CBs live in a stressfull condition and secretes some stress proteins called as heatshock proteins which thought to be a major stimulant of immuneⁱ system resulting in immunulogıcal damage. So you can not leave CB by themselves and should kill them as soon as possible. During this killing process we should be very carefull and not to move too quick to protect ourselves from heavy die-off reactions and pseudorelapses.

Its a really risky strategy you are proposing. You are basically getting rid of any margin for safety and relying on NACⁱ to be a perfect EBⁱ-killer, which it isn't. Is there a dose at which it will kill all EB's? Nobody knows. Even if there is one, it would most likely be a dose which is neurotoxic. Unless you are killing 100% of EB's you are still getting population growth by your method.

Also the main problem people have with the CAPⁱ is not the bacteriostatic agents, its the flagylⁱ.

Finally there is evidence to suggest that Cpnⁱ can transfer between cells without condensing into EB's, which makes NAC useless in such circumstances. 

  I also ask myself that whether we do it better or worse by forcing RBs to turn into CBs by using protein synthesis inhibitors. What would happen ıf we used only NACⁱ and METROⁱ? I don't know the exact answer but most probable scenario is that in my thought; RBs will continiue to replicate in our cells, they will turn to EBs  and then they will get into extracelluler space by bursting cell, NAC will be insufficient to kill all of them and they will enter to other cells. This will go on like this for years and at the and we will have such a big infection and bacterial loadⁱ that adding protein synthesis inhibitors to treatment will not be sufficient to overcome the infection. The risk of getting a resistant strain will also be increased. So it seems to be best that we should beat the CPNⁱ with our all power and shot down it.

Please also recall that your own natural immuneⁱ factors like TNF alpha, plus iron sequestering by macrophages, plus other factors like protein lack (tryptophan for example) will also induce RB's to convert to persistent forms. And as Kerem pointed out, it is in the persistent form that it is more inflammatory and damaging. Add to this that the RB's are using up the most host energy. Lot's of good reasons not to rely on one agent.

We don't know how much NACⁱ (huge doses are given IV for tylenol poisoning) would be needed to maintain tissue penetration and other complex factors, nor how long you' need to do this alone to winnow down Cpnⁱ enough for disease purposes. Some EBⁱ's may not be readily accessible to blood levels of NAC.

What we do know is that PCRⁱ signal for rDNA (which measures the presence of all the forms of Cpn) remained unless agents for all of these phases were employed. If you are only trying to prevent infection, or have a mild disease process, you can experiment in this way. But by the time most folks get here they are sliding down a slippery slope of more serious disease, and too slow a treatment process risks too much.

>Im ny case it is clearly only ONE of several severe and chronic infectionsⁱi - mycoplasmas. borrelia, babesia, and a few viruses.

I suppose that's quite frequent. The intracellularⁱ defenses are based on enzymes that work in an acid environment only. Cpnⁱ is able to totally block a host cells attempt to get more acid rendering its defenses impotent. So, every bugs else that's around there can florish.

In my opinion, that's also the reason why capⁱ takes such a long time to produce results. The body uses natural antibioticsⁱ to fight extracellular bugs and enzymes to fight intracellularⁱ ones. If we had enzymes to apply that have anti-chlamydial power and still work in a neutral surrounding we'd probably kick the whole thing within days.

Andreas

Jim K, I've got this information out of a paper produced by produced by University Heidelberg. There is no translation available. Only the abstract is alternatively given in English and doesn't represent all of the information of the full text.

http://www.p-e-g.org/publikationen/ctj/77_82.pdf

In my translation and in my understanding the full text lines out:

1.

Intracellularⁱ pathogens are attacked by the host cell using enzymes calles lysosome, which try to digest the invader. The host cell also tries to render itself more acid (ph < 4.0). Cpnⁱ (and others) are able to prevent the host cell from getting more acid forcing it to stay neutral.

The German and the English wikipedia article on lysosome (which are not translations out of each other) both confirm this connection stating that lysosome need acid surroundings to be effective:

 http://de.wikipedia.org/wiki/Lysosom

 http://en.wikipedia.org/wiki/Lysosome

 

2.

As far as the effectivness of antibioticsⁱ is concerned, it depends not only on whether they can reach inside the host cell. It also depends on wide spread distribution inside the host cell, to make sure that all areas are covered.

The Macrolides of our capⁱ are rated good in terms intracellularⁱ penetration and distribution. Rifampicin is rated mediocre regarding intracellular penetration but is rated good in terms of intracellular distribution. Tetracyclines are questionable on regard of both aspects (no certainty whether their performance is good or bad, no rating given).

Norman - in my understanding it is said, that it depends on the acidicity of the host cell whether lysosomes are effective (not on whether lysosomes themselves are acid inside). And that Cpnⁱ is able to counter the host cells efforts to become more acid as the host is attacking by producing lysosomes.

That Cpn uses masking techniques is a different topic, but doesn't necessarily contradict what I say. Problably Cpn applies a double strategy to counter host cells' defense measures.