This is the news:  In England, possible antibioticsi to be sold over the counter, to treat CHLAMYDIA!

This is the story form http://www.guardian.co.uk/society/2008/aug/06/health

Oral antibiotics are to be made available for the first time without doctor's prescription under guidelines approved yesterday by the medicines regulator.

A pill to treat chlamydia, the most commonly diagnosed sexually transmitted infection, will become available for purchase in pharmacies across England later this year.

I found a recent 2007 dissertation by M. Paldanius that provides a very good review of the literature and testing procedures for detecting chronic infectionsi and reactivations.  He's on the medical microbiology faculty at the University of Oulu, Finland. His dissertation can be found here: Serological studies on Chlamydia pneumoniae infections.

                             TABLE 11
    Serological and PCRi Responses to Combination Antibiotic Therapy
                                   Months of
                                  Combination
    Pa-                 Titer     Antibiotic 

I had borreliosis last winter and treated it with doxycyclin for 5 weeks 100mg / d.

Last year in summer i had ch. trachomatis which i also treated with a tetracyclin, i don't remember which one exactly. Now to confirm I am no longer infected with borrelia I took a blood test, and tested for borrelia:

IgGi pos but IgM neg. And for chlamydia, and this shows CPni values:

IgA-AK 45 U/ml

IgG-AK 135 U/ml

IgM-AK 1,1 S/CO

Method was an EIA. I have dry coughs sometime, that have been bothering me, so I wondered: Do I have to worry? What treatments are available? From reading some posts in this forum, I know that I'm a really light case, but still any help will be greatly appreciated.

Thanks

Editorial (Rant?)

This is one of my own pet medical peeves, stimulated recently by a thread here on Lyme tests and what bands meet criteria, etc. It relates directly to the difficulties with negative tests for Chlamydia pneumoniae. Yes, I know it's a complex issue, but the basic rule is really a simple one:

A serologyi test, either negative or positive, does not a diagnosis make!

Medical diagnosis is a complex art which includes serologyi, clinical history, symptom patterns, treatment history, and other medical tests. True, some serology carries more weight in the clinical equation that others and may be taken almost defacto as diagnosis. For example, one is treated for many diseasesi on the basis of positive serology, such as for TB or STD's, even if you are asymptomatic and have nothing obvious in your history.

Today I was at the doctor and she told me results of tests- my cpni IgAi titers and KFR are high, almost on the same level as in the beggining. So it seems to her my treatment is not very effective. When I took ofloxin my titers rapidly decreased after one moth.

I was better after first two months into the treatment but then I again got worse and last few weeks I am not really well. (I am finishing fourth month)

I know nothing about testing, but it seems to me strange, does anyone have any idea, why it is? I would be grateful for any reasonable answer.

For some reason, the first thing I saw on the home page of this site is just sinking in. Look at the picture of the parasite-ridden red blood cells on the home page.

No wonder CFSi sometimes shows a low ESR! And the achiness, too, could be due in part to the mechanical difficulty of squeezing those misshapen, oversized RBC's through a capillary.

 Low ESR doesn't exist in the U.S. standard medical training -- it's only associated with inflamatory conditions, and generally only considered significant if it's high (over 20.) I understand that in some of the British standard handbooks, an ESR under 5 is considered abnormal. I found, but don't have the links right now, that low ESR is associated with Giant Cell Arteritisi, another C.Pn. related condition.

Does anyone else who is under treatment for CPNi related conditions happen to know what their ESR was before they started treatment? 

Does it work?

It has been noted that most users of the combination antibiotic protocolsi commenting here have not been on the treatment long enough to give a big enough pool of reports to feel assured of the efficacy of this approach. I had asked Drs. Stratton, Wheldon, and Powell to perhaps tally up at least some basic numbers from their case experience to help us out with this problem, but this would involve problems of confidentiality and use of private data, etc.  

Then, I suddenly realized that we already have a good list of anecdotal reports of response to treatment reported data available to us... right in the Stratton/Mitchell patent materials! (Sheepish, embarrassed grin). So I took it as a project to summarize this data by disease treated. Occasionally I have used the exact wording from the patent materials as they were brief and descriptive. We have the full text referenced in our treatment and links if you want to see more detail.

All reported had with positive serologyi for Cpni using the highly sensitive tests developed by Stratton/Mitchell. I left out a few whose diagnosis was not clear to me, you can see them in the patent materials #6,884,784
All on some form of the combination antibiotic therapy protocol.

Summary of our Cpni Treatment Poll:

The poll was out for two weeks, and represents a snapshot of protocol users at this point in time. We had slightly different numbers participating in each section of the poll, perhaps some questions did not have exclusive answers for those voters. Obviously, 25-28 people is not enough to draw scientifically valid results from, but I intend to speculate on some suggestive patterns in the data.

Gender:
Female: 61% (17 votes)
Male: 39% (11 votes)
Total votes: 28
This ratio is commonly reported in CFSi/FM, MSi and other "autoimmune" diseasesi, so is not surprising. We would expect that if more people with Cardiac diseases were searching out Cpn treatment, with a higher male to female ratio, this might change.

Age:
20-29 years = 7% (2 votes)
30-39 years = 14% (4 votes)
40-49 = 32% (9 votes)
50-59 years = 39% (11 votes)
60-69 years = 7% (2 votes)
Total votes: 28
Our largest group is between ages 40 to 59. I suspect that this age does not reflect the period when people are morel likely to be infected, but rather a range where long term persistent infectionsi are have accumulated enough damage to force us to seek out "desperate measures" such as the multi-antibiotic protocol recorded here.

Primary diagnosis:
Over half the total in the poll have a diagnosis of MS. The second largest group are those with a diagnosis of CFS/FMSi. This likely influences the treatment response reported later which suggest that improvements are noticed most after 5 or more pulses.
CFS/FM = 28% (8 votes)
MS = 55% (16 votes)
Asthmai = 3% (1 vote)
Cardiac disease = 3% (1 vote)
OTHER = 10% (3 votes)
Total votes: 29

Serologyi
Positive blood test for Cpn
48% (12 votes)
Negative blood test for Cpn
16% (4 votes)
Not been tested for Cpn
36% (9 votes)
Total votes: 25
Well over half either have negative or no serologyi for Cpn, suggesting that they are engaging in a completely empirical (based on symptoms or theoretical connection between disease and Cpn) protocol.

Antibioticsi
I take AT LEAST TWO of: doxycycline/azithromycin/roxithromycin/rifamcini/minocycline/INHi-: 73% (19 votes)
Single antibiotic only: 20% (5 votes)
I take only INH: 8% (2 votes)
Total votes: 26
This poll speaks for itself. 73% are already on the dual antibiotics, a small number appear to be early in treatment, confirmed by findings below that 40% have not yet done a pulse of bacteriacidal,  and have only added one agent. As INH is used as a single agent with the flagyl pulses in some versions of the Cpn protocol and, together with NACi for the EBi phase I have reported it separately.

Bacteriacidal Agent Used-
I take metronidazolei (Flagyl) for bacteriacidal pulses
81% (13 votes)
I take tinidazole (Tinactini) for bacteriacidal pulses
19% (3 votes)
Total votes: 16

Pulses of bacteriacidal
I've done NO pulses yet of metronidazole/tinidazole
40% (10 votes)
I've done some partial pulses of metronidazole/tinidazole
4% (1 vote)
I have had LESS than 5 full pulses (at least 5 days each) of metronidazole/tinidazole
24% (6 votes)
I have had MORE than 5 full pulses (at least 5 days each) of metronidazole/tinidazole
32% (8 votes)
Total votes: 25
Over half in this small pole have done at least a full pulse of bacteriacidal agent, with only 8 people reporting 5 full pulses or more. This shows that we are still, as a group, in earlier phases of treatment. As the results below suggest, more significant improvement starts to accrue beyond 5 pulses of the bacteriacidal.

Response to treatment-

1. On 1 0r 2 antibiotics ONLY My primary condition is the SAME or WORSE
13% (3 votes)
2. On 1 0r 2 antibiotics ONLY My primary condition is SOMEWHAT improved
13% (3 votes)
3. On 1 0r 2 antibiotics ONLY My primary condition is SIGNIFICANTLY improved
13% (3 votes)
4. Less than 5 full pulses: My primary condition is the SAME or WORSE
13% (3 votes)
5. Less than 5 full pulses: My primary condition SOMEWHAT improved
9% (2 votes)
6. Less than 5 full pulses: My primary condition SIGNIFICANTLY improved
4% (1 vote)
7. MORE than 5 full pulses: My primary condition is the SAME or WORSE
0% (0 votes)
8. MORE than 5 full pulses: My primary condition SOMEWHAT improved
13% (3 votes)
9. MORE than 5 full pulses: My primary condition SIGNIFICANTLY improved
22% (5 votes)
Total votes: 23

These results are more obvious when grouped.
If we collect together everyone in early phase of treatment (#1-6) and we see that 26% are the SAME or WORSE
28% are SOMEWHAT IMPROVED
17% are SIGNIFICANTLY IMPROVED
Actually, to have 35% already reporting any improvement in their condition this early in the protocol is striking to me. I expected less noticeable improvement at this stage, especially given the numbers being treated for otherwise "intractable" diagnoses such as MS and CFS/FM.

But it is when users of the protocol get to 5 pulses (#7-9) or more, in this small sample, that the number in SIGNIFICANTLY IMPROVED seems to begin to creep upwards. Perhaps when we get a better sample of longer term users we will be able to sort out the "magic number" of pulses where more significant improvements take place. From reports in blogs and forums on this site, somewhere around 7-9 pulses seems to be a period where people are feeling much better and more significant changes in their primary diagnosis are occurring.

 According to http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=145278

"...The diagnosis of acute Chlamydia pneumoniae infection is usually based on the demonstration of at least a fourfold increase in immunoglobulin G (IgGi) antibody levels in serum samples between the acute phase and the convalescent phase or the presence of IgM antibodies in any serum sample..."

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 serologyi. 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!

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.

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.