What follows is an interview with a physician who has significant expertise in treating Cpn who has closely followed the Vanderbilt research over the years. He has garnered a lot of clinical experience, and his insights provide a lot of information both for patients and physicians who are looking to treat for Cpn. He prefers to remain anonymous. We’ll call him Dr. A for this interview. Testing for Cpn JimK- So what about serological testing for Cpn? Dr. A-Testing for Cpn is only useful if you get a positive result. Because Cpn is an intracellular pathogen, PCR testing may be negative unless infected cells containing the DNA of the organism are directly tested. That is a problem for any PCR or antigen forms of testing. Serological testing has two problems. The first is that by middle age, most people have been exposed to Cpn and will have IgG titers against this organism. If you are exposed and have a positive titer, then you most likely have a persistent infection somewhere, but this infection may not be causing symptoms. Thus, a positive serological test cannot distinguish asymptomatic persons from symptomatic persons. The second problem is that even persons with culture-proven Cpn in their coronary arteries only had a 35% positive rate by serological testing in a study done in Germany. The most sensitive test appears to be reverse transcriptase PCR testing for messenger RNA produced by infected cells. This testing, for example, showed 18.5% of blood donors to have messenger RNA from Cpn in their peripheral blood mononuclear cells. JIMK- So there’s no easy way to test for the intracellular phase of Cpn? Dr. A- It’s very difficult to test for the intracellular phase because the organism isn’t readily available to be tested unless you have infected cells to be tested. Testing for messenger RNA from infected cells appears to be the most sensitive method. However, this method is not commercially available. JIMK- So PCR is just the most sensitive test for detecting DNA or RNA floating around in the serum or tissues. Dr. A- If you test for antibodies you are testing for the response of the patient. If you test with PCR you are testing for DNA or RNA from the actual organism. JIMK- You have said that they are useful if they are positive, but not particularly useful if they are negative. Dr. A- Right JIMK- That’s when you might decide to do an empirical course of treatment or something? Dr. A- Exactly. Empirical Diagnosis JIMK- When you make a medical judgment on that, is it based on the disease? Are there also sets of symptoms you might be looking at? In David Wheldon’s web site, he refers to history of respiratory illness. Are there other useful indicators? Dr. A- The problem is that there are no symptoms that will hone in specifically on chronic Cpn infection. So if you have a suspicion, based on symptoms or the disease process, you begin with serology. And if you have positive serology then you may feel you have something to treat. If you don’t have positive serology and you are still convinced that Cpn is causing infection, then my approach would be to try a combination antibiotic protocol empirically, and if the patient has the side effects seen with the so-called “die-off” effect, such as those David Wheldon has described in his WebSite (Ed: these reactions typical of endotoxaemia include fever, chills, sweating, and muscle pains, coryza, widespread arthralgia and myalgia, and temporary worsening of neurological symptoms) then they may well have a Cpn infection. Once you treat for Cpn infection, all these side effects eventually go away! JIMK- What about Borrellia that creates similar side affects when treated with metronidazole? Any way to distinguish based on symptoms? I suggested to one person that porphyria might be a distinguishing factor, any others?) Dr. A- Metronidazole shouldn’t cause these effects, as it has no activity against Borrellia. It is probably killing Cpn. (Ed. Actually, this is not accurate. Dr. A does not treat Borrellia and was at this time unfamiliar with the way Flagyl is active against the cystic form of Borrellia- see Brorson & Brorson 2004, 1999. In I have been told that some Lyme doctors are using Wheldon's protocol as a primary Lyme Disease treatment. It is true that co-infection of Lyme and Cpn may be an unsuspected complication). Length of Treatment JIMK- I’ll tell you, it seems it can take quite a while… Dr. A- It can take years, much as the initial treatment for tuberculosis did. It’s just like treating tuberculosis in that it takes many months to years of combination therapy. JIMK- It Seems like people respond faster or slower. Dr. A- People respond at different rates, which probably has to do with how much Cpn they have, what tissues are infected, and how good their immune system is. JIMK- Supposedly, you’re recovering your immune system function over time from disinfecting the monocytes and macrophages. It seems, just from being on it myself for 10-11 months that different tissues get reached at different times. Also, that different agents reach different tissues. When I added amoxicillin to the doxy/zith/tinadazole I got a big flare up in body areas I had not had pain in for a while. It surprised me how much additional effect I had, since I’d been on antibiotics so long. That’s one of the questions I had. The different protocols use different combinations of antibiotics. Do you find different effectiveness in different antibiotics, or is it more a practical matter of what’s available? Dr. A- I think there are differences in tissue penetration, as well as a lot of other factors that aren’t yet clear. Choice of antibiotics JIMK Do you just tend to have a preference starting with certain antibiotic with a patient? Dr. A- I’m pretty pragmatic and generally use the least expensive and safest antibiotics. I start them on: doxycyccline (Dr. A will attend to patient reaction and have them work up to 100mg twice a day over longer or shorter period, depending on tolerance with any of these medicines), and then I add azithromycin 250 mg working up to once per day Monday/Wednesday/Friday, I work up to 500 mg twice a day for metronidazole. I’ll finally add 300 mg twice a day of Rifamcin to that. But I may start out working up to 500 mg twice a day of amoxicillin rather than doxycycline. JIMK you start out with that because it’s the easiest on the patient? Dr. A- It’s cheap, safe, and tolerated the best. Then after a month or two add the azithromycin Monday/Wednesday/Friday for a month, then the doxycycline, see how they do on all three. I’ve generally added the metronidazole into this and see how they do. I wouldn’t mind pulsing it as David Wheldon does in his protocol (Ed. This is a reference to the Wheldon protocol’s method of pulsing the metronidazole for 5 days every 3 weeks). By pulsing, you can give them time to recover from the side effects. JIMK- But it sounds like you used to give the metronidazole as a constant, then? Dr. A- Yes, that’s generally how I proceed. JIMK- That’s one drug, the metronidazole, that I had the hardest time tolerating. Dr. A- You think that one’s tough, wait until you get to the Rifamcin! JIMK- That’s one my doctor isn’t real enthused about giving me (the Rifamcin). Not sure exactly why. Dr. A- Well, most physicians aren’t familiar with it unless they’ve treated TB. JIMK- Do you think the Rifamcin is a necessary one for this protocol? Dr. A- Let me tell you what Rifamcin specifically does. When chlamydial EB’s germinate and transform into the RB’s, which is the replicating form, the first enzyme out of the EB’s is DNA-dependent-RNA-polymerase that Rifamcin specifically blocks. EB’s are like spore-like infectious form of Cpn. The cryptic form is also different to treat; it is metabolizing but is not replicating (Ed. The cryptic form is what the metronidazole is directed at, since it is metabolizing but in an anaerobic mode. Our expert is noting here that the EB’s are not metabolizing nor replicating, therefore are not affected by antibiotics that interfere either with bacterial metabolism or with bacterial replication. They are effected only by disulphide reducing agents, like amoxicillin, which breaks the disulphide latice bonds of the EB cell membrane). If you have a large EB load you’re going to keep getting cells reinfected. If you stop them before they start, that’s much better than letting them get started and then trying to kill them. JIMK- So doxy/zith is inhibiting the replicating form? Dr. A- Yes. Remember, you are trying to formulate a combination therapy that attacks all of the potential forms of Cpn. And so, N-formyl-penicillamine, which amoxicillin is metabolized to in the body, destroys the EB. It is these spore-like, non-replicating, EB’s, which invade your body’s cells and once inside transform into RB’s capable of replicating. In this transformation the first enzyme employed is DNA-dependent-RNA-polymerase, which allow this transformation. If they are in the RB replicating form, then azithromycin and doxycycline will interfere with that. If they are in cryptic form then metronidazole goes after that. If they are EB’s the amoxicillin takes care of that. If they are transforming from EB’s to RB’s, where they are particularly vulnerable, Rifamcin takes care of that. It takes a lot of different antibiotics because there are lots of different life forms. Otherwise it just goes from one life form to the next. JIMK- So, adding the Rifamcin is to be as complete as possible? Dr. A- It is hard to say if you can get by without the amoxicillan, or the Rifamcin. I suspect that you can in younger healthy persons. I tend to think that they are especially important for those who have been sick for a long time, and likely have a lot of EB’s looking for homes. I want to destroy these EB’s (amoxicillin) or if they are finding homes I want to short-circuit them (Rifamcin). The transformation from EB to RB is where they are particularly vulnerable. JIMK- That is really important information to get out there. Especially for those of us who have, indeed, been sick with this for a long time. I knew when I added the amoxicillin to the Wheldon protocol that I was killing something additional. And it was so clearly, highly inflammatory too; by the amount of pain and inflammation I had in reaction to it. Dr. A- You probably have a high EB load. Those were probably Elementary Bodies that you were destroying. By the way, you can use penicilamine directly, but that’s a very scary drug. JIMK- And that tends to dump a big load of the endotoxin when they get popped? Dr. A- That and a lot of other antigens. The response to the antigens is somewhat dependent on your body’s immune system. JIMK- So you’re getting a cytokine reaction. Dr. A- Yes. JIMK- Do you find tinidazole as effective as metronidazole? Dr. A- I don’t see why it wouldn’t be. It’s just been recently approved in the US, so I have no experience with it, or what they are charging for it! JIMK- I find I tolerate it much better than metronidazole. I got so sick on that, which I believe is more a drug side effect than a kill effect. Dr. A- Well, I wouldn’t necessarily see it that way. My experience is that people who don’t have any Cpn organisms can tolerate metronidazole without any side effects. You’re talking to someone who has had patients taking metronidazole as a post treatment preventative for a number of years without side effects. JIMK- So your bet then would be that I got sick from the metronidazole because it was killing cryptic Cpn, not because of drug side effects (Ed. which would suggest that tinidazole is not as potent in this as metronidazole). Dr. A- There are two explanations as to why you are tolerating tinidazole better. One is that you just knocked down enough of your Cpn load with the earlier metronidazole pulses. And people have done that; they say they can’t tolerate the metronidazole and then after a time they can. The other is that you were getting better penetration with the metronidazole than with the tinidazole. JIMK- So it may be that the tinidazole is not quite as strong, so it may be a good way to gear up over time to the metronidazole. Dr. A- Yes, but if you were to try metronidazole for a couple weeks and you didn’t get any side effects, then you probably don’t have much Cpn. Brain Fog JIMK- You see brain fog a lot in Cpn patients; do you see this as CNS involvement or more as an effect of endotoxin? Dr. A- It is most likely a combination of endotoxins, porphyrins, and cytokines. It may largely be porphyrins for the simple reason that reactions from porphyrins last longer than those from cytokines and there’s no fever. And you know you are better when…? JIMK- So that’s the kind of “gold standard” test: that you can take metronidazole and not get hammered? Dr. A- And Rifamcin. Rifamcin has deep tissue penetration too. So if you can tolerate the metronidazole and then I challenge you with Rifamcin and you tolerate that as well, you have very few Cpn left. I periodically challenge patients with a short course containing metronidazole and Rifamcin to see if they continue to be cleared of Cpn. JIMK- The complete challenge. The more I understand, the more I appreciate how tough a bug this is, and long it takes to get it, how complex it is, and all the tissues you need to penetrate to get there. Dr. A- Not only the tissue penetration, but also both the organism and your cells have active efflux pumping mechanisms to pump out the antibiotic. You have to work against these natural mechanisms to keep adequate concentrations in the cells. Rifamcin tends to inhibit these efflux pumps. I also use another drug, Quercetin, a bioflavonoid that also acts as a cell efflux inhibiter. It works on a different efflux pump than Rifamcin. It’s, also active against Chlamydia on it’s own. JIMK- Plus Quercetin is also an anti-inflammatory and free radical quencher. Dr. A- But the antichlamydial effect may be more important than it’s anti-inflammatory effect. JIMK- How much Quercetin do you use a day—I tend to take three caps with the bromelain. Dr. A- I tend to use 2 caps a day containing 500 mg of Quercetin along with vitamin C. Differences in treating different diseases? JIMK- Do you see differences in treatment based on disease entity, or more on the person. Dr. A- That’s hard to say. My generalization is that: the longer the person’s been sick and the sicker the person has been, the more problematic the therapy is going to be. In addition, the older the person is, the more likely that they’ve had a Cpn load building for a long time without knowing it. Their ability to tolerate treatment can be low, both from the high Cpn load, and from an aging immune system. On the other hand, I know of a young patient who had a very strong family history of cardiac disease. For this reason, his doctor placed him on the regimen. He had very few reactions. He was in his early 30’s. JIMK- He had some reactions, which let you know that he had some Cpn building. Dr. A- Yes. JIMK- I know in my family there’s both cardiac disease and Alzheimer’s, and another sibling has fibromyalgia. So there may be a common link genetically that is more about the susceptibility to Cpn. Dr. A- AOE4 probably has a place in Cardiac disease, Alzheimer’s and MS. I’ve observed that the recent memory problems that come with brain fog for patients can really lift once the Chlamydia is gone, even in those 50 or more. Porphyria JIMK- On the porphyrin stuff- do you think the porphyrin testing is worthwhile, or do you just assume it and treat for it anyway when you are treating for Cpn? Dr. A- The trouble is that you really have to test for the fat soluble porphyrins to get the best data, and that involves a 24-hour stool test, and you have to freeze that sample and so on. You need a 24-hour urine to look for water-soluble porphyrins. There is a poor man’s way to check for porphyrins. It seems that if you have porphyrins, you will have an increased hemoglobin level, on the high end of normal on most CBC’s. JIMK- when I was first treated I was very low on iron, which I understand is heavily used by chlamydial metabolism. Would that make a problem for using hemoglobin’s as an indicator of porphyrins? Dr. A- Initially, low iron would mask the increased hemoglobin you would expect with porphyrins. Once your iron levels are normal, it would no longer mask the elevated hemoglobin. But in general, a high-normal hemoglobin and high-normal hematocrit are both good indicators of porphyrins. JIMK- I can’t tell you how unusual it is to speak to a physician who sees it his or her job to actually investigate and reason out what’s going on in a patient, rather than look to see which already-known-box to put them in. I spoke to David Wheldon about that and he said, “Yes, I know, if I’d listened to those doctors I would be a widower now.” Kind of put home the point.
Agents used to kill micro-organisms.
Zdenicka, as you will see, is a spirited, passionate and stubborn young woman. Her story is very heartening to read, and she holds nothing back in speaking of the trials of dealing with standardized medical treatment with a non-standard condition and protocol. Fortunately, her father Coufal was an early member here and started the Czech version of Cpnhelp, so she had an avenue to find her own help. I've left her very thorough description as she has written it, an amazing job for a non-native English speaker, so that I don't sully the pure charm in her rendition. (Jim K, Editor)
Nature. 2007 Apr 5;446(7136):668-71.
Antibiotic interactions that select against resistance.
Chait R, Craney A, Kishony R.
Department of Systems Biology, Harvard Medical School, 200 Longwood Avenue, Boston, Massachusetts 02115, USA.
(Editor: Karls rather rapid response to the CAP is not necessarily typical of MS patient response. Every patient's response is different. Karl was able to hit the Cpn infection hard and persistently and manage the die-off symptoms adequately in this process. Others must take it much more slowly. His story is inspiring for the persistance it took for him to get adequate treatment, and his thoughtful description of his experience.)
Hi all Cpner's-I've taken the plunge and put my story and pic on www.remedyfind.com : in for a penny, in for a pound! The profile will be used for the Remedyfind's November email newsletter for Fibromyalgia, and then also the December newsletter for Chronic Fatigue. Brett, the site owner, asked me for this quite a while back and has been following cpnhelp with interest, so it's timely now that i have some real improvement to show.I could use your help to make a good showing for the cause. If you don't know it, take a look. www.remedyfind.com is a site consisting of patient ratings for all sorts of treatments in various diseases, encompassing common meds to alternative treatments. It started with CFS and FMS, and now includes MS and many other conditions. I found it a useful reference point over the many years when I was desperate to find something helpful, and it's a great, high integrity and cleverly organized resource. Brett's done a great job, and is a CFS sufferer himself.
This former patient of Dr. Powell asked me to post this story for her. (Jim K) I first learned of Dr. Powell in the summer of 2003. Suffering with chronic neck and back pain most of my life, I tried physical therapy, relaxation techniques, weekly massage and exercise…but could never manage the pain.The numerous doctors I saw over the years could never find anything wrong so they just gave me pills and sent me on my way. By the time I found Dr. Powell, I felt like my body had become toxic with drugs. Everyday, in order to function, I took the following: ∑ For pain: 90mg of Methadone in addition to 8-12 tabs of Norco ∑ For brain function (and to keep me awake): Ritalin and Provigil∑ For depression: Wellbutrin (also helped keep me alert) and Effexor∑ For sinus/allergy issues: Pseudoephedrine and Allegra∑ For sleep: Pamelor among others…My pain level was 10/10 without narcotics and 2/10 with; energy 3/10; brain function 3/10 (serious fibro-fog); and my stress was 9/10. I was working full time and deteriorating fast!One of the first things Dr. Powell had me start was T3 (while carefully monitoring temperature and heart rate daily). Within 3 weeks I started getting my energy back and I felt like a new woman! My pain even started to subside. He warned me this would happen and my inclination would be to over-do it. But I ignored that. I felt so great I seemingly tried to catch up on years of reduced performance. Then I crashed.After cycling through that pattern 3-4 times (slow learner…) I finally gave up and listened to Dr. Powell. The missing piece was changing my behaviors, which had led to years of accumulated stress. I was a People-Pleaser, Performance Maniac, Care-Taker (of everyone but myself) and Perfectionist - and I had to change.This was undoubtedly the most difficult, but the MOST beneficial part of the protocol for me. Through the use of Voice Dialogue, personal therapy, journaling and a lot of emotion (what was THAT?)… I slowly started to change. I stepped out of denial regarding the behaviors that had so depleted me (people-pleasing, over-working, care-taking…) and surrounded myself with people who would support the changes I needed to make. I cannot underestimate the determination it took to accomplish this – but it was 1000% worth every challenging minute!About a year into my treatment, in his scientist/researcher role, Dr. Powell discovered the important relationship bacteria plays in FM, and encouraged me to begin an antibiotic treatment. I have to admit I was reluctant because I was feeling SO much better than before…and I’d heard the antibiotics could make me feel worse – before I felt better, due to the bacteria dying off. I debated the issue for 3-4 months and then decided I should just go for it and see if this could take me the rest of the way to healing. I really didn’t believe I could feel any better, but my improvement was exponential! I had been sick for so long I had no idea what being well really felt like. And, by carefully following Dr. Powell’s recommendations for minimizing the effects of the die-off process, I found the treatment wasn’t nearly as bad as I had feared.Other than a small amount of Wellbutrin and some seasonal allergy meds, which I am almost free of, I no longer take ANY of the drugs listed above! More importantly I have no pain. My brain works, my energy is full and I am excited about life. What is most wonderful is the joy I now experience in my relationships. There was a long period when I was afraid I would never be able to really enjoy life again. Now, my job is just that…a job. I don’t take it home with me or even try to win the kudos I used to long for. Instead, my satisfaction comes from spending time with my family and taking care of myself. I’ll never forget the birthday party my husband gave me when he made a toast “to having his wife back”. In my new life I enjoy playing with my dogs, kayaking with my husband, taking art classes at the local college and exercising regularly so I can go skydiving and surfing with my son on his 21st (and my 50th) birthday. That will be in early 2008 and I have no doubt I’ll be ready!I used to scoff at books that talked about reversing Fibromyalgia, but now I am living proof it can happen. I wholeheartedly trust Dr. Powell and his (often evolving) protocol not only because of the success I’ve experienced, but because I know he is one of a rare few doctors who still practice medicine for the sole purpose of seeing lives restored. I hope you find the same.Pamela McClanahan
This study does a nice job of demonstrating that standard antibiotic treatment with accepted antichlamydials does not get rid of persistent Chlamydia pneumoniae in cells. Note the date. It's been around for a while, and yet "modern" researchers in cardiovascular disease "persist" in treating with 14-30 days of zith and pronouncing with medical authority that antibiotics have not effect on Cpn induced cardiovascular events. Duh! There's still infection. Note too, it's from our old friend Hammerschlag who also has argued strenously against Cpn in MS and Alzheimer's. Win one, loose one.Antimicrob Agents Chemother. 2002 Feb;46(2):409-12.Related Articles, Links Effect of prolonged treatment with azithromycin, clarithromycin, or levofloxacin on Chlamydia pneumoniae in a continuous-infection Model.Kutlin A, Roblin PM, Hammerschlag MR.Department of Pediatrics, State University of New York Health Science Center at Brooklyn, Brooklyn, New York 11203-2098, USA.Persistent infections with Chlamydia pneumoniae have been implicated in the development of chronic diseases, such as atherosclerosis and asthma. Although azithromycin, clarithromycin, and levofloxacin are frequently used for the treatment of respiratory C. pneumoniae infections, little is known about the dose and duration of therapy needed to treat a putative chronic C. pneumoniae infection. In this study, we investigated the effect of prolonged treatment with azithromycin, clarithromycin, or levofloxacin on the viability of C. pneumoniae and cytokine production in an in vitro model of continuous infection. We found that a 30-day treatment with azithromycin, clarithromycin, and levofloxacin at concentrations comparable to those achieved in the pulmonary epithelial lining fluid reduced but did not eliminate C. pneumoniae in continuously infected HEp-2 cells. All three antibiotics decreased levels of interleukin-6 (IL-6) and IL-8 in HEp-2 cells, but this effect appeared to be secondary to the antichlamydial activity, as the cytokine levels correlated with the concentrations of microorganisms. The levels of IL-1beta, IL-4, IL-10, tumor necrosis factor alpha, and gamma interferon were too low to assess the effect of antibiotics. These data suggest that the dosage and duration of antibiotic therapy currently being used may not be sufficient to eradicate a putative chronic C. pneumoniae infection.
In some recent correspondance with Dr. Stratton at Vanderbilt University, he kindly answered some of the questions which had formed as I've understood more about the combination antibiotic protocol and about Cpn. From the patient's perspective I wanted to correlate some observations about treatment reactions with his deeper understanding about the biology of the Cpn. I'll list the questions I put to him, and then his generous response below.1. In an earlier correspondance you had mentioned pulsing the INH band metronidazole together. * Why do that rather than take it continuously? * My understanding is that INH is one of the anti-replicatives, and the point is to use these continuously to drive the bug into the cryptic phase where it will be obliterated by the flagyl/tini. Does INH act differently than the other antireplicatives? * I also understood that we use a dual abx to prevent developing resistance. Why can we use INH alone without developing resistance?
Summary of our Cpn 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 CFS/FM, MS and other "autoimmune" diseases, 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 infections 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/FMS. 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) Asthma = 3% (1 vote) Cardiac disease = 3% (1 vote) OTHER = 10% (3 votes) Total votes: 29 Serology 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 serology for Cpn, suggesting that they are engaging in a completely empirical (based on symptoms or theoretical connection between disease and Cpn) protocol. Antibiotics I take AT LEAST TWO of: doxycycline/azithromycin/roxithromycin/rifamcin/minocycline/INH-: 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 NAC for the EB phase I have reported it separately. Bacteriacidal Agent Used- I take metronidazole (Flagyl) for bacteriacidal pulses 81% (13 votes) I take tinidazole (Tinactin) 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.
Here is a paper describing development of resistence in CPn in vitro studies using subinhibitory concentrations of the drug. CPn developed resistence after 12 cycles. It is not recommended to use single agents for CPn infection in chronic illness. The combination of macrolide and tetracycline effectively makes resistence impossible.