antibiotic therapy reducing gut microflora

[Guest guest]

This is Sam Donta's opinion re why abx (metronidazole for eg) work transiently by reducing the gut flora and therefore the metabolic products which participate in the neuro probs we (Lyme patients) experience.

http://www.lymediseaseaction.org.uk/conference/prog04.htm

Can someone comment as to why Donta seems to be so adamant that Bb are not affected by imidazoles (and I suppose Chlam.pneum)? Does anybody know why Donta chooses to completely ignore the cystic/cryptic forms of the bacterias?

Nelly (just had the most horrifying 3 days after 3 days of tinidazole as my second stint with it as per Wheldon/Stratton, yet I have already taken loads of tinidazole)

Now, there is an interesting thing here and this raises a big question about what it is that we do with treatment. And it is a little bit of a digression but I think perhaps it is an important one. Metronidazole, Flagyl, as it is called in the United States, has been used in Lyme Disease based on the idea that it might affect the cyst form but when you look at the genome of the Borrelia they do not contain any sequences to metabolise Metronidazole so there is no way the Metronidazole can have a direct effect on the Borrelia. So, how is it that clinically some patients who are on this seem to have a transient response? I have thought about this for a while and it takes me about 4 or 5 years to figure things out but whether I have figured it out or not but what I think may be happening and here is the analogy: When you have a patient who has cirrhosis of the liver from either alcoholism or from Hepatitis, one of the things that they do is to go into a coma or not necessarily a coma but confusional state and that is thought to be due to the absorption of some metabolic products of the intestinal bacteria. So what do we do in that case, we give them Neomycin, an antibiotic which just stays in the intestine, and it reduces the amount of the intestinal flora and thereby decreasing the metabolic products which have to be detoxified by the liver and in that case the liver is impaired. Well how do I jump from that to the Lyme patient and Metronidazole and let me put Cholestyramine in the picture too and perhaps any antibiotic, scary as that may be. What if we are, in the Lyme patient, that in the non- Lyme patient the metabolic products don't make any difference. Not as far as we know. This is our brain, this is our state of confusion, our state of memory. What if the Lyme patient is sensitised because we know the Lyme patient is sensitised to wherever their focus is they are sensitised to stimuli, they may be de-sensitised too, but what if some of the metabolic products with an intact liver are creating a problem with the sensitivity of the neurons and maybe what we are doing with the Metronidazole or Cholestyramine in the case of binding metabolic products and temporarily making a person feel better. What if some of our antibiotic therapy is reducing some of the other microflora and we are transiently then reducing some other. In other words, what if this is a secondary effect. How do we know that it is a direct effect on it.