Serology

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Tissue testing for bacterial signs.

Now it begins . . . perhaps!

My CFSi Dr. is starting me with a serologyi test for CPni -- IgGi and IgM -- and will be getting backup from Dr. Stratton as needed. I really appreciate the two Drs. stepping up like this -- what I've read here and experienced over the past 18 mos tells me they're unusual.

 Dr. S suggested starting with serology. I suppose if it comes back elevated, then it's an easy sell to start the protocol. So, if it does come back elevated, it (treatment) begins. I kind of hope that CPn serology comes back positive. Hopefully the beginning of the end for this bug and its sequelae.

 If not, well, I'll just take the next step, which will be deciding on a next step, I suppose. My story with CFS (at least that's what I think it is) has only been a year and a half -- nothing to most of you, but plenty for me!

Dr. Michael Powell: A Rheumatologist Treating Cpn in CFIDS, FM, Lupus and other "auto immune" disorders

I spoke with a rheumatologist in California, Dr. Michael Powell, who is cautiously using a combination of antibioticsi in conjunction with standard therapeutics for the treatment of nanobacterium (including Cpni) in patients suffering from FM, CFSi and autoimmune disorders. His results with this treatment program have been encouraging. He faxed me some examples of patient feedback forms, excerpts from which you can see below. Recovery is not instantaneous, but tends to occur over a 6 to 12 month period. The graphs of subjective improvement are drawn from visual analogue scores compiled during each visit. When summarized in this manner these data give a time-lapsed impression of the response to treatment.

One of the interesting things he mentioned was in relation to negative patient serologyi for Cpn when other clinical signs lead him to suspect some involvement. Serologic assays for IgGi, IgM and IgA are sent to confirm infection prior to treatment. He would like to see a positive serologyi in patients before engaging them in a combination antibiotic protocol, but recognizes that patients may not have antibody reactions. This may be due to the ability of intracellulari organisms like Cpn to evade a humoral response (antibody production), immunoglobulin depletion, or other factors. In these cases, when there is a high index of suspicion for the infection without a humoral response, he tests the spouse of the partner for Cpn. He sees the "non-symptomatic" partner as a good indicator of Cpn in the patient, given the infectious nature of Cpn. Thus far, most spouses are positive when an ill family member is non-reactive.

In our discussion Dr. Powell pointed out the many similarities between TB and Cpn.  Both organisms  can evade our immune system.  Both organisms can be carried from the lungs, the original site of infection, and infect other tissues. Both require prolonged treatment with multiple drugs to eradicate the infection.  Both are sensitive to stress levels. Optimal therapy is being evaluated at various research centers and new medications for Cpn are on the horizon (see activbiotics.com).

INHi and supplementsi for endotoxinsi-
Dr. Powell finds most patients improve on a standard combination antibiotic protocol for Cpn. Rheumatologist have apparently been using doxycycline for many years with success for inflammatory arthritis but there is evidence that using doyxcycline in combination with rifampin is even more effective. Some patients plateau after about 8 months of treatment he has found variations in the treatment protocol have made a difference. One protocol he uses involves the use of NACi 600 mg twice daily, INH 300 mg once daily before breakfast, and metronidazolei 500 mg twice daily pulsed with 5 days on and two weeks off.  It is essential to start each agent separately and gradually increase the dose over weeks or months as tolerated.  The use of Vitamin C 500 - 1000 mg four times daily (the half life of vitamin C is 30 minutes and little remains after 3 hours) to offset the release of toxins during therapy.  B6 is important to control INH related peripheral neuropathy.  Monthly laboratory evaluation of AST, ALT, Cr, and CBC are recommended for all who engage in this protocol.  It is not uncommon for liver enzymes to show a mild elevation during the initial stages of treatment.  Antibiotic therapy should be temporarily discontinued during periods of toxicity, should it arise. He emphasized the importance of insuring that yeast and fungal infectionsi do not overgrow during protracted antibiotic use. He recommends the use of acidophillus, nystatin, diflucan, oregano oil, and/or grapefruit seed extract as needed to prevent secondary opportunistic infection during treatment.

Covering for the possibility of yeast and fungal overgrowth during antibiotic therapy is essential.  If diarrhea develops, stool must be evaluated for antibiotic associated diarrhea (C. difficile).  This is not a simple protocol and it is best if it is guided by an experienced clinician who is familiar with the medications and methods of minimizing toxicity related to killing the nanobacterium.

A link to Dr. Powells clinic may be found on our links page. Dr. Powell does do telephone consultations by arrangement and may be a resource for those who have had difficulty finding a Cpn knowledgeable doctor in their area. He requires an initial visit with a physical examination before initiating therapy (lab work can be performed prior to the initial visit to facilitate diagnosis and treatment), and monthly laboratory testing with monthly phone consults are then the norm. Treatment of related hormone imbalances in the thyroid system and nutritional support, temporary antidepressant support as needed, and sleeping medications are useful adjuncts to the antibiotic protocol. It is necessary for patients to have a primary care physician to monitor health matters that are unrelated to FM, CFS and autoimmune disease.

David Wheldon's story: Cpn Treatment of Cardiac & Myalgic symptoms

I was born in 1950; I’ve always been very active. As an adolescent I had recurrent and painful sinusitis; this vanished in my late teens. Amongst my activities I listed caving (spelaeology) which requires some physical fitness. I continued cave exploration until well into my forties.

In 1999 my wife, Sarah, and I both caught a respiratory infection which started off as a sore throat; in a fortnight it had become a mild pneumonia. Sarah developed frank asthmai which required a Salbutamol inhaler. I also had a wheeziness, particularly on exertion. This eventually cleared. I also suffered with sinusitis again. I didn’t seek medical advice.

A few months later I began to find turning my head not only painful but difficult. As I cycle to work this grew to be problematic. I found that if I wished to turn right (UK) I had to dismount and walk across the road. At about this time I noticed that I was developing soft-tissue swellings in my neck; these began to grow quite quickly. Shortly after this I found I had myalgia in my shoulders and the long muscles of my back. Sarah noticed that I was walking very awkwardly; if I wished to turn my head I had to turn all my body. Flexion of the spine was difficult, too.

In 2002 I noticed that my resting heart-rate had increased, and there were increasing numbers of dropped beats. These were quite alarming in the dead of night. Sarah noted that my apex beat was really hard and actually audible at night. I was worried by this time, but was more concerned with Sarah’s aggressively advancing MSi, which was much more troubling.

By 2003 All my symptoms increased in intensity; they now included constant pleuritic pain (a sharp pain in the side when breathing) on the right. Also there was an exquisitely painful longitudinal white streak along the nail of my left forefinger. I began to feel vertigo when moving suddenly: it was as though I were standing on either side of a small see-saw. My blood pressure was 150/95. I had my blood tested for Chlamydia pneumoniae antibodies; the IF titres were 1:128. This level is seen in many asymptomatic people. Low titres mean little; they certainly don’t exclude the infection. Borrelia antibodies (Western Blot) were negative.

I began a course of empirical antichlamydial treatment; it was very similar to Sarah’s, namely doxycycline 200mg daily and roxithromycin 300mg daily. (it doesn’t matter whether you take all the daily dose at once with these.) That night I felt sweaty and ill; this feeling carried on for five days; it was worse in the evenings, and was accompanied by an odd state of mind.  All kinds of visions went through my mind, and Sarah says that I was babbling, changing the subject almost in mid-sentence. But this subsided. After three months I began a short course of metronidazolei in addition to doxycycline and roxithromycin. Towards the end of this course I had a rather ominous feeling that something was about to happen. Three weeks later I began another five-day course of metronidazole. On the fourth day I began to feel pain in the muscles of the back of the neck and in the soft tissue swellings to the side of my neck. That evening I began to sweat profusely, and had very strong muscle fasciculationsi over my torso. These continued for a week or so after stopping the metronidazole; again they reached their peak in the evening, so I was able to work during the day. (Evening fevers seem quite common with resolving intracellulari infectionsi.) They were followed by crushing pains in both upper limbs, which I take to be a mild form of Reflex Sympathetic Dystrophy. Fortunately these eased within weeks. My weight dropped from 95 to 81 Kilos within a few weeks. Within three months the neck swellings had almost subsided. Reactions to the third pulse of metronidazole were slight. Reactions to the fourth, fifth and sixth were negligible. My blood pressure dropped to a typical morning BP of 115/75; the apex beat became actually quite difficult to feel, and my pulse became very soft and even. All the ectopics had gone.

Now I am on intermittent antibioticsi and supplementation; this includes N-acetyl cysteine 600mg twice daily for the purpose of bursting any chlamydial elementary bodies which remain. I still have a little trouble with vertigo and ringing in the ears, but not enough to stop me riding my bicycle. I’m pain-free and supple, and have full movement of my spine and head. There is an impression of ongoing soft-tissue remodelling.

Sarah and I had a similar respiratory infection; she developed frank asthma, and I an intermittent wheeziness. So though I have no hard evidence that we both had an infection with Chl. pneumoniae it seems clinically likely. No other known pathogen causes a respiratory infection after the pattern described. Often this is a clinical diagnosis. We have to accept that, on an individual basis, present-day laboratory tests may have little diagnostic value.

I managed to work full-time during this illness, coming home to cook for us both. We kept our household together. Some of our social friends were alarmed and lost touch, but, well, I don’t suppose they were really friends.

Sarah’s recovery from secondary progressive MS (where recovery is not a part of the natural history of the disease) is recounted elsewhere on this site.

Serological evidence of CPn LPS antibodies in atherosclerosis of various vascular regions

Vasa. 1999 Nov;28(4):259-63. Related Articles, Links

Serological evidence of Chlamydia pneumoniae lipopolysaccharidei antibodies in atherosclerosis of various vascular regions.

Korner I, Blatz R, Wittig I, Pfeiffer D, Ruhlmann C.

Department of Cardiology/Angiology, University of Leipzig, Germany. koei@medizin.uni-leipzig.de

BACKGROUND: The role of Chlamydia pneumoniae in the pathogenesis of atherosclerosis has so far mainly been investigated in patients suffering from coronary heart disease; the other vascular regions have virtually been ignored. The aim of this study was to carry out a statistical survey of serological markers of a C. pneumoniae infection in patients with different patterns of atherosclerosis manifestation. PATIENTS AND METHODS: 340 patients were examined for the atherosclerotic alteration of peripheral arteries of the lower limbs, carotid arteries and coronary arteries by ultrasound scan and/or angiography. Immunoglobulin(Ig)G and IgA-rELISA were used to measure chlamydial lipopolysaccharide antibodies. Species determination was performed using the IgG micro-immunofluorescence test. RESULTS: 24.0% of atherosclerotic cases (A) and 52.3% of controls (C) were negative for C. pneumoniae lipopolysaccharide antibodies (p = 0.00002). By contrast, 45.1% of atherosclerotic cases and 16.9% of controls were positive for both IgG and IgA (p = 0.00002). The mean antibody titers of the atherosclerosis group were higher than in the control group (IgG positive xAIgG = 344, xCIgG = 272; IgG and IgA positive xAIgG = 576, xCIgG = 486 and xAIgA = 120, xCIgA = 91). Concerning atherosclerosis manifestation in various vascular regions, no significant differences were found between IgG and IgA antibody titers and prevalence. CONCLUSIONS: The results show that a persistent C, pneumoniae infection with evidence of lipopolysaccharide immunoglobulin G and A is equally associated with the atherosclerotic alteration of coronary arteries, carotid arteries and peripheral arterial occlusive disease, irrespective of the severity of atherosclerosis and with no predisposition to any particular vascular region.

Cpn Treatment Information

The links below will take you to pages with specific information involved in the treatment of Cpni.

Diagnostic Testing For Cpn<
Information on serological testing and the problems of this in Cpn.
Combination Antibiotic Treatment Protocols for Cpn<
Links to pages on the current versions of Vanderbilt/Stratton and Wheldon Protocols for treating Cpn infectionsi in various diseasesi.
Experts Comments<

Commentary and interviews  with various experts in treating Cpn which help guide and inform about various facets of treatment.
Treatment Reactions<
Information on some of the kinds and sources of treatment reactions one can expect on combination antibiotic protocols in treating Cpn, including cytokinei reactions, endotoxini reactions, secondary porphyriai and other reactions. These are often lumped under the term "herx," an inaccurate term and not as useful as really understanding what's going on.

 

The Basics Page

Hello and Welcome!

This site is focused on treatment of chronic disease like Multiple Sclerosis (MSi) Chronic Fatigue Syndromei (CFSi) and Fibromyalgia (FMSi) an many other diseasesi with antibioticsi. Recent research indicates that Chlamydia Pneumoniae (CPni) plays a role in these diseases.

Here are the basics that make it easier for people new to the site to get going (if your brain isn't ready for even this much right now-- we've all been there-- read Cpn Simple< first):

Is this a sexually transmitted disease? No. this is chlamydia pneumoniae, a bacteria that can cause pneumonia. It may soon be called chlamydiophilia (meaning in the family of).

Is chlamydia pneumoniae (CPn) rare?

PCR Analysis

Here< is a link to a detailed and technical paper on PCRi analysis that evaluates and outlines the problem with culturing CPn and the variations in abilities in different labs. It also talks about the results of split samples and concordance between some PCR approaches and discordance with others. Though this is highly technical, it answers the question of how can it be that there are still some researchers producing papers saying, for example, that they tested patients with MSi for CPn and found the incidence to be no higher than controls, such as this article here< but note that this one used antibody tests, a ridiculously ineffective way of looking for CPn in cryptic form in the brain.

Results, and Clinical Performance of Five PCR Assays for Detecting Chlamydia pneumoniae DNA in Peripheral Blood Mononuclear Cell

J. B. Mahony,1,2,* S. Chong,1 B. K. Coombes,1 M. Smieja,1 and A. Petrich1,2
Hamilton Regional Laboratory Medicine Program, St. Joseph's Hospital,1 and Department of Pathology and Molecular Medicine, McMaster University,2 Hamilton, Ontario, Canada
Link here<

Received 18 January 2000/Returned for modification 31 March 2000/Accepted 4 May 2000

Chlamydia pneumoniae has been associated with atherosclerosis and coronary artery disease (CAD), and its DNA has been detected in atheromatous lesions of the aorta, carotid, and coronary arteries by a variety of PCRi assays. The objective of this study was to compare the performances of five published PCR assays in the detection of C. pneumoniae in peripheral blood mononuclear cells (PBMCs) from patients with coronary artery disease.

Serological evidence of Chlamydia pneumoniae in asthma.

Serological evidence of infection with Chlamydia pneumoniae is related to the severity of asthma. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=10706488&dopt=Abstract
  • Chlamydia pneumoniae as an Emerging Risk Factor in Cardiovascular Diseasei<
  • Murat V. Kalayoglu, MD, PhD; Peter Libby, MD; Gerald I. Byrne, PhD , JAMA. 2002;288:2724-2731 http://jama.ama-assn.org/cgi/content/abstract/288/21/2724
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