CDC slide, based upon a seriously flawed study has been used ad nauseum by “experts” and the media to push gene therapy injections upon children.

Go here for this savvy mom who fact-checks public health ‘experts’ and a bought-out media and believes this faulty study should be fully retracted. 

SUMMARY:

  • Their Covid numbers came from NCHS which includes deaths where Covid is listed anywhere on the death certificate which over counts Covid deaths because it includes death that had a different underlying cause.
  • While the pre-print article states “we only consider COVID-19 as an underlying (and not contributing) cause of death”, this is blatantly false. This same error was addressed previously where the author was called out and subsequently posted follow-up where he admitted it was wrong to compare multiple causes of death data with underlying causes of death data.
  • The time periods used are also faulty and end up being ranked TWICE for each age group.  This is completely misleading.
  • The CDC used the rankings for cumulative COVID deaths further overcounting deaths compared to other causes of death.  Please see the article for the corrected rankings and deaths.
  • Even corrected rankings overstate the impact of COVID because the top few causes of death far outweigh the causes further down the list.  For example:
    • Ages 1-4, accidents account for almost 25 times as many deaths as Covid-19 on an annualized basis
    • for each of the 4 age groups covered by the CDC slide, the very broad “accidents” is the leading cause of death. If we break that down further, causes of death like drownings, vehicle crashes, drug overdoses, would be individual causes of death greater than Covid in various age groups. Actuary Mary Pat Campbell explains this well in a couple of blog posts on pediatric Covid deaths.
  • Why did they use data from 2019 and not 2020 or 2021 when aspects of COVID response affected some of the leading causes of death?
  • Why did a group of UK researchers analyze US deaths instead of for their own country?  Could it possibly be due to the fact the US counts Covid deaths very generously, so our data made it easier to present Covid as a leading cause of death? And why did they inflate the counts by including 18 and 19 year olds in the data, when the pediatric population is generally accepted to be 0-17?
  • How did Dr. Katherine E. Fleming-Dutra, MD at the CDC and pediatrician and doctor of emergency medicine not realize this data was seriously flawed and out of line with all other data?
  • How did a preprint get used in an ACIP and FDA presentation with no oversight and without the quality of data being fully vetted? And how come a mother, on her own personal time, become more knowledgeable about COVID deaths in children than academics and public health ‘officials’ whose job it is and who are paid by tax-dollars?

Important excerpt:

We are forced to believe that the CDC researchers who put this data together are either incompetent or liars, and when all the mistakes go in the same direction, it certainly seems like the CDC uses whatever data they can find to push their agenda without any consideration to its veracity. ~ Kelley, Pediatric News

The author is completely correct when she states that this is an international and national disgrace, and that the CDC and much of the academic and pubic health community have utterly failed the American public.

BRAVO!  Thank God for moms!

https://rumble.com/v18s66i-bombshell-dr.-clare-craig-exposes-how-pfizer-twisted-their-clinical-trial  Video Here (Approx. 4 Min)

And another astute woman, Dr. Clare Craig a diagnostic pathologist, breaks down another horrific example of fraudulent COVID shot trials on children.

SUMMARY:

  • out of 4,526 children, (6 months to 4 years) 3,000 didn’t make it to the end of the trial!
    • this is often due to severe side-effects
    • for this reason alone, this trial should be deemed null and void
  • 6 of the children (2 to 4 years) in the “vaccinated” group were diagnosed with “severe COVID,” compared to just one in the placebo group
  • the only child requiring hospitalization was in the “vaccinated” group
  • in the 3 week follow-up, 34 “vaccinated” children were diagnosed with COVID compared to 13 of the unvaccinated
  • Between doses 2 &3 which had an 8-week gap, “vaccinated” children again experienced higher rates of COVID
  • After the 3rd dose, “vaccinated” children again experienced higher rates of COVID
  • They only counted 3 cases of COVID in the “vaccine” arm but 7 cases in the placebo group, literally ignoring 97% of all the COVID cases that occurred during the trial to conclude that the shots were “effective” in preventing COVID
  • While they claimed the 3-dose regimen reduced COVID, 12 kids actually caught COVID TWICE in the 2-month follow-up – 11 of which were “vaccinated”!
  • Confidence interval for Pfizer’s shot is -370% at the lower end of the 95% which suggests kids who get the shot are nearly FOUR times more likely to become ill with COVID than their unvaccinated peers

Robert F Kennedy explains the dirty little secret that it’s imperative the ‘powers that be’ get the COVID shots recommended for children because when that happens “vaccine” manufacturers are protected legally from any liability. 

This is the end-game.  Your children for their profit.

And this insightful interview with Dr. Tess Lawrie explains why the COVID shots should be recalled.

Three more perfect examples of getting straight, transparent answers outside corrupt research institutions and conflict riddled public health ‘authorities‘.

There is an urgent need to break the public health monopoly that has been used to enslave the public.

Category:

Activism, research, vaccines, Viruses

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Non-Funded Study Shows LDN is a Broad-Spectrum Analgesic

https://www.futuremedicine.com/doi/10.2217/pmt-2021-0122

Low-dose naltrexone, an opioid-receptor antagonist, is a broad-spectrum analgesic: a retrospective cohort study

Samuel J Martin, Heath B McAnally, Paul Okediji and Moshe Rogosnitzky

Published Online:15 Mar 2022https://doi.org/10.2217/pmt-2021-0122

Abstract

Aim: To evaluate the use of low-dose naltrexone (LDN) as a broad-spectrum analgesic. Methods: Retrospective cohort study from a single pain management practice using data from 2014 to 2020. Thirty-six patients using LDN for ≥2 months were matched to 42 controls. Pain scores were assessed at initial visit and at most recent/final documented visit using a 10-point scale. Results: Cases reported significantly greater pain reduction (-37.8%) than controls (-4.3%; p < 0.001). Whole sample multivariate modeling predicts 33% pain reduction with LDN, with number needed to treat (for 50% pain reduction) of 3.2. Patients with neuropathic pain appeared to benefit even more than those with ‘nociceptive’/inflammatory pain. Conclusion: LDN is effective in a variety of chronic pain states, likely mediated by TLR-4 antagonism.

Plain language summary

Naltrexone has historically been used to treat various substance use disorders, but recent discoveries have sparked interest in using low-dose naltrexone (LDN) to manage chronic pain. This study compared pain levels reported by patients before and after at least 2 months of LDN treatment to those reported by patients with the same painful diseases, who did not take LDN. Overall, patients who took LDN reported significantly more pain relief than patients who did not take LDN. How LDN alleviates pain seems complex, but apparently involves an anti-inflammatory effect on cells in the brain and spinal cord. LDN is extraordinarily safe, with no known risks (unlike most standard pain medications), and should be studied more in the treatment of chronic pain.

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**Comment**

And this has been our personal findings as well.

I wish more offices did this internal research.  The data is all there begging to be collected, organized, and published.  This is a perfect example of how we can get answers without  corrupt, conflict riddled research institutions, government, and government collecting (bought out) researchers.

For more on this:  https://madisonarealymesupportgroup.com/2022/06/29/the-urgent-need-to-break-the-public-health-monopoly/

For more on LDN:

Category:

Lyme, Pain Management, research, Treatment

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