Submitted by Jim K on Tue, 2006-09-12 16:57

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 Cpn 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 Stratton on Chlamydia Pneumoniae (Cpn) Infection August 2006   I recently had a phone conversation with Dr. Charles Stratton and he brought me up to date on his current thinking about Cpn. A conversation with Dr. Stratton is always an enjoyable thing in of itself as he’s such a friendly and interesting person, but he’s also a remarkable scientist keenly observant of emerging findings in related fields.   Dr. Stratton has been carefully observing the emerging literature and research on Cpn, as well as the clinical trials of new anti-chlamydial agents. His unique and expert microbiological perspective on Cpn puts these emerging findings into a different light such that their implications may be understood by those with less appreciation of Cpn microbiology. I have tried to summarize his observations in the following presentation. Please remember that these are his theoretical speculations based on his review of prior and emerging research, as well as on his considerable clinical experience treating Cpn infections. The picture he presents has helped me to make clearer sense of the multiple pathways and illnesses caused by Cpn, as well as the difficulties in the treatment process.   Dr. Stratton has paid particular attention to findings by Dr. Stewart that supposedly young, healthy blood donors are showing positive cultures and flow cytometry for Cpn. Her study showed a number of very important findings with implications for our understanding of Cpn transmission and proliferation in the body.   The first is that approximately 25% of buffy coat samples (a buffy coat is the WBC— white blood cell— portion of spun blood) were culture positive for Cpn. This is not an antigen test, but means that Cpn could actually be cultured or grown in the lab from 25% of white blood cell samples. This means infectious Elementary Bodies are circulating in the blood stream.   The second significant finding in Dr. Stewart’s study, was that approximately 25% of WBC’s were seen by Flow Cytometry to have intracellular Cpn. The work of Yamaguchi, demonstrating messenger RNA from peripheral blood mononuclear cells, suggests that these intracellular Cpn found by Stewart are viable. Thus, we know that viable Cpn in WBCs and infectious Cpn elementary bodies circulate in the blood stream and can go anywhere blood goes and can infect any tissue. I will go into why Dr. Stratton sees this finding as so important in a bit.   Dr. Stratton also notes that, in her study, this 25% of donors infected with viable Cpn, both intracellular and free EB’s, occurred in so-called “young healthy blood donors.” That is, while they were culture-positive for Cpn, they have no disease symptoms and were considered to be a “normal” control sample. Dr. Stratton links this finding to reports from the Pfizer drug trials for Rifabutin, a highly potent anti-chlamydial. In the drug trials for Rifabutin there were some cases of liver failure and also of plummeting white blood cell counts in “healthy” volunteer subjects. This has been interpreted in some places as a potential side effect of the medication.   From Dr. Stratton’s perspective on the biology of Cpn, and utilizing the evidence from Stewart, Yamaguchi and others, if 25% of “healthy” volunteers are in fact infected with Cpn, including potentially liver and immune system (white cells) cells as important sites of infection (see explanation below), then a highly potent anti-chlamydial agent will kill many Cpn in parasitized cells. This could initiate large-scale apoptosis (natural cell death) of those body cells that have been inhibited from apoptosis by the Cpn which previously infected them.   Let me say that again, a little differently. We know that Cpn inhibits apoptosis of its host cell so that the host cell stays alive and the infecting Cpn survives. If you kill the Cpn invader, the host cell is no longer being prevented from it’s natural death and replacement cycle. And If you kill a bunch of Cpn all at once, you have a bunch of your body or organ cells dying all at once, and it takes time for them to be cleared by the immune system and then replaced by the natural cell replacement process. It is this, on a more gradual scale, which David Wheldon has noted makes for continuing die-off like symptoms after a Flagyl pulse has been completed.   So, if a whole bunch of liver cells undergo apoptosis at once then liver failure or liver problems could occur. Similarly, if a whole bunch of immune cells undergo apoptosis then, then macrophages and white cells die and severe neutropenia (lowered white count) could occur. From Dr. Stratton’s perspective, these reports may not be a side effect of the Rifabutin, i.e. an unintended effect of a medication, but rather could be due to it’s main effect—killing Cpn.   Dr. Stratton’s Current Theoretical and Clinical Thinking: These observations also inform Dr. Stratton’s current thinking about the course and pattern of Cpn infection. I’ve attempted to diagram this below to give the reader a feel for the sequence and locus of Cpn in the body, as well as the resulting disease picture.   The initial entry into the body for Cpn infection is through the respiratory system. Studies have demonstrated that Cpn crosses from the lungs into the blood stream via infecting macrophages, the first response immune cells which are trying to combat the respiratory infection.   These circulating infected macrophages both produce EB’s, the infectious spores of Cpn, directly into the blood stream where they attach to and are carried by red blood cells throughout the body (see the picture on our home page), and are taken up by the natural filter organs of the body where they infect those organs with Cpn.   The Inflammatory Trigger: Stage is now set for focal diseases: any source of inflammation attracts infected macrophages and white cells as well as EB carrying red cells as part of the body’s natural repair process. Cpn then transfers from damaged macrophages via EB’s and sets up shop in inflamed areas.   At this point in the infection cycle, the type and locus of the Cpn infection then determines which disease will result and manifest symptomatically (the following is meant for example only, and is not intended to be a complete or exhaustive list):   Inflammation Sources     Infected immune cells aggregate at inflammation site and infect it with Cpn   >>>>>>>>>>>>>>>>> >>>>>>>>>>>>>>>>> >>>>>>>>>>>>>>>>>   >>>>>>>>>>>>>>>>>   >>>>>>>>>>>>>>>>> >>>>>>>>>>>>>>>>> >>>>>>>>>>>>>>>>> >>>>>>>>>>>>>>>>>   >>>>>>>>>>>>>>>>> >>>>>>>>>>>>>>>>> >>>>>>>>>>>>>>>>> >>>>>>>>>>>>>>>>> >>>>>>>>>>>>>>>>> Resulting Cpn-related disease Accident/injury Bone & soft tissue “itis” (chronic inflammation), fibromyalgia, etc. Muscle wear and tear Fibromyalgia Joint wear and tear Arthritis Brain capillary inflammation (vasculitis) Virally inflamed meningal or brain tissue Multiple Sclerosis, Behcets, Alzheimer’s Lung irritation (smoke, chemical, other) Asthma, COPD,  Emphysema Bone marrow/immune CFIDS Spider or other inflamed insect bite Skin infection Inflamed skin capillaries (especially from EB’s) Rosacea Gut epithelial inflammation from dysbiosis, viral, fungal or bacterial origin IBD, Crohn’s, esophagitis, Cardiovascular inflammation Cardiac disease Small vessel inflammation Small vessel disease Bladder inflammation Interstitial cystitis Prostate infection/inflammation Chronic prostatitis   Where specialists, and patients, tend to look at a particular disease as the problem, the microbiological perspective Dr. Stratton brings sees the problem as one of a systemically based infection.   Dr. Stratton now posits that the primary infection in Cpn is of the immune system: immune cells & bone marrow.

  • It is this which, in part, causes such difficulty in getting rid of Cpn.
  • It also causes continuous reinfection if the full spectrum of Cpn infection is untreated.
  • It also lowers the body’s ability to cope with other bacterial and viral infections.
  • This, in turn, fosters further sources of inflammation, and even has the potential (through immuno-incompetence) to compromise the body’s ability to fight cancer and other diseases.

  It also answers some common questions that arise in Cpn Combined Antibiotic Protocol (CAP) treatment.   Why do viruses and cold sores “surface” during CAP treatment? This could be due to apoptosis (cell death) of infected immune cells and resulting neutropenia which temporarily lowers your immune response until these cells are replaced. Hence latent but suppressed viruses and fungi emerge as immune cells, which previously held them in check, die.   Why is aggressive or rapid treatment of Cpn potentially dangerous? In addition to the misery of massive endotoxin release from killing Cpn, and related cytokine (inflammatory) responses of pain and brain fog, massive kill of Cpn infected cells in the body could potentially cause crashing white counts and potential organ dysfunction or even organ failure (E.G.. liver failure) as large scale apoptosis of infected immune and organ cells occurs. As there is no quantitative measure of infectious load, and no way other than symptoms to know which organs are significantly infected, it behooves physicians treating Cpn to start gradually until some measure of the patient’s response indicates how quickly one can “ramp up” to full treatment. This also suggests that highly potent anti-chlamydial agents such as Rifabutin are not the best first-line treatment, even though they appear to be more effective at killing Cpn more quickly. Once the load has been brought down through gradual introduction of the regular CAP, then a cautious trial of such other agents can be considered.   Dr. Stratton has been paying close attention to reports of drug trials of Rifabutin, a very potent new anti-chlamydial. Even healthy young volunteers showed lowered white cells and liver problems during the Pfizer trials.   Given that Dr. Lee Stewart’s findings that 20-25% of young, healthy blood donors were found to be  flow cytometry positive for Cpn, Dr. Stratton believes that these effects could be not so much side effects of Rifabutin, as it has been currently viewed, but rather a main effect of the drug, that of killing Cpn and resulting death of previously infected cells.   In other words, since Cpn infection is ubiquitous and often sub-clinical, and “side” effects from potent antichlamydial agents in so-called “healthy” volunteers are actually main effects--- the subjects were not healthy after all, just not clinically ill.   Multi-year treatment process- Treating Cpn is a multi-year treatment process because of it’s potential to be widespread throughout in body organs, the vascular system, and immune system, as well as it’s toxicity in treatment (from endotoxins, porphyrins, inflammatory and cellular apoptosis). The more body systems involved, the longer and more difficult it is to treat, both in terms of tolerance of treatment from endotoxins, porphyria and apoptosis, as well as being able to get to all the tissues involved, which have differentials in terms of how antibiotics may concentrate in them. Cpn cells also have active pumps which try to lower concentrations of noxious substances (like antibiotics) which also have to be overcome.   How long treatment will take depends, of course, on the degree of infection, amount of bacterial load, severity of infection and number of organs involved, and so on. We don’t have any quantitative measures of infection currently. A good clinician, knowledgeable about the conditions which Cpn can cause, may be able to make an educated guess as to how many organ systems are involved on the basis of history and symptoms. Dr. Stratton sees the degree of reaction to NAC as a useful rough indicator of EB load—the more you react to it the more EB’s you have built up. He also sees the length of time one has been infected (when symptoms may have started) as a rough indicator of the length of treatment (note: one can only guess at this, as we may have initiated Cpn infection from what seemed a mild respiratory infection many years ago, and did not demonstrate serious problems such as MS until years later).   Dr. Stratton’s rule is “Go as fast as you can but no faster,” i.e. as rapidly as your own particular condition can tolerate given the above factors.   He sees that towards the latter phase of treatment, when one is no longer responding with significant reactions to metronidazole pulses, doing a course of 2 weeks on Flagyl and 2 weeks off while continuing with dual antibiotics, is a useful process to clear remaining tissues. When this is tolerated without significant side effects, a cautious trial of Zithromax and Rifabutin as a final test of Cpn clearance could be tried under careful supervision (watching for plummeting white cells and liver toxicity). At this point one should have cleared organs sufficiently that any apoptosis from the potency of Rifabutin would likely be easily tolerated.   The “Flagyl Free” Treatment Example- When asked about the example posted by Astrodiana of having apparently cured her Cpn infection by dual antibiotics without the Flagyl pulses prescribed in the CAP, Dr. Stratton made a couple of interesting observations.  One was that, while in the original Vanderbilt research PCR signal for Cpn was not cleared fully until all three agents were used, there are suggestions from later studies that the regular antibiotics may also have some anti-cryptic phase effect. So long term use could potentially clear cryptic organisms. He also notes that their conclusion that Flagyl is specifically anti-cryptic was a theoretical conclusion, based on it’s chemistry. They did not have specific evidence that cryptic organisms were rendered non-viable. There is also evidence that Flagyl, in addition to it’s believed effect on cryptic Cpn, could be killing other phases of Cpn. What they knew for certain was that their highly sensitive PCR test did not show clearance of the Cpn signal unless all three types of antibiotics were used.   He added that he would want to “test” the cure, if it was his own patient, by doing at least a couple of months of a regular CAP, then adding Rifampin. Or, if Flagyl/tinidazole are reacted to for other reasons (other than die-off) such as true allergy or intolerance, a well monitored trial of azithromycin and Rifabutin while carefully monitoring both white count and liver enzymes. If white cells drop or liver enzymes increase, he would take it as a clinical sign that there is still Cpn infecting the body despite symptomatic cure, and would continue with treatment.   I would comment, in closing, that a conversation with Dr. Stratton is always educational and illuminating. And it only took me four edits to understand  and represent the conversation well enough for me to finally get it right!   Jim K   Related References-     Prevalence of viable Chlamydia pneumoniae in peripheral blood mononuclear cells of healthy blood donors. Yamaguchi H, Yamada M, Uruma T, Kanamori M, Goto H, Yamamoto Y, Kamiya S. Transfusion. 2004 Jul;44(7):1072-8.    Department of Infectious Disease, Division of Microbiology, and the Department of 1st Internal Medicine, Kyorin University School of Medicine, Tokyo, Japan.   BACKGROUND: Demonstration of viable Chlamydia (Chlamydophila) pneumoniae in peripheral blood mononuclear cells (PBMNCs) is essential to understand the involvement of C. pneumoniae in atherosclerosis. Nevertheless, the prevalence of viable C. pneumoniae in the blood of healthy donors has not yet been studied. STUDY DESIGN AND METHODS: The presence of C. pneumoniae transcript in PBMNCs from blood of healthy human donors was assessed by real-time reverse transcription-polymerase chain reaction (RT-PCR) with primers for C. pneumoniae 16S rRNA, which is more sensitive than genomic-DNA-based analysis, and by the use of staining with fluorescein isothiocyanate-conjugated chlamydia monoclonal antibody (MoAb). RESULTS: Thirteen of 70 donors (18.5%) showed the presence of bacterial transcript in cultured PBMNCs. The prevalence of bacterial detection and bacterial numbers was significantly increased in PBMNC cultures incubated with cycloheximide. Immunostaining of PBMNCs with antichlamydial MoAb also revealed the presence of bacterial antigen in the PBMNCs judged as positive. Nevertheless, cultivation of C. pneumoniae from all PCR-positive donors was unsuccessful. There was no signifi-cant correlation between the presence of chlamydia and either sex or current smoking habits. A possible age variation, however, in the presence of chlamydia in blood of healthy donors was suggested by the results obtained. CONCLUSION: The bacterial transcripts in PBMNCs obtained from healthy donors were detected by the RT-PCR method. Viable C. pneumoniae may be present in healthy human PBMNCs.   Detection of Chlamydia in the peripheral blood cells of normal donors using in vitro culture, immunofluorescence microscopy and flow cytometry techniques BMC Infectious Diseases 2006, 6:23     doi:10.1186/1471-2334-6-23 Frances Cirino ( Wilmore C. Webley Nancy L. Croteau ( Chester Andrzejewski Jr. ( Elizabeth S. Stuart (   Eur J Haematol. 2005 Jan;74(1):77-83. Detection of Chlamydophila pneumoniae in the bone marrow of two patients with unexplained chronic anaemia. Nebe CT, Rother M, Brechtel I, Costina V, Neumaier M, Zentgraf H, Bocker U, Meyer TF, Szczepek AJ. Central Laboratory, University Hospital Mannheim, Mannheim, Germany. Anaemia of chronic disease (ACD) is a common finding involving iron deficiency and signs of inflammation. Here, we report on two patients with ACD where a persistent infection with Chlamydophila (Chlamydia) pneumoniae (CP) was detected in bone marrow (BM) biopsies. Infection was suspected by routine cytology and confirmed by immunofluorescence, electron microscopy, polymerase chain reaction (PCR) including different primer sets and laboratories and sequencing of the PCR product. This is a first report of chlamydial presence in the BM of anaemic patients. The cases are presented because persistent chlamydial infection may contribute more frequently to chronic refractory anaemia than previously suspected.   Tolerance and Pharmacokinetic Interactions of Rifabutin ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 0066-4804/01/$04.000 DOI: 10.1128/AAC.45.5.1572–1577.2001May 2001, p. 1572–1577 Vol. 45, No. 5 Copyright © 2001, American Society for Microbiology. All Rights Reserved. and Azithromycin RICHARD HAFNER,1* JAMES BETHEL,2 HAROLD C. STANDIFORD,3 STEPHEN FOLLANSBEE,4 DAVID L. COHN,5 RONALD E. POLK,6 LARRY MOLE,7 RALPH RAASCH,8 PRINCY KUMAR,9 DAVID MUSHATT,10 AND GEORGE DRUSANO11 FOR THE DATRI 001B STUDY GROUP† This multicenter study evaluated the tolerance and potential pharmacokinetic interactions between azithromycin and rifabutin in volunteers with or without human immunodeficiency virus infection. Daily dosing with the combination of azithromycin and rifabutin was poorly tolerated, primarily because of gastrointestinal symptoms and neutropenia. No significant pharmacokinetic interactions were found between these drugs.   Severe neutropenia among healthy volunteers given rifabutin in clinical trials CLINICAL PHARMACOLOGY & THERAPEUTICS DECEMBER 2003 591 Glen Apseloff, MD The Ohio State University College of Medicine and Public Health Columbus, Ohio CLINICAL PHARMACOLOGY & THERAPEUTICS Letters to the Editor DECEMBER 2003, p. 592     Comparison of azithromycin and clarithromycin in their interactions with rifabutin in healthy volunteers. J Clin Pharmacol. 1998 Sep;38(9):830-5 Apseloff G, Foulds G, LaBoy-Goral L, Willavize S, Vincent J.   Department of Pharmacology, The Ohio State University College of Medicine, Columbus 43210-1239, USA.   A 14-day, randomized, open, phase I clinical trial was designed to examine possible pharmacokinetic interactions between rifabutin and two other antibiotics, azithromycin and clarithromycin, used in the treatment of Mycobacterium avium complex infections. Thirty healthy male and female volunteers were divided into five groups of six participants each: 18 received 300 mg/day of rifabutin, 12 in combination with therapeutic doses of either azithromycin or clarithromycin; the remaining 12 received azithromycin or clarithromycin alone. On day 10 the study was terminated because of adverse events, including severe neutropenia. Fourteen participants who received rifabutin developed neutropenia, including all 12 participants who received azithromycin or clarithromycin concomitantly. Analyses of serum revealed no apparent pharmacokinetic interaction between azithromycin and rifabutin. However, the mean concentrations of rifabutin and 25-O-desacetyl-rifabutin (an active metabolite) in participants who received clarithromycin and rifabutin concomitantly were more than 400% and 3,700%, respectively, of concentrations in those who received rifabutin alone. Physicians should be aware that recommended prophylactic doses of rifabutin may be associated with severe neutropenia within 2 weeks after initiation of therapy, and all patients receiving rifabutin, especially with clarithromycin, should be monitored carefully for neutropenia.  

Jim, thank you and Dr. Stratton for all of this information. It is very succinct and makes so much sense. It cetainly helps me to understand the robust nature of the strange side effects that continue to surprise me through the protocol. By their very appearance in the different parts of the body where they manifest, it is easy to see how far the Cpn has travelled.

CAP 2/14/06 for Cpn-CFS/FM/Cardiovascular Disease

Wow.  I KNOW I have to read this one a few times to get it all, but right now ... WOW.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

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

Thank you, Jim! What a clear and concise exposition you have given of your talk with Dr. Stratton. What I see in the big picture is what I have thought all along---one disease with many manifestations. All the labels we place on various conditions are just variations of Cpn infection. I am particularly intrigued by the reports on the new drug Rifabutin. Don't think I want to take that one anytime soon.Also, finding such a large percentage of young supposedly healthy people with Cpn infection reinforces my belief that it is rampant in the school systems--especially in high schools and colleges. And the part about lowering white cell counts explains to me why Dr. P. is monitoring my white cell count. I didn't quite connect the dots on that one. (And yes, it is coming up over the months) Many thanks!! RavenCawing on the CAP since 8-05 for Cpn and Mycoplasma P. for MS and/or CFS 

Feeling 98% well-going for 100. Very low test for Cpn. CAP since 8-05 for Cpn/Mycoplasma P.,Lyme, Bartonella, Mold exposure,NAC,BHRT, MethyB12 FIR Sauna. 1-18-11 begin new treatment plan with naturopath

Gracious--this bug is bad juju. In the bone marrow--yuck--churning out elementary bodies--blah!--Jim, you have shared a ton of info, and I am sure that was very difficult to put so clearly on the site for us. A big thank you. And of course thanks to Stratton, et al, too.Lexy

"Chance favors the prepared mind." --Louis Pasteur

Husband treating MS with CAP


Excellent work Jim.   Thanks so much.   And please pass along thanks to Dr Stratton.A quick question about the interview.   I noticed that "Inflamed skin capillaries (especially from EB’s)" was listed as a source for Rosacea.   It's the only area where a Cpn form is mentioned.   Did Dr Stratton by any chance mention why he thinks EBs might be so important here?   Thanks again so much...    On Combined Antibiotic Protocol for Cpn in Rosacea since 01/06

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-

Red- Only an example. Of course, where there are EB's there are probably infected vascular and epidermal cells and RB's, cryptic forms (hence the use of Flagyl cream), etc. Dr. Stratton in the interview only referred to EB's getting stuck in small vessels. I extrapolated to the rosacea for the table, although he reviewed the whole thing and approved it. The table is just meant to give an idea of the Cpn site>> disease connection, not as a definitive description.Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndrome & Fibromyalgia- Currently: 150mg INH, Doxycycline/Zithromycin, Tinidazole pulses. Northern Ohio, USA

Big thank you, Jim and also to Dr. Stratton for such a illustrative explanation.Prague, The Czech Republic, On Wheldon protocol for Cpn and Mycoplasma since 02/18/2006.

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

Thanks, Jim and dear Dr. Stratton!    I have a strong feeling, after reading this latest, that it is correct, not just speculation, and that I  survived my 1st year of abx by "going as fast as I could".  I think if I had gone faster,  I would have been a really bad "host" -  i.e. - a dead one!  This would explain the loss of memory,  the toxicity, all the rest that I "suffered" and would happily again, if need be.  Here I am, on the 4th day of my 31st pulse, able to read and absorb this!  Need I say more? Rica        EDSS 6.7 at beginning - now 2 Ignorance is voluntary bad luck.  Lauritz S.   A true Viking If you come to a fork in the road, take it. Yogi Berra

3/9 Symptoms returning. Began 5 abx protocol 5/9 Rifampin 600, Amox 1000, Doxy 200, MWF Azith 250, flagyl 1000 daily. Began Sept 04 PPMS EDSS 6.7 Now good days EDSS 1 Mind, like parachute, work only when open. Charlie Chan  In for the duration.&am

Thank-you Jim,Makes me feel better as I am disappointed that I am not going faster with this treatment - feel like I am moving at a turtles pace but I will get there soon - my body is telling me I am not ready yet.  But soon  On Wheldon protocol for MS since April, 2006.  doxy 200 mgs daily, zithromax 250 mgs 3x/ week , LDN 2004

5oo mgs Ceftin 2 x/day, 500 mgs Zithromax, 500 mgs 2 x tini pulses,100 mg diflucan, 4.5 ldn; Wheldon protocol for MS April, 2006 to May 2008. 2008 MRI shows NO NEW DISEASE ACTIVITY, 2012 MRI no new disease activity.

Another WOW and thank you. Combined Antibiotic Protocol for chlamydia pneumoniae in fibromyalgia- minocycline/Zithromycin, Tinidazole

minocycline, azithromycine, metronidazole 2007-2009, chelation for lead poisoning, muscle pain, insomnia, interstitial cystitis (almost well), sinus, dry eyes, stiff neck, veins, hypothyroid, TMJ, hip joints (no longer hurt)

Jim: Excellent, excellent pedagogy. I didn't need to read it with a pencil! Thank you. One phenomenon explained -- two pulses back, I pulled a muscle in my left knee at yoga. My knees have always been good, especially my left. It felt like a minor pull, but during the next pulse the whole left side of my body hurt, my knee swelled, I ran a fever, and I felt so toxic that I thought I was going to have to stop the pulse early.After the pulse, my knee slowly returned to normal. The pulse I'm currently doing hasn't been nearly as bad; my knee feels worse than it did between pulses, but nowhere near as bad as last pulse. Given the data above, it seems reasonble to conjecture that:

  • having CFIDS indicates that my primary site is the bone marrow/immune system.
  • the strain in my knee attracted a large number of infected, incompetent, immortal immune cells (4-i's!)
  • my knee didn't heal because the cells are incompetent
  • the pulse about flattened me because the infected cells are out where the abx can really hit them hard.
  • now that the infected cells are clearing, the knee is healing up again.

Now, would it be a good idea to deliberately inflame a muscle between pulses to get the immune cells out where they can be killed? Someone (else) ought to try that!Ron On Stratton protocol for CFS starting 01/06 (NE Ohio, USA).

RonOn CAP for CFS starting 01/06 (NE Ohio, USA)Began rifampin trial 1/14/09Currently: on intermittent


Makes sense Jim.  Thanks again as always... On Combined Antibiotic Protocol for Cpn in Rosacea since 01/06

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-

Dr. Stratton and Jim,  Thanks for this terrific educational tool---lots of info in a small package.Ron,  If your conjecture should prove true, then maybe it's a good thing for MSers to bump into things and fall down while pulsing.  Perhaps the old adage about getting back up on that horse when you fall off is better advice than we ever thought.Joyce~~~MS scaregiver and madvocate practicing for 10/31

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

Joyce- I think that would make the adage "Get up after you fall off the horse, so that you can fall off again..."I must say, as the officiant of this site, that Ron's method of getting at immune cells is explicitly not recommended as a treatment method or as any part of the CAP. I can see the headlines now: Alternative Treatment Site Says to MS'ers: Let Them Fall!" Class action suits, Federal Agents coming to confiscate my computer, languishing without meds in jail. Ron, will you send me care packages of antibiotics and supplements?Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndrome & Fibromyalgia- Currently: 150mg INH, Doxycycline/Zithromycin, Tinidazole pulses. Northern Ohio, USA

Jim, since it was my idea, I'll probably just need to roll the pills through my own bars and over to your cell.Seriously, though, it was interesting to see the whole process in such a short period of time. I had heard about old injuries/symptoms being exacerbated during a pulse, but had not thought about more recent injuries doing the same.The exaggerated general feeling of toxicity was surprising to me as well. RonOn Stratton protocol for CFS starting 01/06 (NE Ohio, USA).

RonOn CAP for CFS starting 01/06 (NE Ohio, USA)Began rifampin trial 1/14/09Currently: on intermittent

Just in case I might have been too subtle, everyone please read the signoff on my earlier comment.  Joyce

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

Subtlety and observation are not my strong suits, Joyce!  Cute!  We are always in the barn feeding and milking, and have a long driveway with trees between the road and the barn and house - all dark!  No visitors - it's too much like a cemetary.  What breed were your friend's goats? Rica        EDSS 6.7 at beginning - now 2 Ignorance is voluntary bad luck.  Lauritz S.   A true Viking If you come to a fork in the road, take it. Yogi Berra

3/9 Symptoms returning. Began 5 abx protocol 5/9 Rifampin 600, Amox 1000, Doxy 200, MWF Azith 250, flagyl 1000 daily. Began Sept 04 PPMS EDSS 6.7 Now good days EDSS 1 Mind, like parachute, work only when open. Charlie Chan  In for the duration.&am

CNS is not mentioned in this fascinating info from Dr S.  Jim, it would be interesting to hear when/how CPN reaches the CNS in people with MS.  Also is there any evidence from non MS people that CPN reaches nervous tissue or does it stay outside the CNS ?  OK techie thoughts but I wonder how CPN crosses the BBB or is a leaky BBB needed ?.....................MarkCNS=Central Nervous System  BBB=Blood Brain Barrier.Mark Walker - Oxford, England.RRMS since 91, Dx 97, CFS Jan03.  Patient of David Wheldon Feb06, started CAP Mar06. Pharmaceutical Consultant (until I stopped working in Jan03).

Mark Walker - Oxford, England.RRMS Nov 91, Dx 97. CFS Jan03. Copaxone + continuous CAP (NAC, Dox, Rox) Feb06 to May 07. Met pulses from Jun06. Intermittent Abx from June 07 onwards.

 Thanks Jım for thıs update...Cpn crosses the BBB ınsıde the t-cells(ımmune cells) , as far as ı know..On CAP's protocol for Cpn in PPMS since June 2004Currently:  Doxy/Roxy, Metronidazole pulses 

On CAP's protocol for Cpn in PPMS since June 2004 - Currently: Doxy 100mgx2/day - Roxy 150mgx2/day - Flagyl 500mgx3/day (Continuous protocol since sept.2006)

Good question, Mark. Other comments in the past have cited the immune cells (which cross the BBB), as well as David Wheldon's comments on MS spreading along vascular lines in the brain, implying that vascular endothelial Cpn infection (not different really from larger vessel findings of Cpn infection in heart disease) creates the entry point for infection into the brain. I always assume once it's in the brain, EB's can reach spinal cord sites via the cerebrospinal fluid, but don't really know of specific evidence of this. Certainly they test for DNA particles of Cpn in the PCR studies.Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndrome & Fibromyalgia- Currently: 150mg INH, Doxycycline/Zithromycin, Tinidazole pulses. Northern Ohio, USA

Mark,I don't know alot about this. However, as I recall, B. Balin's latest involves nasal inoculation of intact, wild-type mice with Cpn, which became demonstrable in the brain area by immunohistology. I don't know whether they specifically showed the immunorecognition to be on the brain side of the BBB, by excluding the possibility that it could be inside the BBB structure itself. (I'm following this source which considers both the luminal and abluminal cytoplasmic membranes of the endothelial cell layer to belong to the BBB, so the endothelial cytoplasms would thus lie within the BBB structure).By the way, invasive borreliae and treponemes are rapidly CNStropic in intact hosts; I'm not sure if the mechanism is well explored or what. There are many other CNStropic agents too.

WOW!  What an exciting piece!  It contains so much information which I can relate to personally from my own experiences and those of my son.  I remember a couple of years before i was dx'd with cPn, watching a  "live cells analysis" of my blood which was fascinating, a macrocosm within a microcosm of what was going on in my body. Reading this brought to mind, seeing in that one drop of my blood, put on a slide and under a microscope, and then viewed on a screen before me, as I was shown by the technician the markers which pointed to signs of weakness in my kidneys and lungs, evidence of past bouts of pneumonia I had,  and especially the look I got at the lively and plentiful bacteria swimming around in my bloodstream and the poor, bloated, half-dead looking micophage white cells as the bacteria swam swiftly past them, only to have them react in a slow "drunken" sort of  manner, way too late, to being to move toward the spot where the bacteria had been and to begin very slowly to assume the shape they would need to surround that invader - then, just give up, when it realized the villian was long gone. I laughed and said "that's just how I feel! It's as though I know I am full of bacteria, as evidenced by how good I feel whenever I can get some antibiotics from a doctor and get them into me, and how tired out and overwhelmed I feel, knowing the bacteria is so plentiful and so ahead of the game that I can never catch up with it." Espeically since doctors never found anything "wrong" with me and my full time job had become figuring out ways to try and "score" an antibiotic on my office visits. It would probably have been easier to get an illegal drug more often!It scares me to think - did my son, a "healthy" college aged blood donor, who was told by one MD to get rid of his high iron level by donating blood every six weeks, actually infect others with his blood?  He donated nearly every six weeks, from age 21 - 26 and was found at age 29 to have cPn and two species of mycoplasms. His high iron level had been found NOT to be hemochromatoisis, the inherited  iron storage problem, and so donating seemed the thing to do. The blood bank nurse used to comment on "how much heavier" a bag of his blood was compared to the norm, "probably due to the iron".  I was quite interested to learn the connnection with the cPn and the high iron.  Mine had also always been high. (within normal range now).I am going to read and re-read is so fascintaing to understand more and more about cPn and it's various permutations and modus.  Thank you, Jim, for being our translator. I have the capacity to understand scientific things, but somehow, not the patience or focus at this stage of my life. I know this wasn't easy for you to understand fully, digest, and then bring it to us in such a basic and well explained manner. You are just wonderful. You and Dr. Stratton, both.Diana

Thanks so much for going to the trouble of explaining Dr. Statton's work. I can see you are deluged with messages of gratitude, but let me add to the collection. This information you have shared has the potential to give me my life back! Thank you and also thank Dr. Stratton for his excellent work on cpn.Melissa