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50% rate of infection?

According to this ScienceDaily release<, half of all Swedish 20 year olds are "carriers" of C.Pn.


Full text< of the dissertation is available, but it's 100 pages long, and I haven't find the citation for that "50% carriers" factoid.

Loads of good, good stuff about the plaque formation and vessel damage that was described in The Potbelly Syndrome -- worth a look. I'll look harder for the citation later, but it's 4am, and I have rested enough to sleep some more, so that's my next job.



Joyce's CAP Log: The Beginning

May 15, 2007 was my start date. I took 100mg doxycycline for 5 days with very mild reactions: 3-1/2 year old hysterectomy scar turned red and itchy for 2 days, eyes red-rimmed for a day, residual puffiness and redness underlying 3 month old surgery scars on cheek and upper lip increased for 1 day, then "deflated" to a lower profile than before.

"The Heart Attack Germ Book"

I ran across this while surfing the Web today.... anything worth reading in it?<

Blessings to all,


Help I am so confused

I am still trying to get a grasp on Chlamydia Pneumoniae, I just found out on 4-11-07.  But I have been sick for awhile  Cry.  I am just starting Antibioticsi again......eeeeek Foot in mouth.  My symptoms have been sinus infectionsi and uppper respitory infections , Phlaringitis, Broncotitis, Asthmai.  In and out of the Dr. office the month of April, and my throat swelled shut I could go on and on.  I ended up at an Infetious disease Dr.


Bacteriophage are viruses that infect specific bacteria, sometimes killing it. I saw a TV show about Russian doctors treating bacterial infections by giving the patients the proper phage.

Apparently a certain bacteriophage for Cpni  makes Cpn more pathogenic. Phage-containing strains of C. pneumoniae are uncommonly found by isolation but may commonly infect individuals with vascular disease.<

Another article said those phages were commonly found in aortic arterial aneurisms.

 Phage-bearing strains of Chlamydophila spp. are more pathogenic than phage-free strains is being investigated in vascular disease; phage-bearing strains of bacteria are often more pathogenic than phage-free strains.

Blood pressure changes

Blood Pressure and cpni.

I thought I'd start this as a new thread, not wishing to hijack a previous and significant one of Marie's.
Ron's study of BP after starting antibioticsi opens something unknown.
I had untreated hypertension">i, BP being typically in the morning, 155 / 95. This is pathological, and I had (foolishly) staved off getting treatment.
On starting doxycycline and roxithromycin the pressure dropped, over a few months, to a typical and steady 110 / 75.
When I started to add metronidazolei the pressure became very erratic; during the second pulse (when I felt ill and had major reactions) it wandered from 100 / 65 to 170 / 100 within an hour, evidence of the latter pressure borne out by a pounding apex beat.
When reactions to metronidazole grew less, my BP began generally to stabilize at about 110 /75, at which it remained, whether metronidazole was taken or not.
This is only one person's experience, and using only one BP machine.
Occam's Razor shaves again (it never gives answers, but only apportions credence to the questions): were carotid baroreceptors being purged of their infection load during that bacteriocidal metronidazole addition?

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 inflammationi 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

Blood Pressure Experiences

Blood Pressure Experiences

One of the most remarkable (and objectively measurable) effects of CAPi seems to be the normalizing of blood-pressure. I thought it might be worth while having a forum on this subject, so that people can voice their findings.

My own experience is that of a rapid reversal of what had been worsening for 25 years. My blood pressure before starting treatment was typically 155 / 95 and rising. That's a pulse pressure of 60, which is wide for someone in their late fifties. The usual thoughts cross the mind: 'I'm healthy, I have a reasonable diet, I go cycling to work every day, I enjoy what I do.' And then you look towards the future. And then you think of colleagues who have had coronary problems, some much younger than you. For you the future course of events is that the systolic blood pressure will continue to rise, and the diastolic pressure will plateau and then slowly fall. This results in an ever-widening pulse-pressure which is known to precede strokes and coronary artery disease. Well, in my case, when I began taking antibioticsi, I noticed a regular fall in both systolic and diastolic blood pressure over the weeks (I had bought a little Seinex sphygmomanometer a year or two ago.) I measured my BP every other morning or so. I'm now on intermittent antibiotics and my BP runs along at a typical 115 / 75. It's also far more responsive to exercise and even emotions. If I'm really calm and the sunlight is streaming through the window, then it can go down to 95 / 65. It rises during exercise and then quickly falls. The pulse-rate echoes this. Before treatment it was typically 85; now it is typically 60 - 65. It recovers very quickly after exercise. All this strikes me as amazing, and, scattered through various threads, it seems that several others have had similar experiences. I recall Ron saying:

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 Disease (IBD)
Interstitial Cystitisi (IC)
Fibromyalgiai (FM)
Autonomic nervous dysfunction (AND neural-mediated hypotension);
Pyoderma Gangrenosum (PG)
Chronic Fatigue (CF) and Chronic Fatigue Syndromei (CFSi).

Atherothrombotic events and CPn

Chronic Chlamydia pneumoniae infection in patients with symptomatic atherothrombosis.

Halfon P, Limal N, Penaranda G, Khiri H, Sene D, Andreu M, Feryn JM, Rotily M, Serra R, Piette JC, Cacoub P.

Virological Department, Alphabio Laboratory, 23 Rue de Friedland, 13006 Marseille, France.

OBJECTIVES: The aim of the present study was to search for an association between chronic Chlamydia pneumoniae infection, indicated by elevated antibody titers against the pathogen, atherothrombosis and the occurrence of arterial ischemic events. METHODS: We studied 52 patients presenting at baseline with at least one symptomatic episode of atherothrombosis. A screening for fasting blood glucose and a lipid profile was performed on all patients who had no known history of diabetes or hypercholesterolemia. RESULTS: The prevalence of IgG and IgA anti-C. pneumoniae antibodies at baseline was 90% (95% CI: 79-97) and 81% (67-90), respectively. Forty-two of the 52 patients (81%) experienced a new arterial ischemic event after a mean follow-up of 9 years [heart: 19 (37%); brain: 12 (23%); lower limbs: 8 (15%); and other: 13 (25%)]. Occurrence of a new arterial ischemic event was related to age (p=0.003), sex (p=0.009), and tobacco smoking (p=0.06). Prevalences of IgA and IgG anti-C. pneumoniae were significantly higher in patients with atherothrombosis at baseline than that in controls. CONCLUSION: Our study confirmed the links between C. pneumoniae and atherothrombosis. However, neither IgA nor IgG antibodies for C. pneumoniae was a significant predictive factor for new ischemic arterial events in patients with atherothrombosis.

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