Post-Vaccine autopsy reports continue to miss out on critical information.
Why is there so much that is still not being investigated?
Otherwise Healthy…
We’re dealing with the unfortunate reality that some people are dying after receiving their COVID vaccines. At the same time there’s no clear evidence towards the actual extent of death and harm occurring, with most evidence having to rely on case reports or highly messy excess death data.
So far minimal autopsy reports have come to light to provide some much-needed insights into the deaths of some individuals- it’s another circumstance of the harsh reality that is going on. And yet even with this data there appears to be so much that continues to be missing. More importantly, evidence towards consilience continues to be lacking, as consilience would provide the most evidence towards finding the mechanisms of these vaccine harms.
But this also comes as reports on these autopsies tend to lack more critical assessments. Rather, it’s become the norm to post a case report and argue that the individual being examined is otherwise healthy.
That is to say, if we excuse a deceased individual’s comorbidities they will appear healthy, and then we can make a claim that many otherwise healthy people are dying.
This narrative is a strange one because it makes an otherwise unnecessary argument.
It is not the intention of those seeking answers to question the prior health of the individual, but rather to look at the harms and deaths post-vaccination through the lens of an individual’s personal health history to understand whether this history may have played some additional role in the unfortunate outcomes.
Consider that one of the first autopsy reports was of two teenage boys who died days following a second dose of the BioNTech vaccine as reported by Gill, et al.1, with initial reports on Substack and other websites remarking that these teenage boys were healthy/had no prior medical history prior to dying due to the vaccines.
On the contrary, one teenager was diagnosed with ADHD and was reported as taking amphetamines/dextroamphetamines during school for his ADHD while the other teenager was reported to have been obese.
This led me to write a series on catecholamines, partially due to a hypothesis proposed by Dr. Cadegiani2 which argued a hypercatecholaminergic response as a consequence of the vaccines. And as I came to find, there appears to be an intrinsic relationship between catecholamines, ADHD, and some of the ADHD medications in use.
This also corroborates with the contraction band findings which are similar to those who experience takotsubo cardiomyopathy3, which is also possibly caused by a hypercatecholaminergic response.
This hypothesis doesn’t appear to have taken off much, but this may be due to other myocarditis reports that point to different pathophysiological changes in the heart post-vaccination, such as older adults appearing to have a greater bias towards lymphocyte infiltration relative to young vaccinees that, with the limited data available, seem to be biased towards innate immune infiltration (leukocytes such as neutrophils and eosinophils).
Altogether, if one were to propose a hypercatecholaminergic response in regards to the vaccine, then wouldn't someone diagnosed with a disorder associated with catecholamine dysfunction who may also be taking medications intended to alter a catecholamine response have a different risk factor for a vaccine that may increase the risk of a hypercatecholaminergic, response as opposed to the general population, and wouldn’t this factor be worth investigating?
What this tells us is that we cannot exclude the diagnosis of ADHD (as well as the prescription medications) as possibly having some effect on this teenage boy. Rather than argue that he is healthy and sidestep his medical history, it’s within the context of his medical history that we may paint a clearer picture of whether his disorder and medications may have had some effect as well in the adverse reactions.
So far this point is a mere speculation because we don’t have any way of investigating this idea further.
This same issue with respect to one's prior medical history came about when it was reported that an elderly man with Parkinson’s fainted two weeks after receiving his booster and later died.4 It was suggested that this man had suffered from encephalitis as his cause of death with evidence of myocarditis as well (as was noted after his first vaccine dose where he complained of cardiovascular issues and required treatment).
What’s interesting is that in this case this man had symptoms following his second dose, including behavioral and psychological changes, as well as worsening PD and motor symptoms which didn’t appear to subside by the time he received his booster.
This is all important, because there is some evidence to suggest that symptoms of encephalitis may be missed as signs of worsening PD.
After reporting on this case report I came across this article in Parkinson’s News Today with the following headline:
The article points to a a case report5 which noted a woman with a 2-year history of PD who eventually showed signs of slowing as well as unresponsiveness to L-dopa treatment. Because this woman had signs of bradykinesia it was assumed that these symptoms were an indication of worsening PD symptoms rather than something else, and her condition continued to worsen over the course of months.
After various clinical tests it was found that this woman apparently had developed N-methyl-d-aspartate receptor antibody-mediated encephalitis, or NMDAR-E for short.
NMDAR-E is an autoimmune disorder in which IgG antibodies target NMDA receptors, leading to various cellular processes such as uptake of receptors that lead to cellular dysfunction and the end result of encephalitis. The cause of this autoimmune disorder is generally unknown, although some evidence notes that cross-reactive antibodies associated with tumors or viruses may be responsible for the priming of anti-NMDAR antibodies.
More can be read on NMDAR-E here.6
The case report provides the following remark in the Discussion [context added]:
In our patient NMDAR-E diagnosis was extremely challenging, since her symptoms were interpreted as a deterioration of PD for some months. In this setting, clinical clues, such as a history of autoimmunity, the complete lack of response to L-dopa, and the progressive evolution to frank mutism led us to consider alternative causes, and perform a lumbar puncture, which, in turn, proved to be fundamental to generate the hypothesis of intrathecal immune activation, after the detection of unique-to-CSF OCBs [oligoclonal IgG bands]. On the other hand, routine CSF analysis with cell count were normal, with the exception of the presence of OCBs, confirming that autoimmune encephalitis in elder patients can present with few signs of CSF inflammatory signature (Escudero et al., 2017). Ultimately, the presence of disease-specific antibodies in the CSF (100% specificity, using two techniques (GresaArribas et al., 2014)) strongly supported the diagnosis of an NMDAR-E.
This information has actually made me consider whether the Mörz, M. case report of worsening PD may have been an indication of NMDAR-E that was overlooked as worsening PD symptoms, and could have possibly been caught prior to the booster which could have exacerbated the autoimmune response (remember that this is only relevant IF NMDAR-E was the cause of death, of which we may not find out).
In corroboration of this assumption some evidence have come out of NMDAR-E occurring post-COVID infection as well as post-COVID vaccination.
A case report from 20217 noted a young woman in her 20s who began experiencing psychosis following her first dose of the BioNTech vaccine.
Note that the study also notes prior evidence of NMDAR-E occurring post-COVID infection as well.8
The case narrative notes the following:
A female in her 20's presented to the Emergency Department (ED) with a chief complaint of urinary frequency 1 week after receiving her first dose of the Pfizer-BioNTech COVID-19 vaccine (Figure 1). The patient's family stated she had increasingly frequent bouts of anxiety, decreased mentally acuity, insomnia, and a fixation that she suffered from irritable bowels and kidney disease. She displayed waxing and waning hypochondriacal delusions that she had contracted COVID-19 and that “her body was shutting down.” The patient was also noted to have some motor dysfunction and a transient bout of aphasia during this time. There were no complaints of antecedent infection, fever, or headache. Family history and past medical history were non-contributary. The physical examination showed tachycardia and hypertension but otherwise unremarkable. Hematology and metabolic labs and urinalysis were normal.
Due to various factors, including the patient’s deterioration immediately following her COVID vaccine, the researchers suggested a possible autoimmune response brought on by the vaccine, with later diagnostic results noting very high anti-NMDA titers confirming this hypothesis.
This, again, highlights the important of understanding a patient’s prior history and examining adverse reactions within that context.
This raises questions with respect to PD symptoms following both a COVID infection or vaccination, and how these may be cases of autoimmune-mediated encephalitis that may be overlooked as something else.
But it also emphasizes the point that clinicians should take care not to overlook symptoms, especially in those with comorbidities which may mask the actual presentation of other symptoms such as encephalitis in this case.
Those who have had a prior history of NMDAR-E may be more prone to encephalitis following a COVID infection or COVID vaccination, and yet this likely doesn’t appear as a possible contraindication for the administration of these vaccines.
This same remark is made within the conclusion of the Flannery, et al. case report (emphasis mine- note that this summary also uses the phrase "previously healthy” while also arguing the case of checking if someone had a prior case of anti-NMDAR encephalitis):
In summary, we present the first case of anti-NMDAR encephalitis complicating SARS-CoV2 vaccination in a previously healthy young woman. This case provides an important reminder that (i) psychiatric clinical presentations warrant a thorough medical workup, including brain imaging, CSF analysis, anti-NMDAR antibody testing, and a vaccine history; (ii) combined therapies of blocking (IVIG), reducing production of (rituximab), and even removing (plasmapheresis) harmful anti-NMDAR may be the optimal strategy to reverse the neurological and psychiatric symptoms driven by anti-NMDAR antibody production. Fortunately, prompt therapy targeting anti-NMDAR antibodies resulted in achieving and sustaining an excellent clinical outcome. In addition to providing clinicians the opportunity to identify potential vaccine-associated anti-NMDAR encephalitis, particular attention may be needed to patients receiving COVID-19 vaccine who have previously have had anti-NMDAR encephalitis.
This further emphasizes a serious issue when we overlook prior comorbidities and act as if they have no bearing with respect to a vaccine injury.
A recent case report of multi-organ inflammation
This post did not come out of nowhere, as it was spurred on by a recently circulated case9, such as reported on by Stephanie Brail of Wholistic in response to Dr. Campbell’s video being removed from YouTube which covered this autopsy finding.
The report notes a Japanese 14-year old girl who died 2 days after receiving a BioNTech booster.
The case report notes the following:
The day after vaccination, she developed a fever of 37.9 °C, which resolved by the same evening. Her sister, who had slept with her that night, reported that she woke up briefly because she was having difficulty in breathing, talked with her sister, and went to bed soon after. The following morning, her mother noticed that she was not breathing and had a pale appearance, and she immediately called an ambulance. The patient was in cardiopulmonary arrest when the ambulance crew arrived at their house and attempts to administer advanced life support were unsuccessful. She died 45 h after the third vaccination. After the first dose of vaccine on 12th September 2021, she had arm pain without fever. The day after the second dose on 3rd October 2021, she missed school because she had a fever of less than 38 °C. All three vaccines were made by Pfizer. An autopsy was performed the following day to evaluate the cause of sudden death.
Histological examinations of various organs noted lymphocyte infiltrates such as CD3+ and CD68+ T-cells, as well as eosinophils similar to findings from Gill, et al. and Mörz, M. Although eosinophils were found, the infiltrates appear to have been dominated by T-cells and macrophages:
Lymphocyte cellular infiltrates, including eosinophils, were observed in the lungs, pericardium of both atria and adjacent myocardium, liver, kidneys, stomach, duodenum, and diaphragm (Fig. 1 ), and mild cellular infiltration was also observed in the pericardium of the right ventricle. The brain showed congestion. In the hippocampus a slight lymphocytic infiltration was observed. Immunostaining with an anti-CD3 antibody (Dako 1:200) (Fig. 1) and anti-CD68 antibody (Dako 1:200) (Fig. 1) revealed that most of the infiltrating cells were T cells and macrophages.
In addition, this young girl appeared to have extremely elevated levels of SARS-COV2 antibodies (43600 U/mL) as well as the cytokine IL-6 (226 pg/mL).
In the end, it appears that myopericarditis was the main cause of death (emphasis mine):
A diagnosis of vaccine-related multiple-organ inflammation was made based on the absence of bacterial or viral infection, lack of a past medical history suggestive of autoimmune disease, no allergic reaction, and no drug exposure other than the vaccine. Myopericarditis is a form of multiple-organ inflammation. Although pneumonia is involved, pneumonia alone is rarely a cause of sudden death, and the presence of erythrocyte-laden macrophages as well as congestive edema of the lungs on histology suggested signs of heart failure from the previous day. Although the extent of inflammation was relatively narrow, the presence of foci centered on the atria and breathlessness are the findings that raise the suspicion of heart failure several hours before death. This led to the diagnosis that the cause of death was vaccine-related myopericarditis, which led to severe arrhythmias and progressive heart failure.
Overall, this information is rather alarming. It’s rather concerning that such a fate had to occur in this young girl, especially for something that could have been completely prevented.
And yet, at the same time I found this autopsy report frustrating for a completely different reason, and that’s because this report is another failure to capture critical information.
This review didn’t appear to have included immunohistochemical staining for the spike protein which other autopsy reports have done, so this doesn’t provide us insights as to whether spike may have been detected all throughout the body. This is made critical given the fact that myopericarditis is being argued to have been the cause of death which raises questions with respect to spike-induced inflammation.
The authors also noted a very high level of SARS-COV2 antibodies. Were these antibodies bound to vaccine spike or unbound? A prior report of myocarditis in adolescents tells us that bound/unbound spike dynamics may be different in adolescents and is something worth investigating, as well as the ratio of S1/full spike. One thing that must be considered is whether this adverse reaction is one caused by the spike effect or one caused by the immunological response with the possibility of autoimmunity occurring. There continues to be a lack of characterization of these antibodies and whether some may be cross-reactive with human proteins such as myosin in the heart.
There also isn’t any information provided with respect to this young girl’s response to the prior vaccinations and whether there were indications that something may have been amiss before receiving the booster.
But once again there appears to have been one critical thing that the researchers appear to have glossed over via a remark about this young girl appearing “healthy” (emphasis mine):
Despite her history of orthostatic dysregulation, she was healthy by nature and was active in her middle school athletic team.
The researchers haven’t taken to using the language of “otherwise healthy”, but here they reported a history of orthostatic dysregulation but didn’t appear to provide any context to this issue.
Orthostatic dysregulation refers to an impairment in which the body cannot compensate for changes in blood flow and gravitational dynamics when one stands up (orthostatic). People who experience orthostatic dysregulation may show signs of vertigo, loss of consciousness, heart palpitations, and may faint, among other signs and symptoms.
There’s some evidence to suggest that orthostatic dysregulation is associated with autonomic dysfunction, and there appears to be a correlation between those with OD and sleep disorders and issues with circadian rhythms.
Remember that the autonomic system is heavily influenced by none other than catecholamines.
So here we have a young girl who appears to have a possible impairment (OD) stemming (speculatively) from autonomic dysfunction and may be related to catecholamines in some way.
This brings us back to Cadegiani’s hypothesis as well as the autopsy findings from Gill, et al.
That is to say, was this young girl predisposed to some form of catecholaminergic dysfunction, which may have contributed to the widespread inflammation, the myopericarditis, and her eventual death?
Again, the biggest problem here is that we just don’t know! Because investigations still continue to miss out on key details.
It’s as if there are bits of information here, ready to get closer to some form of consilience, and yet there seems to always be enough missing to leave us wanting more than just having to speculate.
Suppose that there was someone who was morbidly obese, contracted COVID, and unfortunately died. Suppose that in this scenario the autopsy report noted the following:
Aside from the morbid obesity the patient appeared otherwise healthy prior to his infection.
We would already know that this would be a highly contentious statement- obesity is related to MANY comorbidities, and we also know that those who are overweight or obese are more at risk for COVID hospitalization and death.
So would we find it fitting for an autopsy report to make the claim that aside from one’s comorbidities the person seemed fine when it is the comorbidity that may have increased the risk of worse outcomes?
And yet this continues to be some of the language used in both case reports and online discourse.
As this post has become much longer than I had hoped I will leave the consilience analysis for the next post.
But hopefully this is a reminder that we are still missing out on critical information when trying to answer why some people are experiencing these adverse reactions post-vaccination, and why we shouldn’t be quick to jump on the narrative of proclaiming “otherwise healthy” if it prevents people from digging deeper and trying to piece things together.
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James R. Gill, Randy Tashjian, Emily Duncanson; Autopsy Histopathologic Cardiac Findings in 2 Adolescents Following the Second COVID-19 Vaccine Dose. Arch Pathol Lab Med 1 August 2022; 146 (8): 925–929. doi: https://doi.org/10.5858/arpa.2021-0435-SA
Cadegiani F A (August 11, 2022) Catecholamines Are the Key Trigger of COVID-19 mRNA Vaccine-Induced Myocarditis: A Compelling Hypothesis Supported by Epidemiological, Anatomopathological, Molecular, and Physiological Findings. Cureus 14(8): e27883. doi:10.7759/cureus.27883
Ahmad SA, Brito D, Khalid N, et al. Takotsubo Cardiomyopathy. [Updated 2023 Jan 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430798/
Mörz M. (2022). A Case Report: Multifocal Necrotizing Encephalitis and Myocarditis after BNT162b2 mRNA Vaccination against COVID-19. Vaccines, 10(10), 1651. https://doi.org/10.3390/vaccines10101651
Gastaldi, M., Arbasino, C., Dallocchio, C., Diamanti, L., Bini, P., Marchioni, E., & Franciotta, D. (2019). NMDAR encephalitis presenting as akinesia in a patient with Parkinson disease. Journal of neuroimmunology, 328, 35–37. https://doi.org/10.1016/j.jneuroim.2018.12.002
Samanta D, Lui F. Anti-NMDA Receptor Encephalitis. [Updated 2022 Dec 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK551672/
Flannery P, Yang I, Keyvani M and Sakoulas G (2021) Acute Psychosis Due to Anti-N-Methyl D-Aspartate Receptor Encephalitis Following COVID-19 Vaccination: A Case Report. Front. Neurol. 12:764197. doi: 10.3389/fneur.2021.764197
This is taken from Table 1 of Flannery, et al. Keep in mind the neurological symptoms and findings for differences in presentation.
Nushida, H., Ito, A., Kurata, H., Umemoto, H., Tokunaga, I., Iseki, H., & Nishimura, A. (2023). A case of fatal multi-organ inflammation following COVID-19 vaccination. Legal medicine (Tokyo, Japan), 63, 102244. Advance online publication. https://doi.org/10.1016/j.legalmed.2023.102244
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Why?
They'd just as soon it never be investigated.
They already have the answers, just nobody that likes them.
Forgive and most of all, forget.
Marburg is coming, the sooner you forget about SARS-CoV-2 the better.