So more members who have had good results with the Disulfiram? I do agree with the way the different laboratories induce persisters.
Zhang has the best method as far as my very limited knowledge of microbiology can tell.
Zhang has said Disulfiram was rather weak in a video which is no longer available online. Lewis is not referring to the drug in public but a lecture in a university ended up online.
When Lewis determines the drug effect he doesn't take into calculation biofilms. His rationale is: the drugs must freely diffuse into the biofilm because food does too and the molecular size of nutrients and antibiotics do not differ much.
He says the reason for biofilm persistence is only persister cells. Zhang and Sapi have a different approach to that rationale. Herbert Allen's hypothesis with regards to spirochetes causing dementia is also different.
Allen suggests the spirochetes reach a certain amount in the colony and trough quorum sensing roll out a biofilm. Because the immune system does not reach the bacteria due to the biofilm they damage the surrounding tissue.
He also suggests biofilm prevent penicillins from working and thinks drugs like rifampin are needed to punch holes in the biofilm.
Zhangs oral combination is based on this idea:
Doxy/mino : kills exponentially growing forms.
Rifampin: kills stationary forms / punches holes in the biofilm.
Dapsone: affect biofilm and kill the most resistant persisters.
I have not seen publications about
how disulfiram works or the publications in mice. I have also not seen published results from lab studies.
This makes me wonder if Lewis found disulfiram kills the exponentially and stationary forms but not took into consideration matured and aggregated biofilm-like forms.
The farmacological properties of disulfiram are very promising with regards to tissue penetration, half life bioavailability and cns penetration.
However, Bartonella could still be an overlooked infection, which can cause many subjective symptoms mainly due to endothelial inflammation and small vessel disease.
It is very hard to kill because most antibiotics are only bacteriostatic and it is intracellular and can survive in erythrocytes, endothelial cells, progenitor cells, marcophages, neurons and glial cells. It can also interact with B cells and functions somewhat as a polyclonal B cell stimulator.
mino/rifamp will help with that infection but I am really interested in knowing which drug combinations are able to kill Bartonella.
Also, the concentrations reached in the body are of concern, the concentrations reached inside cells is even more difficult to predict. Also, in which compartment of the cell the Bartonella survive and if the drug can reach that...
Zhang is also the mastermind in fighting Tuberculosis and finding new strategies so intracellular infections are his specialty. However, with Bartonella you have another problem, wild strains are very difficult to culture.
With the Houston-1 strain this is much easier but that doesn't correctly reflect what happens in natural infection.
Either way, exciting developments. I cried a little bit because eventually people will no longer have to suffer these diseases we have all gone trough.
owner of Lyme-basics.com