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Body response, often an immune/cytokine response, to infection or other foriegn agent.

RCPN & Thoughts on the Thyroid

First of all, since my last blog post - I have made a Dr.'s Appt.  I think with some of the craziness I've read I'm going to coin a new term "Responsible CPNi'ing" or RCPN...

Is taking 30 days of Flagyli, Zithi and Doxyi right out of the start gate RCPN'ing?  No.  In my case, is self treating an out of control thyroid RCPN'ing?  No.  So there.  I'm a rather blunt person.  Anyway, I'm totally RCPN'ing because I want to get better in the safest and quickest way possible.

Now about the thyroid.  Today a totally strange thing happened to me.  My thyroid gland swelled up some and it hurts.  In the meantime, my heartrate and the other hyperthyroid symptoms I've been having are starting to retreat.  This works for me, I'll trade the Minnie Mouse heartrate for a swollen thyroid anyday.


Hi CPNers,  My basic disorder is fibromyalgiai which many doctors think carries the autoimmune factor.  I've had sporadic bouts with it since 1989.  Fibro symptoms are heavy muscular pain, fatigue, brain fog and itchiness.  The present acute attack began in 10/06, brought on by mega stress factors in my life.  When I failed to respond to gamma globulin injections and home treatment, and instead worsened, my doctor ordered a CPN test which came back positive on 11/7/06.  The test further indicated that I'd had CPN for years, but I never felt CPN symptoms before this.  I've praised my doctor for being so knowledgeable on CPN.  He visits CPNHELP.ORG frequently.

This year I had a 5-month bout of severe exhaustion, undiagnosed; coulcn't do anything nor go anywhere.  In 2004 I had 7 weeks of even more severe exhaustion, undiagnosed.  I wonder if the strange exhaustion was caused by CPN.

Reflex Sympathetic Dystrophy

I seem to have developed some reflex sympathy dystrophy. It is in my shoulders (mostly left) traveling to my elbows and fingers. I have had it wake me up 2 nights now at 4 am. severe traveling pain. It got better yesterday only to return. My question is ...... can and what do I take for it that might help. How am I going to lift an 18 pound turkey? Am I a textbook case or what?

hormonal factors and chlamydia<

This article states that chlamydia is found more rapidly at the end of the cycle. Could that possibly mean it is more active at different times of the cycle.

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

Repeated Chlamydia pneumonia infection, persistence, caridovascular disease, luteolin

I don't believe we have this linked to our Research Pages (Marie?). This is a brilliant dissertation from the Finnish group, some of the world's experts on Cpni as some of the faculty in Helsinki were part of the original group who discovered the very existence of Cpn.

This dissertation demonstrates a number of important findings:

  • Repeated infection with Cpn "...induced persistent chlamydial DNA and inflammation in lung tissue and development of mouse Hsp60 autoantibodies."
  • Repeated infection with Cpn "...significantly increased subendothelial lipid accumulation in the aortic sinus area."
  • That "A flavonoid, luteolin, was shown to effectively decrease the chlamydial load and inflammatory reactions in lung tissue." Note: luteolin is not the same as lutein.
  • Conventional antimicrobial treatments are not effectively to eradicate persistent infection.
Go to the link and you can download the whole thing in pdf form.
Experimental Chlamydia pneumoniae infection model: effects of repeated inoculations and treatment

Liisa Törmäkangas

Lääketieteellinen tiedekunta, Oulun yliopisto


Cortisol elevation is common in MSi patients. I recall having tested high for cortisol when I was very ill. I used to treat it with licorice(capsules and tea). Here's an abstract I found that mentions HPA axis activation and cortisol.


HLA-B27 & C.Pn.

I was googling around a little, and started down a trail that looks promising<, except that I can't read most of the papers without a subscription. Undecided

 I was looking at connective tissue diseasesi and HLA-27B kept popping up, and C.Pn., but I can't get the connection - at least, not without buying access to a bunch of papers, most of which will be dead ends.

Does anyone know what the connection is? Or, even better, does anyone know where I can read about it without spending a fortune?


End of Day One Fred

I first posted this in response to Paul's comments on another thread, so I'm just repeating it here so it's part of my "Fred" blog. Here's how I've learned to sort my reactions out in terms of my own experience, correctly or not!

  1. Endotoxini reactions seem to typically include feeling chilled, cold, cold hands and feet, and so on. Dr. Powell had a great biochemical explanation as to why this is so, for the life of me I can't recall what it was. I just remember it as typified by chill, cold extremities and peripheral vasoconstriction.
  2. Cytokinei (immunei) reactions are typified by inflammation, consequent pain, swelling or congestion of tissues, and cascade of other responses like histimine release and so on.
  3. Porphyric reactions seem typified by a feeling of loggyness, depression or anxiety, nausea, disorientation, discoordination (when not caused by loss of muscle control function, see below) bowel disturbance, fatigue, hypersensitivity to light, sound and other stimuli. You note, Paul, that the porphyrins also bind to nerve receptors, especially GABA receptors, and thus interfere with the modulating functions the correct neuroransmitter would perform, hence increased pain sensitivity and anxiety and depression (both modulated by GABA). But increased pain sensitivity is not the same as pain-causing, and I know inflammatory pain feels quite different from hypersensitivity.
  4. Cell deathi seems typified by loss of baseline function (eg worsening of hand function in MS), pain, and so on followed by slower recovery and then improvement above baseline. 

 I see this in my reactions to the Fred pulse. When the dose hit a couple hours after taking it, I started to feel increased chill and cold despite all the things Dr. Powell has me on to counter endotoxin which usually do well to counter these symptoms. Then I had a rather rapid porphyric response (over the next hour or so) where my coordination, mental focus, disorientation really increased. Mac noted how visible my typing problems were on the chat. What they didn't see was how many times I had to type and retype a word before I could complete a sentence, and that poorly spelled and error laden even so.

Reactions to CAP Treatment: That "Kissed by a Dementor" kind of feeling*

Bacterial Endotoxini reactions, Cytokinei (immunei) reactions and inflammationi<

These are often casually. but inaccurately, referred to as “herx” reactions, or scientifically as “herxheimer-like” alluding to the Jarisch-Herxheimer reaction to bacterial toxins specifically from syphilis. All gram-negative bacteria, of which Cpni is one, have contain Lipopolysaccharidei endotoxinsi as well as HSPi's (heat shock proteins) which are released as a matter of course during infection and are in part responsible for the on-going symptoms of the infection.

When these bacterial are killed en masse during treatment, they release relatively large amounts of endotoxin, causing significant symptoms especially during initial phases of treatment, as well as when an additional antibiotic agent is added to the protocol. If the amount of endotoxin exceeds the body's ability to get rid of it, these toxic effects can be life threatening. But even in less threatening amounts, the endotoxins and the resulting reactions can cause oxidative stress and damage to body organs.

Book Review

Russell Farris and Per Marin MD PhD

The potbelly syndrome: how common germs cause obesity, diabetes and heart diseasei.

Basic Health Publications Inc, Laguna Beach, CA

Pp 246 ~ Paperback $17.95 (US) $23.95 (Canada)

Reviewed by David Wheldoni MB FRCPath

This book explains how common, non-resolving intracellulari infectionsi can, over long periods of time, subvert the body's defences by causing chronic elevation of cortisol while provoking chronic activation of pro-inflammatory cytokinesi; this has serious repercussions, including type II diabetes, atheroma and heart disease. Much of what we put down to ageing is caused by chronic infection.

Diseases associated with Cpn: the exhaustive list

I have culled from Mitchell & Stratton patent #6,884,784 an exhaustive list of diseasesi where Cpni has been implicated as a possible cause or co-factor (reference: Mitchell & Stratton patent #6,884,784):

Diseases where an association has been discovered between chronic Chlamydia infection of body fluids and/or tissues with several disease syndromes of previously unknown etiology in humans which respond to unique antichlamydial regimens include:

Editorial comment: Strong findings from their research. If you have any of these it suggests to me that at least an empirical course of the combination antibiotic therapy is strongly indicated, with or without serologyi.

Multiple Sclerosis (MSi)
Rheumatoid Arthritis (RA)
Inflammatory Bowel Diseasei (IBD)
Interstitial Cystitisi (IC)
Fibromyalgiai (FM)
Autonomic nervous dysfunction (AND neural-mediated hypotension);
Pyoderma Gangrenosum (PG)
Chronic Fatigue (CF) and Chronic Fatigue Syndromei (CFSi).

Trouble ahead w/abx conflict

Houston, there's a problem.  I am on David Wheldoni's protocol, almost to the letter, and it's been going just ducky.  Something happened two days ago and I may have a problem ahead.  I woke to find four little 'pimples' behind and below my right ear.  They itched.  I figured heat rash or chafing from a high parka collar.  I happened to run into a friend who's a nurse and she said 'that looks like spider bites'.  They were swelling a bit and starting to itch and hurt.  Another friend said it looked like an allergic reaction to something (but there is NO other outbreak anywhere but this one spot).  The little spots now look like angry mosquito bites and there is swelling below this 'bitten' area, extending downward, which I think might be a gland (?).  It seems to me I should not be reacting like this as I am ON abxi.  What if I need a different abxi to treat whatever this swelling is?  Do I hiatus from the protocol (NOT something I want to do, by any means)?   Could another antibiotic be safely added to the current cocktail?  And it HURTS, like the occasional throbbing/stabbing pain at the beginning of an earache, though it's not in the ear, but below it.  Can I take aspirin?  Yes, yes, I know; I'll see a real doctor if it doesn't begin to subside tomorrow.  I was allergy tested before starting abx and I doubt it's that, but this is scary.  Does spider venom do this?  So many questions! 

Mechanisms of Chlamydophila pneumoniae Mediated GM-CSF Release in Human Bronchial Epithelial Cells

Am J Respir Cell Mol Biol. 2005 Dec 9; [Epub ahead of print]

Mechanisms of Chlamydophila pneumoniae Mediated GM-CSF Release in Human Bronchial Epithelial Cells.

Krull M, Bockstaller P, Wuppermann FN, Klucken AC, Muhling J, Schmeck B, Seybold J, Walter C, Maass M, Rosseau S, Hegemann JH, Suttorp N, Hippenstiel S.

Department of Internal Medicine/Infectious Diseasesi, Charite, Universitatsmedizin, Berlin, Germany.

Chlamydophila pneumoniae is an important respiratory pathogen. In this study we characterized C. pneumoniae strain TW183-mediated activation of human small airway epithelial cells (SAEC) and the bronchial epithelial cell line BEAS-2B and demonstrated time-dependent secretion of granulocyte macrophage colony-stimulating factor (GM-CSF) upon stimulation. TW183 activated p38 mitogen activated protein kinase (MAPK) in epithelial cells. Kinase inhibition by SB202190 blocked chlamydia mediated GM-CSF release on mRNA- and protein-level. In addition, the chemical inhibitor as well as dominant negative mutants of p38 MAPK isoforms p38alpha, beta2, and gamma inhibited C. pneumoniae-related NF-kappaB activation. In contrast, blocking of MAPK ERK, c-Jun kinase/JNK or PI-3 Kinase showed no effect on Chlamydia related epithelial cell GM-CSF release. UV-inactivated pathogens as compared to viable bacteria induced a smaller GM-CSF -release suggesting that viable Chlamydia were only partly required for a full effect. Presence of an anti-chlamydial outer membrane protein-A (Omp-A) antibody reduced and addition of recombinant heat-shock protein 60 from C. pneumoniae (cHsp60, GroEL-1) enhanced GM-CSF -release suggesting a role of these proteins in epithelial cell activation. Our data demonstrate that C. pneumoniae triggers an early proinflammatory signaling cascade involving p38 MAPK dependent NF-kappaB activation resulting in subsequent GM-CSF release. C. pneumoniae-induced epithelial cytokinei liberation may contribute significantly to inflammatory airway diseases like chronic obstructive pulmonary disease (COPD) or bronchial asthma.

Differences in cell activation by Chlamydophila pneumoniae and Chlamydia trachomatis infection in human endothelial cells

Infect Immun. 2004 Nov;72(11):6615-21. Related Articles, Links

Differences in cell activation by Chlamydophila pneumoniae and Chlamydia trachomatis infection in human endothelial cells.

Krull M, Kramp J, Petrov T, Klucken AC, Hocke AC, Walter C, Schmeck B, Seybold J, Maass M, Ludwig S, Kuipers JG, Suttorp N, Hippenstiel S.

Department of Internal Medicine/Infectious Diseasesi, Charite, University Medicine Berlin, Augustenburger Platz 1, 13353, Germany.

Seroepidemiological studies and demonstration of viable bacteria in atherosclerotic plaques have linked Chlamydophila pneumoniae infection to the development of chronic vascular lesions and coronary heart disease. In this study, we characterized C. pneumoniae-mediated effects on human endothelial cells and demonstrated enhanced phosphorylation and activation of the endothelial mitogen-activated protein kinase (MAPK) family members extracellular receptor kinase (ERK1/2), p38-MAPK, and c-Jun-NH2 kinase (JNK). Subsequent interleukin-8 (IL-8) expression was dependent on p38-MAPK and ERK1/2 activation as demonstrated by preincubation of endothelial cells with specific inhibitors for the p38-MAPK (SB202190) or ERK (U0126) pathway. Inhibition of either MAPK had almost no effect on intercellulari cell adhesion molecule 1 (ICAM-1) expression. While Chlamydia trachomatis was also able to infect endothelial cells, it did not induce the expression of endothelial IL-8 or ICAM-1. These effects were specific for a direct stimulation with viable C. pneumoniae and independent of paracrine release of endothelial cell-derived mediators like platelet-activating factor, NO, prostaglandins, or leukotrienes. Thus, C. pneumoniae triggers an early signal transduction cascade in target cells that could lead to endothelial cell activation, inflammation, and thrombosis, which in turn may result in or promote atherosclerosis.

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