Key Takeaways from my Chat with Brenda Wilson, PhD.
- Megan McCue
- Jun 30
- 3 min read
Updated: Jul 11

I wanted to share some key takeaways from a Zoom call I had with Dr. Brenda Wilson, a microbiologist and professor at the University of Illinois, Urbana-Champaign.
Her research focuses on bacterial toxins, including botulinum toxin and tetanus toxin. One of the projects she is working on is trying to create an antidote to botulism - a protein that could target BoNT-affected nerve cells and degrade the toxin (help break it down so that it's no longer potent). You can read more about her lab and research here: https://mcb.illinois.edu/directory/profile/wilson7
Botulinum toxin can persist in nerve cells for extended periods of time.
Botulinum toxin is stored in the presynaptic nerve terminal (the end of one nerve cell, where it meets up with the next nerve cell and transmits chemical messages via neurotransmitters). It becomes encased in other proteins, antibodies, and antigens, which help stabilize and “store” the toxin at these terminals. More toxin can then be continually released if those surrounding proteins break down or are disrupted, potentially causing the waxing/waning of symptoms and what us sufferers know as “relapses”. Some triggers for this release of more botulinum toxin may include things like certain medications (anticholinergics, certain antibiotics, etc.) or even things like acupuncture and chiropractic adjustments. Dr. Wilson’s best guess was that, depending on how much toxin has spread into the nervous system, BoNT can remain stored in nerve cells for years. One interesting anecdote from her lab was that mice who were given BoNT and who had become paralyzed and recovered, became re-paralyzed at a later time period, proving that at least some of the toxin had been stored and re-released.
MCAS and other delayed autoimmune responses to botulism are not surprising. Dr. Wilson told me that it’s expected that the body would have an immune response to the toxin, and was not surprised to hear that many people get MCAS after botulism. She explained that the antibodies our immune system makes to target the toxin release mast cells and histamines.
Botulinum toxin, if it spreads into the central nervous system, can cause not just flaccid paralysis, but also spasticity - including muscle tremors and spasms. Despite popular belief - BoNT can cause spastic symptoms in addition to flaccid symptoms if it spreads into the central nervous system
BoNT can and does spread into the CNS - affecting more than just acetylcholine. This has been proven time and time again in the medical literature, and was confirmed by Dr. Wilson. I asked her about CNS symptoms, like brain fog, slow processing speed, word finding difficulties etc. I wanted to know if these symptoms possibly took longer to heal due to CNS neurons being less “resilient” than PNS neurons (or, not able to regenerate as quickly). She said that might be true, but she wasn’t sure.
Many of us sufferers have so many questions for which there are no good answers. The biggest takeaway from my conversation with Dr. Wilson is that there are many unknowns about how this toxin acts in the body once it spreads, and what can potentially help with healing. I know this is frustrating for us all to hear, but I’m hopeful for a future where scientists will begin to show interest in botulism and potential therapies beyond antitoxin, since so many of us are denied treatment at the hospital.




Comments