Posted 6/27/2024 2:11 PM (GMT -5)
After around 2 months, the bruising and microclotting has gone away somewhat. I still have one red/purple spot on my finger.
I took valacyclovir for around a year and didn't have this severe of a problem. Why did I get this now?
The answer seems to be that I backed off the antibiotics and other meds that I was taking. If valacyclovir kills borrelia, why risk the side effects of azithromycin/minocycline/valproate?
In retrospect, this was a bad idea. Antibiotics like azithromycin leave the spirochetes in a dormant state and immobile. Acyclovir apparently does not. Acyclovir kills the bacteria by blocking the DNA polymerase, allowing DNA mutations to accumulate. This is a random process, and some bacteria may survive depending on what part of the genome the mutations are in. Without the ribosome-blocking antibiotics, the surviving bacteria are mobile and may try to hide intracellularly, damaging the endothelium and causing blood clots.
I also started getting a horrific odor that smells like burning. I'm guessing this is some sort of oxidation product from neutrophil superoxide production. It smells different than the vinegar-and-butter smell (byproducts of glycolysis) that I got from killing borrelia with valproate. Why did I not get this smell before? I'm assuming that this is because more superoxide is produced in response to live bacteria than dead ones.
Excessive superoxide production is bad. It kills the bacteria, but also damages human tissue.
I am wondering though, why is TTP reported with acyclovir/valacyclovir but not other inhibitors of borrelia DNA polymerase such as nevirapine and lamivudine? Maybe it does happen and just hasn't been reported.