Cryptic form

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Under stringent conditions, RB's in the cell can transform for survival into an low-metabolizing and non-replicating form which is not killed by regular antibiotics.

Continuous Treatment

I haven't blogged my treatment for a while, as I've been waiting to see if I would stick with a shift in protocol. So far, still with it, so thought it might be time to report in and get other's thoughts. New folks, please read this as informational only. It does help clarify Dr. Stratton's use of the continuous rather than pulsed protocol, but the rest of the hypotheses here are presented as my own speculations, not scientific fact.

adipose tissue's role?

I was at the gym last night and reflecting on the events prior to my diagnosis with MSi and leading up to it. One of the things that stands out in my mind is that my condition worsened greatly over the course of a year just prior to the diagnosis which was happening at the very same time I was losing large amounts of weight. In fact, the onset of the active form of my condition was 2 - 3 months after I set off into attempting weight loss.

could it be all cryptic? help with getting a diagnosis

Hi everyone!

I really hope you can help me, because I have yet to be diagnosed with much of anything.  I have a huge variety of symptoms including life-long asthmai and sinus/bronchial infection issues.  Throw on a healthy dose of mind-numbing fatigue, brain fog, joint pain, muscle weakness (relatively minor, not like the MS stories I have read), etc, etc... I've been getting worse and worse year after year.  It presents a pretty confusing picture to doctors.

Only only two things have helped me.  1) Flagyli, and 2) Secnidal (another drug in the same family as flagyl.)  I did a 5 day course of the first and a 10 day course of the second.  I felt nearly about 70% improved on the first, and nearly perfect after the second.  Both of these were shots in dark, and I went back to being ill 2 weeks after the antibioticsi were finished.

Essential Observations by Dr. Charles Stratton on Chlamydia Pneumoniae Infection and Disease

I am very excited to present the following article that summarizes Dr. Stratton's recent observations on Chlamydia pneumoniae infection. Putting it together has contributed greatly to my own understanding of Cpni as well as to my appreciation of Dr. Stratton's generosity with his time, and his great depth of knowledge of this area. Thanks to him for his contribution.

Jim K

Recent observations by Dr

Recent observations by Dr. Charles Strattoni on Chlamydia Pneumoniae (Cpn) Infection

Morning after 2 grams pulse

Waking up after having downed 2grams of Tini last night. Took it with gliSODin which I also did again at bedtime along with 1000mg vitamin C and usual bedtime stuff and 3 ibuprohen. Surprisingly this morning I'm a foggier, but the main symptom is burning/tingling in hands and feet and general acheyness.

Paul's April Fools post gave a big and much needed laugh which let me know my humor (bad as it is) was intact! ROFF ROFF! (see comments after his post for this to make sense http://www.cpnhelp.org/?q=vanderbilt_university_res<). This is my third single high-dose pulse which I've been doing weekly, working up from 1.5grams to the two grams I did last night. I'll see how symptoms proceed today, and may do a second dose of 1.5grams today if it feels like I'm managing well.

Dr. Stratton Answers Some Questions:

In some recent correspondance with Dr. Stratton at Vanderbilt University, he kindly answered some of the questions which had formed as I've understood more about the combination antibiotic protocol and about Cpni. From the patient's perspective I wanted to correlate some observations about treatment reactions with his deeper understanding about the biology of the Cpn. I'll list the questions I put to him, and then his generous response below.

1.  In an earlier correspondance you had mentioned pulsing the INHi band metronidazolei together.
        * Why do that rather than take it continuously?
        * My understanding is that INH is one of the anti-replicatives, and the point is to use these continuously to drive the bug into the cryptic phase where it will be obliterated by the flagyl/tinii. Does INH act differently than the other antireplicatives?
        * I also understood that we use a dual abxi to prevent developing resistance. Why can we use INH alone without developing resistance?
 

literature on the mysterious cryptic form

Im not certain what everyone means by the cryptic form? And I may be going over old ground here. But one definition of the cryptic form is chlamydial infection of a cell which is not detectable by light microscopy with appropriate stain. Such an infection is detected only because reversion to forms visible by light microscopy later occurs.

Apparantly this phenomenon was first observed by Moulder in 1980 in C. psittaci, and has never been really clarified much in the intervening 25 years:

http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=6262243<

Page 172, top of column 2 here (warning, huge pdf file):

http://www.pubmedcentral.gov/picrender.fcgi?artid=372804&blobtype=pdf<

Cpn Slides

This link< for slides on the different life stages of Cpn.

The immune system, atherosclerosis and persisting infection

Vestn Ross Akad Med Nauk. 2005;(2):17-22. Related Articles, Links

[The immune system, atherosclerosis and persisting infection]

[Article in Russian]

Pigarevskii PV, Mal'tseva SV, Seliverstova VG.

The paper demonstrates that lymph nodes situated in the vicinity of magistral blood vessels are the source of immune and inflammatory response to LDL as the main pathogenetic factor in atherosclerosis. The activation of T-cell-mediated immunity takes place in them at the very early stages of the disease, resulting in forming of CD4+T-lymphocytes, activated mononuclear cells and immunostabilizing B-lymphocytes. The cell changes in lymph nodes correlate with the severity of atherosclerotic lesions in the vessel intima and closely reflect the peculiarities of immune inflammation development in fatty streaks and atherosclerotic plaques in human atherogenesis. A paradoxical reaction was observed in cases with Chlamydia pneumoniae found in the wall of aorta and paraaortal lymph nodes. No evident immune response on the part of immunocompetent cells took place, but, on the contrary, the function of mononuclear cells, including T-lymphocytes, was suppressed. This phenomenon may be explained by the fact that intracellulari localization of Chlamydia pneumoniae hides it from immune system control or by the possible microorganism capability of direct immunosuppressive influence on lymphoid cells both in the blood vessel wall and in regional lymph nodes.

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