Treatment: the End-Game


Treatment of chronic C. pneumoniae infection in Multiple Sclerosis: The End Game.


The question is: how do you know when to finish? And the answer seems to be to take the response to treatment as a guide.


I’ve noticed quite often, in treating persons with MS, that, after a year or so of combined antibiotics, they get worse on stopping; this seems to happen quite quickly, even as soon as a few weeks. Often they have flu-like symptoms and loss of energy. Surely this is far too short a time for the regrowth of bacterial numbers (which after all took years and even decades to cause severe chronic disease.)

I think the answer must lie in the withdrawal of the immunomodulant action of doxycycline or minocycline. These antibiotics inhibit macrophage activation in the CNS and have a profound action on many cell types in the immune system; they downregulate pro-inflammatory cytokines. It seems very likely that the symptoms which occur soon after stopping antibiotics are due to a strengthening of the immune system in its activity against bacterial fragments. The fact that they include flu-like symptoms, those of ‘coming down with something’ seems to point to increased cytokine activity.

I’ve made a small note of this on my web-page which deals with the sequelae of treatment: comments are very welcome.

What a complicated disease this is!

And then there's the phenomena of those of us too apprehensive to come off the darned antibiotics... I keep saying, 'one of these days'.

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

How interesting idea, David, thanks for that caution. But I guess there can be another answer as well. The other undiagnosed infection, which was suppressed by cap, but not eradicated and as soon as atbs are stopped it takes place again. Most of us old timers started cap just with tests on cpn or empirically without testing. Now with growing possibilities of extensive testing, many people find out there are more pathogens in their game: ehrlichia, lyme, bartonellas, babesias, yersinia, anaplasma etc. Some are covered by cap, but many are not and need harder or different approach.

Stratton/Wheldon protocol 02/2006 - 10/11 for CFS and many problems 30 years


Hey DW, Interesting. In addition to other immuno-modulating effects, there are some studies that suggest antibiotics might interfere with apoptosis (at least in certain cases). Could removing the antibiotics, particularly when a patient is also on vitamin d3 too, also lead to an increase in apoptosis and a spilling of cell contents (including porphyrins and bacterial fragments) into the system?

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

It doesn't even have to be another undiagnosed infection. It can be Cpn, which was suppressed by the antibiotics, then emerged from the cryptic state when antibiotics were withdrawn. Then, once the body realizes this, it activates the immune system, turning up interferon-gamma, and puts the germs back into the cryptic state. In this scenario, the immune system had been lazing along, letting the antibiotics do the work; then it had to become active. The patient feels that activity as sickness. There is likely also to be a brief interval, before that feeling of sickness, during which the germ is not suppressed by any mechanism, and thus grows rapidly. (Although the original infection took years to establish itself, Cpn can grow and spread much faster than that when not suppressed. You may have whittled down the infection to one cryptic body in a cell; but given twenty-four hours of free activity, it might grow and divide into ten RBs.)

As for the "immunomodulatory activities" of antibiotics, it's likely that many of the experiments establishing those activities were done on cell lines contaminated with Cpn — as Stratton has reported many cell lines to be. To be trustworthy, they probably would have to be redone with cell lines cleared of Cpn — because when they're done on infected cells, one is, at least in part, measuring the cell's response to the suppression of the infection with antibiotics. That naturally yields a reduction of the inflammatory response. (Killing the infection might increase the inflammatory response, but suppressing the infection — putting it in a cryptic state — naturally decreases inflammation. And it does seem to be the "bacteriostatic" antibiotics, rather than the "bacteriocidal" ones, which have reputations for "immunomodulation".) It's not just cells; whole lab animals, too, are reported by Stratton to commonly come already infected.

At one point, a few years ago, I had a look at the literature about immunomodulatory effects. There was one paper I ran across which reported that it didn't find such effects in a lab strain of cells, but did find them in cells of the same type taken from patients. They mumbled something about the genetics possibly being different, but didn't even mention patients' infections as a possible explanation for why immune cells taken from patients might behave differently. And when I looked at a paper purporting to establish effects of minocycline on matrix metalloproteases, what I saw was that it really established that there were no significant effects at the dosages normally used on patients, only at dosages fifty times higher.

One might also ask where those chemical compounds went, which were developed as analogs of tetracyclines which had the immunomodulatory activity but lacked any antibiotic activity. Given all the concern over antibiotic overuse, one would be expecting them to be widely used by now — unless, for some "unexpected" reason, they failed their clinical trials and were quietly dropped.

There is a review of the topic titled Interference of Antibacterial Agents with Phagocyte Functions: Immunomodulation or “Immuno-Fairy Tales”? Unfortunately it does not really answer the question posed in the title, but instead is a rather dry summary of what various research groups have reported.

Given these considerations, my own approach to the endgame has been substantially more aggressive — probably overly so.

DW~   Yes indeed, a complicated disease it is.  Especially when one is dealing with more than one infectious pathogen.  

In my case, it seems likely that my illness started from a steroid shot to my knee.  3 weeks to the day after that shot I became ill with many and varied symptoms.   I continued to fall apart and no doctor could figure out why.  A few years later I was tested for Lyme disease at a major medical university and was thought that it was the probable cause of my illness.  I was started on IV rocephin and gained significant improvement, only to relapse exactly 3 weeks to the day of when the picc line was pulled.    

Whatever pathogen I had appeared to have a 3 week replication time before it made me very sick.  And we are saying very sick....not a little bit ill, but hit like a freight train ill.   Rocephin does not have immunomodulating properties (that I'm aware of), so it wasn't that.

In hindsight I don't know if I was dealing with Lyme or Cpn at that point in time.  It is clear that Cpn is a player in me now based on lab tests.

I also struggled with C. diff.....for 11 long months.   One strategy that was tried on me (but which did not work) was pulsing.   After 2 weeks of vanco, I'd go off for a day, then on for 2 days, then off for 2 days, then on for 2, then off for 3 days, etc.    The idea being that any C. diff spores would germinate during the time off antibiotics and would then be hit again by the antibiotics.   If one reached 10 days off antibiotics they were considered cured.   I never made it.  It was the rifaximin chaser that cleared the C. diff in me.  

So, when it comes to Cpn treatment, of course I've given it a lot of thought.  I am also dealing with other infectious pathogens though, so they must be taken into consideration as we plan my treatment.  

The antibiotics I'm on has dropped my IgA level for Cpn significantly.   I would idealy like to add in some flagyl or tini next time I see my doctor.  And perhaps drop back on the amount of rifampin I'm on.   I must admit though that what I'm taking appears to be working based on test results.  Once my IgA is in the normal range, I would consider pulsing the antibiotics (not rifampin of course), but something that hits the Cpn.  I'd carefully monitor the IgA levels as I do this.   If the IgA levels stay down then at some point I'd consider stopping the antibiotcs altogether.   Of course, my doctor gets the final say in all this, and I'm fortunate that we have the ability to work together on treatment planning.   I'll be interested to hear his thoughts the next time I see him.

DW, you did not mention testing at all.  Do you not use this to determine either when to start pulsing, do intermittent therapy or end treatment?  It seems in those patients who have high IgG and high IgA antibody levels that it could yield useful information for treatment planning.

Best to all,


on valtrex 500 mg tid




DW- good to hear your accumulated observations and reasoning on this. The question I'm left with is, "What gets worse?" Fatigue and flu-like symptoms can cover a lot of possibilities, including bacteria converting from cryptic to replicating as Norm mentioned. Worsening of MS symptoms suggests inflammation of infected lesions in the nervous system which argues the immune boost direction. What are you seeing?

Timaca- according to my last chat with Dr. Stratton, rifampin seems to be the most broadly potent antichlamydial. I've still not had the guts to try it again, but if you are able to use it I think you are getting the most bang for the effort on the Cpn side of things. If your IgA levels stay down, you might consider doing at least a course of metronidazole to cover any cryptic load induced. I've found that this can sneak up on you.


CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral