Lyme Disease

Important quotes 1. They isolated the biofilm-like microcolony (MC) and planktonic (spirochetal form and round body) (SP) variant forms…. 2.  They were “more tolerant to the current Lyme antibiotics,” but [the biofilm Lyme bacteria] also caused more severe arthritis in mice….” 3.  Only the combination of daptomycin, doxycycline, and ceftriaxone could kill the biofilm form.” I strongly believe the biofilm killing was done only by

These are smart and fine doctors I respect. They do not read definitive books like our #1 Artesunate, Artemisinin, Artemether, Artemisia annua herb book. You can drown a sumo wrestler in artemisinin, and it will not cure babesiosis. Ten milliliters a day of atovaquone yellow paint rarely has any effect. Our $3.8 million in self-funded research showed that the common

Routine Lyme medicines bounce off Lyme biofilms unless you use very strong treatments, which I outlined in 2014. Our Combatting Biofilms is still number one on the topic. But doctors have full waiting rooms, insurance that takes their time, and low reimbursement—hence, fast appointments. They have no time to read many books in a year. Dominico and fellow researchers offer these

The problem with using phages to treat Borrelia is their variable genome, exchange of genetic material and the fact that no two Borrelia are alike in living hosts (as opposed to lab cultures). One would have to engineer an array of phages and give them all each time. Even with this, some bugs may escape. Some feel there needs to

Hundreds of articles show that doxycycline and amoxicillin/Augmentin and IV/IM Ceftriaxone do not kill persisters or biofilm forms. Ceftriaxone [Rochephin] Pulse Dosing Fails to Eradicate Biofilm-Like Microcolony B. burgdorferi Persisters And yet these Lyme are killed well by Daptomycin + Doxycycline + Cefuroxime without Pulse Dosing Feng and coauthors suggest one possibility for persistent illness in some treated Lyme patients… “… is due to Borrelia burgdorferi persisters that current antibiotics

In previous studies, we showed that fibroblast growth factor receptors (FGFRs) contribute to inflammatory mediator output from primary rhesus microglia in response to live Borrelia burgdorferi. We also demonstrated that non-viable B. burgdorferi can be as pathogenic as live bacteria, if not more so, in both CNS and PNS tissues. In this study we assessed the effect of live and non-viable B. burgdorferi in inducing FGFR expression from rhesus frontal