There is a lot of confusion about biofilms and Lyme disease. I have frequently heard from patients that a “biofilm-buster” is needed. Biofilms consistent of colonies of microorganisms who live within the confines of a protective membrane made of mucopolysaccharides with odd pieces of DNA. These molecules are long chain sugars. We know that biofilms provide a protective niche permitting the survival of Lyme spirochetes and many other bacteria. Most of what we know about biofilms is derived from in-vitro, test tube studies which focus on surface infections, for example, diabetic wounds and cytstic fibrosis. Most of this research has focused on Pseudomonas, a notoriously stubborn pathogen associated with these diseases. We have precious little information about Lyme biofilms.
Biofilms comprised of Pseudmonas aeruginosa have experimentally been treated with a number of topical agents, like xylitol, with some success. Ammons found that lactoferrin has biofilm activity for surface Pseudomonas. How well does this translate? One mechanism of action is the chelation of iron. While this may work with Pseudomonas it may not work with Lyme (even topically), because these spirochetes use manganese in lieu of iron. Other agents, like stevia, have had some success treating Lyme biofilm-like colonies but these finding are from test tube studies and likely do not apply to systemic infection.
Proteolytic enzymes have been widely touted as ‘biofilm-busters.” This has never made sense to me since biofilms do not contain protein.
Yeast have biofilms. Cremer et al, current Antimicrobial Agents Chemotherapy, screened 1600 drugs/agents and found that Artemisinins were synergistic with miconazole for the treatment of Candida albicans biofilm related infection. This synergy did not occur with several other anti-fungal drugs studied. I am sure many readers have personal experience with stubborn Candida biofilms on their tongues. This highlights the fact that drugs used for a single purpose (artemisinin for Babesia) may help in unexpected ways (Candida).
The recent study from Hopkins about Lyme persisters and the original studies of Sapi are at odds with one another. The Hopkins study lumps cysts or round bodied forms together with biofilm-like colonies calling them stationary phase bacteria. Sapi considers cyst or round body forms and biofilm forms to be two separate entities. Hopkins reports that doxycycline, amoxicillin and Flagyl have no effect on stationary forms. Sapi found amoxicillin and Flagyl have anti-cyst effects and that Tindamax works well against cysts and also kills spirochetes within biofilms. More study is needed.
An explanation of Tindamax’s greater effect against biofilms may be due to disruption of quorum sensing: a process by which bacteria within the biofilm communicate with each other by molecular signaling (very complicated stuff). In Pseudomonas models a number of antibiotics have been shown to interfere with quorum sensing and associated virulence factors.
Experimentally, these have included: Zithromax, Flagyl, Tindamax and Cipro.
The take-away point is that the best biofilm-buster might be a specific antibiotic or combination of antibiotics.
Cyst forms, round body forms, L-forms, biofilms forms: now we have a new buzz word to add to the list, quorum sensing (QS).
I think parsing ‘Lyme” into these parts and trying to tailor therapy for each one is generally not helpful. These notions are helpful in a general sense only; patients respond differently, unpredictably. Experience remains our best teacher. Theory is no substitute for that which is tried and true.