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.
Treatment protocols for Chlamydia Pneumoniae, usually using combination antibiotics.
For those currently on or completed a CAP who have been diagnosed with Chronic Fatigue Disorder or Myalgic Encephalitis:Take the survey #6 on this page: http://www.cpnhelp.org/UCCASSv1.8.1/index.phpIt's open, and shouldn't require a password. This will only be around for a week, so get to it you tired and slow friends! Once we accumulate the results, you can use the filtering system on the results page to look at subsets of the data, eg filter for only those on CAP for 1 year or more, etc.Current results link
We have been preparing this for an eventual overhaul of the Handbook, but there have been a number of requests, especially by new folks, to help clear up confusion.
(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.)
To all of you who took the survey in October, my thanks... and apologies. In looking at the data analysis it appears that some questions were misunderstood, leading to possible skewed data... as in "all skewed up!" With a rather small N=53, that leaves little margin for error. Rather than try and smooth out the data I have decided that better science requires a complete redux. Again, my apologies, but the work you all did on the last one helped us refine and expand to this present offering. It still ain't perfect, but getting better!So, I'm going to rely on your fundamental good natures (at least I believe most of you have one when not undergoing a pulse!) and ask you all to do the CAP Treatment Survey over again.
Rica-- known as katman in her www.cpnhelp.org membership, has been an intrepid user of the CAP for Chlamydia pneumoniae in treating multiple sclerosis, well before this website even existed. She finally put together her most impressive story of recovery and we are proud to present it here. You'll find this and more about her journey in her blogs on this site.Jim K, editor In the 28th month of relentless, daily treatment, I feel that I have earned the right to stand at the vantage point of a second or third tier trailblazer. I stand as Pancho to Don Quixote or Tonto to the Lone Ranger. There are a couple of operatic characters nibbling at my sub-conscious but you get the point. Now, I have a very real problem with sharing MY body with all the (bacterial) freeloaders who are doing just that. I am indignant - I have worked very hard for my place in life and the workplace and when I found that these nasty little devious creatures were stealing my life, I had to fight back. After spending much too much time in their immediate presence and on their level, I am leaving them behind.
Remedyfind published my story again, this time in their CFS/CFIDS newsletter. Isn't having multiple-diagnoses efficient! Same article, but if you missed it you can find it at http://remedyfind.com/newsletters/Dec_06_CFS.htmlWe will no doubt be seeing some new guests and members from this, so you'all make 'em welcome, ya hear?
Cpnhelp.org widmet sich dem besseren Verständnis und der Behandlung von Chlamydia pneumoniae, eines Bakteriums, welches eine Rolle bei vielen menschlichen Erkrankungen spielt. Cpnhelp.org ist nicht kommerziell, die Seite wird von Freiwilligen betrieben und gewartet. Sie wird weder finanziell noch anderweitig durch andere Interessengruppen gefördert. www.cpnhelp.org wurde durch mündige Patienten ins Leben gerufen, die selbst eine kombinierte Antibiotikabehandlung (CAP) gegen Erkrankungen anwenden, bei denen C. pneumoniae mitwirkt, u.a.: Multiple Sklerose MS, Chronisches Erschöpfungssyndrom / Müdigkeitssyndrom CFS, Erkrankungen des Herzens, Interstitielle Zystitis, Prostatitis, Morbus Crohn, entzündliche Darmerkrankungen, Morbus Alzheimer, Asthma, Arthritis, Fibromyalgie, chronische refraktäre Sinusitis, Makuladegeneration, Bluthochdruck (Hypertonie) und andere.
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.
When I first started www.cpnhelp.org one of my dreams was to be able to gather some real data about users experiences and results on cpn protocols. I know from my training as a psychologist that having such a ready data pool is a priceless opportunity. It would allow us to go beyond mere anecdote to some real, statistically relevant results. I was joined in this by Marie Rhodes whose training and intelligent understanding of medical research gave her an interest in gathering some "hard" data, i.e. medically sanctioned measures such as EDSS scores, blood results and the like. But when I started the site 33 weeks ago and put up the first survey, we had only 4 people who had met the three month criteria and could fill out the survey. It took us 8 months to make for reasonable numbers that I felt were worth reporting on. The results of that survey can be found at Survey #1 Results. Since that report, I've seen others referring to it, like me grateful to have some kind of data they can point to. We aren't just going on our personal impressions any more. Having been worried about the lack of data, now I'm getting worried about how data is being used and misused. In case you haven't gathered by now, I'm a worrier by nature. This could be a genetic defect on my part. You've heard the joke about the Jewish mother who gives her son two ties for his birthday? The next morning he comes down proudly wearing one of them, and she says "What's the matter, you didn't like the other one?" My worries- that these very preliminary results will be referred to as firm findings. The data group is so small (23) that anything in this survey is merely suggestive. And barely that. This is even more true with any results derived from breaking down findings into subgroups, like the MS/CFS-FM groups. In that case we have even tinier groups, and less validity to draw on. Such fndings are even less generalizable because each group is now so small that any large differences by any one member within the group will skew the results of that group. I almost regret having broken the results down this way, especially with those damned charts of which I was so proud, because the charts make everything look so official. Slick presentation impresses us beyond the actual validity of the data itself. However, our numbers are growing every day. I put up a poll up recently to get a clearer idea of how many people are actually doing the protocol: 35, plus 3 people additional actually done with the thing! Thirty-eight is not bad. When we hit 50+, we might even have some data worth doing statistical analysis on. Getting closer to that every day. The results of this first survey have inspired Marie and I to take the next step, and build a survey which is much more detailed and will include some hard measures of functioning in it as well. It will take time to develop, but it's coming. In the mean time, I want to ask everyone to please be cautious about how you refer to any findings of the current survey. If you refer to these findings, please, please use qualifiers like "It looks like..." and "preliminary survey results have suggested..." and the like. It's good to be enthusiastic about the CAP's and your own personal experience, but be tentative about how firmly you make claims based on this data. Make sure newbies know that, while the survey found one thing, their own results may differ, and that there is a big range of response within the survey reports. Thanks to everyone who contributed to Survey #1. I'll be relying on you all to provide even more data next time!