Insane in the membrane - getting ahead of the meningitis fear curve
Don't just get in line like you did last time, please
Meningitis is inflammation or swelling of the meninges: the protective membranes covering your brain and spinal cord. Pretty bad stuff! I would imagine that this is the culprit with regard to the COVID-19 AEs reported, but this article isn’t about the COVID-19 shots.
Read the article entitled: “Meningitis after Vaccination in United States, a Report from the CDC/FDA Vaccine Adverse Event Reporting System [1990–2010] (P03.243)”. It was published on April 23, 2012 in the journal Neurology and it concludes that meningitis cases reported to VAERS post vaccine were probably the result of the vaccine.
The unbalanced distribution of reports of meningitis in the first 6 weeks after vaccination is suggestive of the possibility that some cases may be triggered by vaccination.
Here’s a bullet point summary for you:
Significant number of meningitis reports post-vaccination - From 1990 to 2010, the VAERS database (CDC/FDA Vaccine Adverse Event Reporting System) recorded 722 cases of meningitis following vaccination in the United States, with a mean patient age of 9.3 years (range 0.1–74.7 years). Many cases were serious, including 76% requiring hospitalization and 6.9% resulting in disability.
Timing suggests possible association - Among cases with known vaccination dates, meningitis onset occurred within 6 weeks in 57.5% (415 cases) and within 2 weeks in 45.2% (327 cases), showing a clustering soon after vaccination rather than a uniform distribution over time.
Reports linked to multiple routine childhood vaccines - The highest number was after Hib vaccine (314 cases, 43%), followed by hepatitis B (115 cases, 15.9%), oral polio (114 cases, 15%), DTP (104 cases, 14.4%), DTaP (89 cases, 12.3%), pneumococcal conjugate (88 cases, 12.1%), MMR (84 cases, 11.6%), and IPV (67 cases, 9.2%). The authors conclude that this unbalanced early-onset pattern is suggestive that some cases may be triggered by vaccination.
So lots of cases of meningitis in temporal proximity to vaccination and many were linked to other vaccines as well. Considering there are absolutely no studies done on counter-indications with regard to pumping young people full of so many vaccines, this doesn’t come as a surprise to me.
The current meningococcal (meningitis) vaccines on the market in the U.S. as of March 22, 2026 are Menveo, MenQuadfi, Bexsero, Trumenba, Penbraya, Penmenvy. The ones most associated with AEs in VAERS is Bexsero and Trumenba.
There’s something you need to know about these products and in particular, about Bexsero and Trumenba. They both use recombinant technology and the latter uses synthetic versions of the triacyl lipoproteins. Lipoproteins are like delivery trucks made of protein and fats and the triacyl part just implies the cargo inside these trucks. Chylomicrons are examples of triacyl lipoproteins. You can read this article to learn about chylomicrons and to visualize the role of triacyl lipoproteins.
These are not the same as bacterial triacylated lipoproteins. Bacterial ones are membrane-anchored proteins on bacterial cells with three fatty acids directly attached to the protein itself. Human ones are large floating particles in blood that carry many triglyceride molecules inside a protein/phospholipid envelope. The distinction is important but the design is the same.
Bacteria of all kinds contain triacyl lipoproteins as well.1 These bacterial triacyl lipoproteins are potent activators of the innate immune system, primarily through Toll-like receptor 2 (TLR2), often in complex with TLR1 or TLR6, triggering inflammatory responses. TLR2 (Toll-Like Receptor 2) is one of the main first-line-of-defense alarm sensors that is found on the surfaces of many immune cells like macrophages, dendritic cells, monocytes, neutrophils, B cells, and natural killer cells, and can also be found on epithelial cells and nervous system cells. They detects invaders as a pattern recognition receptor (PRR) via pathogen-associated molecular patterns (PAMPs) which are conserved molecules on microbes. PAMPs found in all sorts of things like bacteria, fungi, viruses, and parasites when “seen” quickly trigger inflammation and immune responses.
These invader detection mechanisms provide protection against infection and this is clear in individuals with TLR2 defects or polymorphisms - they can be more susceptible to certain infections or have altered responses.234 They are also important for adaptive immunity bridging. By activating dendritic cells, TLR2 helps present antigens to T cells and promotes antibody production.
The thing about these guys is the following: overactivation can contribute to excessive inflammation in chronic conditions like autoimmune diseases, atherosclerosis, some cancers, or severe sepsis and underactivation might let pathogens slip through. Such a wonderful and balanced system.
Enter vaccines.
As I mentioned, the MENB vaccine Trumenba uses synthetic versions of triacyl lipoproteins to trigger immunological responses5. These are synthetic/recombinant versions of these molecules that mimic natural bacterial lipoproteins (they are not purified from bacteria but produced in E. coli with the same triacylation). So what do you think will happen if we inject molecules that mimic the foreign molecules that trigger potent immunological responses? This isn’t a hard question to answer.
The lipidation of this vaccine makes it self-adjuvanting: it activates TLR2 (often with TLR1). This enhances antibody production against the protein part (fHbp) for “protection” against MenB disease. But what about molecular mimicry? Concerns about molecular mimicry do exist in the context of certain meningococcal proteins (factor H binding protein (fHbp)) with some human proteins that could lead to autoimmunity.6 So the problem isn’t just overactivation and excessive inflammatory responses being activated, it could be much broader.
Triacylated lipoproteins from Borrelia burgdorferi (causative agent for Lyme) induce both pro-inflammatory (IL-6) and anti-inflammatory (IL-10) cytokines via CD14, mimicking sepsis.7 [8]
As TruthCures recently pointed out on X:
The bottom line is that it is completely insane to willingly inject a synthetic version of the triacyl lipoproteins that cause serious bacterial infections. It’s insane to claim these are vaccines.
I couldn’t agree more.
Trumenba does contain two recombinant lipidated factor H binding proteins (fHbp variants from subfamilies A and B, specifically rLP2086-A05 and rLP2086-B01). These are produced in E. coli as native lipoproteins and are triacylated at the N-terminal cysteine with fatty acids (typically 14–19 carbon chains). The lipid moiety is crucial for structure, immunogenicity, and TLR2-mediated immune activation. Official Pfizer product monographs, FDA/EMA assessments, and peer-reviewed characterizations (ie: 2016 study on lipid roles) confirm this. The antigens are synthetic/recombinant versions of natural meningococcal lipoproteins.
Bexsero uses recombinant proteins (fHbp, NadA, NHBA - some as fusions) produced in E. coli, but these are non-lipidated (no triacyl lipid attachment on the fHbp component). Its fourth component is detergent-extracted outer membrane vesicles (OMVs) from a natural N. meningitidis strain, which contain native bacterial lipoproteins (including triacylated ones), lipooligosaccharide (LOS/endotoxin), and other outer membrane components. OMVs do include lipoproteins and residual LOS (a TLR4 agonist). So Bexsero’s immunogenicity partly relies on OMV-associated TLR agonists.
Borrelia burgdorferi (Lyme guy) expresses multiple triacylated lipoproteins (ie: OspA, OspC) that potently activate innate immunity via TLR2/CD14 pathways, inducing both pro-inflammatory cytokines (ie: IL-6, TNF-α) and anti-inflammatory/regulatory cytokines (ie: IL-10). This dual cytokine response contributes to immune dysregulation, persistent inflammation, and sepsis-like features in disseminated Lyme disease (ie: cytokine storms or immune suppression in chronic cases), as shown in studies on Borrelia lipoproteins and monocyte/macrophage responses.891011
So Trumenba’s triacylated fHbp antigens activate TLR2 similarly producing a parallel innate immune signature, including IL-6/IL-10 induction. [5] Bexsero has some TLR2 agonists via native lipoproteins in its OMVs (though reduced by detergent extraction) and residual LOS (TLR4 agonist), but its main fHbp is non-lipidated, so the triacylated lipoprotein aspect is much less prominent than in Trumenba.
What of adverse events?
I’ll just leave this here.
Overall, in Studies 2-5, among 3,058 participants aged 10 through 25 years who received at least 1 dose of BEXSERO, 66 (2.1%) participants reported serious adverse events at any time during the trial. In the 3 controlled trials (Study 3, Study 4, Study 5) (BEXSERO n = 2,716, control n = 2,078), serious adverse events within 30 days after any dose were reported in 23 (0.8%) participants receiving BEXSERO and 10 (0.5%) control recipients. In Study 4, among participants who received 3 doses of BEXSERO (n = 628), 15 (2.4%) participants reported serious adverse events at any time during the trial.12
Serious adverse events (SAEs) within a month of injection were more prevalently reported in the individuals who got the vaccine (0.8% vs. 0.5%), and the individuals who got 3 shots reported 3 times more SAEs than the individuals who received fewer. Gee. I wonder if these SAEs were death?
In my opinion, these vaccines are highly problematic in terms of AEs and SAEs, and cause more problems than they could ever solve.
As just because this is my schtick, VAERS paints the picture with safety signals as it is designed to do.
The lull in 2021 probably has a lot to do with vaccination in student housing.
Josh Guetzkow pointed this out on X, and yes, there were a lot fewer students living in dorms during COVID, so that likely drove the dip.
Listen, before you think about lining up to appease the upcoming fear mongering as part of plandemic 2.0, think about what you’re thinking of injecting into yourself. It might be more prudent to use common sense instead of panicking and injecting yourself with more crap - especially considering we have no idea what the impact will be in the context of the COVID-19 shots.
Many, many people are still suffering the harms inflicted upon them from those shots.
I would anticipate that these shots cause more problems than they solve, and the precautionary principle dictates a more balanced approach to health outcomes. A huge percentage of the population is still clearing spike protein from their COVID-19 shot experiences, so I would suggest not going yippie-kay-yay on the latest new vaccine.
We have immune systems. There is exceptional complexity and balance therein and the great news is is that we can optimize this system with proper nutrition to include essential elements and compounds, Vitamin C, D, and body movement. The sunshine is gold with respect to immune and energy optimization. Fear is an immune system killer, and more often than not, injected toxins and foreign molecules are bad.
Remember, nature didn’t design our gorgeous immune system to respond to injections - we’ve forced this idea into the realm of science and onto nature itself. The immune system is optimized to respond via inhalation, ingestion and skin exposure.
All in all, it’s been demonstrated that MENB shots can give you meningitis. I’ve provided more evidence that it can induce other AEs and SAEs and induce molecular mimicry and it’s even possible that you could give yourself Lyme-like disease pathology. And more!
So in lieu of taking these known risks, my advice as a non=practicing MD is to simply act with common sense. Know how to spot symptoms of meningitis and keep yourself immunologically and spiritually optimized.
My two cents: Natural immunity reigns.
Think first. In silence.
Nakayama, H., Kurokawa, K. and Lee, B.L. (2012), Lipoproteins in bacteria: structures and biosynthetic pathways. FEBS J, 279: 4247-4268. https://doi.org/10.1111/febs.12041
Texereau J, Chiche J-D, Mira J-P. The importance of Toll-like receptor 2 polymorphisms in severe infections. Clin Infect Dis. 2005;41(suppl 7):S408-S410. doi:10.1086/431990. https://academic.oup.com/cid/article-abstract/41/Supplement_7/S408/665381
Stappers MHT, Thys Y, Oosting M, et al. TLR1, TLR2, and TLR6 gene polymorphisms are associated with increased susceptibility to complicated skin and skin structure infections. J Infect Dis. 2014;210(2):311-318. doi:10.1093/infdis/jiu080. https://academic.oup.com/jid/article-abstract/210/2/311/2908555
Behairy MY, Soliman NA, El-Sokkary RH, et al. Investigation of TLR2 and TLR4 polymorphisms and sepsis susceptibility: a pilot study and in silico analysis. Int J Mol Sci. 2022;23(18):10982. doi:10.3390/ijms231810982. https://pmc.ncbi.nlm.nih.gov/articles/PMC9504743/
Luo Y, et al. The Dual Role of Lipids of the Lipoproteins in Trumenba, a Self-Adjuvanting Vaccine Against Meningococcal Meningitis B Disease. AAPS J. 2016;18(6):1577-1585. doi:10.1208/s12248-016-9979-x
Kanduc D. Molecular mimicry between meningococcal B factor H-binding protein and human proteins. Glob Med Genet. 2023;10(4):331-340. doi:10.1055/s-0043-1776985. https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0043-1776985
Sahay B, Bashant K, Gaji RY, et al. Induction of interleukin 10 by Borrelia burgdorferi is regulated by the action of CD14-dependent p38 mitogen-activated protein kinase and cAMP-mediated chromatin remodeling. Infect Immun. 2018;86(4):e00781-17. doi:10.1128/IAI.00781-17URL: https://journals.asm.org/doi/10.1128/iai.00781-17
Giambartolomei GH, Dennis VA, Philipp MT. Induction of pro- and anti-inflammatory cytokines by Borrelia burgdorferi lipoproteins in monocytes is mediated by CD14. Infect Immun. 1999;67(1):140-147. doi:10.1128/IAI.67.1.140-147.1999. https://journals.asm.org/doi/10.1128/iai.67.1.140-147.1999
Murthy PK, Dennis VA, Lasater BL, Philipp MT. Interleukin-10 modulates proinflammatory cytokines in the human monocytic cell line THP-1 stimulated with Borrelia burgdorferi lipoproteins. Infect Immun. 2000;68(12):6663-6669. doi:10.1128/IAI.68.12.6663-6669.2000. Accessed March 22, 2026. https://pmc.ncbi.nlm.nih.gov/articles/PMC97764/
Dennis VA, Lasater BL, Blanchard RK, Israel BF, Philipp MT. Interleukin-10 anti-inflammatory response to Borrelia burgdorferi, the agent of Lyme disease: a possible role for suppressors of cytokine signaling 1 and 3. Infect Immun. 2006;74(10):5785-5793. doi:10.1128/IAI.00271-06. Accessed March 22, 2026. https://pmc.ncbi.nlm.nih.gov/articles/PMC1594918/
Brown JP, Zachary JF, Teuscher C, Weis JJ. Dual role of interleukin-10 in murine Lyme disease: regulation of arthritis severity and host defense. Infect Immun. 1999;67(10):5142-5150. doi:10.1128/IAI.67.10.5142-5150.1999. Accessed March 22, 2026. https://journals.asm.org/doi/full/10.1128/iai.67.10.5142-5150.1999
https://www.fda.gov/media/90996/download
This is the report I have been waiting for! The pressure on education-aged people is insane again, not least from the fearful parents. It's like no-one learned from the events of only 5 years ago.
Me thinking silently, "Never inject anything".