Initial and following blood work is not just a matter of Cpni [2] related indicators, but also relevant to your particular history and case, as determined by your doctor. Suggestions drawn from experts treating Cpn in a variety of conditions include the following.
Initial blood work can be obtained for the following tests:
- CBC & Differential
- Liver function tests
- Uric acid
- Serum iron studies (typically depleted by Cpn: low iron levels are more diagnostic, and are not necessariy indicators to supplement, which may actually increase Cpn infection-- see references below).
- Red blood cell ALA dehydratase
- Red blood cell PBG deaminase
- Vitamin B-12 level
- Homocysteinei [3] levels
- Serum methymalonate level.
- Vitamin Di [4] levels
- Thyroid panels (standard plus free T4, free T3, revers T3) [Endocrine disturbances common in Cpn and associated diseasesi [5]]
- Creatinine
- AST
- ALT
- 24-hour urine and 24-hour stool specimens for porphyrins
Dr Stratton has noted relative to porphyrins:
Homocystine levels are elevated with B12 and folatei [6] deficiency, but can be reduced by folate alone. On the other hand, serum methyl malonate levels are elevated in B12 deficiency and are not changed by folate. Therefore, serum methyl malonate levels are the best indicator of B12 deficiency.
Another indicator, according to Dr. Stratton, is high hemoglobin and high hematocrit.
Dr. Powell notes:
I also tst DHEAi [7]-S and free testosteron in perimenopausal females. Both increase nitric oxide levels, which kills Cpn. No point heading into treatment with low androgens.
Regular Followup Tests
- CBC & Differential
- Liver function tests (especially important when using medications such as INHi [8] or Rifamcini [9] which can have liver toxicity, and because die-off of liver cells infected with Cpn can affect liver function)
- Vitamin D levels (if supplementing deficiency)
- Thyroid panels (standard plus free T4, free T3, reverse T3) (if supplementing deficiency)
- AST
- ALT
- Others as determined by doctor relevant to your particular condition.
Some References-
Iron and the Role of Chlamydia pneumoniae in Heart Diseasei [10], http://www.cdc.gov/ncidod/eid/vol5no5/letters.htm [11]
Weinberg ED. Patho-ecologic implications of microbial acquisition of host iron. Reviews in Medical Microbiology 1998;9:171-8.
Freidank HM, Billing H. Influence of iron restriction on the growth of Chlamydia pneumoniae TWAR and Chlamydia trachomatis. Clinical Microbiology and Infection 1997;3 Suppl 2:193.
Chapuy MC, Preziosi P, Maamer M, Arnaud S, Galan P, Hercberg S, Meunier PJ. Prevalence of vitamin D insufficiency in an adult normal population. Osteoporos Int. 1997;7(5):439-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dop... [12]
Lips P, Chapuy MC, Dawson-Hughes B, Pols HA, Holick MF. An international comparison of serum 25-hydroxyvitamin D measurements.Osteoporos Int. 1999;9(5):394-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dop... [13]
Holick MF. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis. Am J Clin Nutr. 2004 Mar; 79(3):362-71.
Heaney RP. Functional indices of vitamin D status and ramifications of vitamin D deficiency. Am J Clin Nutr. 2004 Dec;80(6 Suppl):1706S-9S.
May E, Asadullah K, Zugel U. Immunoregulation through 1,25-dihydroxyvitamin D3 and its analogs. Curr Drug Targets Inflamm Allergy. 2004 Dec;3(4):377-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dop... [14]
Emerging Stratton Protocol 4/2008: a new approach to an old set of problems
Reported by Jim K
A number of dilemmas appear in treating Cpni [2]. As we all know here at Cpnhelp, treating with protein-synthase inhibitors alone induces chlamydial persistence---conversion to the cryptic/persistent form of "aberrant" non-replicating RB's. Infectious EBi [15]'s still remain in extracellular fluids and tissues to reinfect once antibiotics are withdrawn. The CAPi [1] which addresses all three phases has been the answer to this multi-phase nature of Cpn, but it has problems of its own. The biggest problem is the tendency to induce strong reactions to treatment which have been attributed to bacterial release of LPSi [16] endotoxini [17] and inflammatory HSP60 endotoxin, and to secondary porphyria. This makes for the additional problem, which is the requirement of a gradual, slow, and long term process of treatment when addressing Cpn infections. There are more potent anti-chlamydials around, but using them kills the Cpn too fast for the body to tolerate resulting in mass apoptosisi [18] of infected cells and subsequent organ failure or neutropenia.
Existing CAP protocols have been focused on first halting replication, kill a lot of the RBs and force the rest into non-metabolizing and non-replicating cryptic/persistent form, with the notion that this will stop the progression of the disease. The cryptic Cpn can then be dealt with at one's leisure, gradually over time.
But emerging research has been suggesting that Cryptic Cpn is not benign even if it is not replicating. Cryptic Cpn is essentially a stressed form of Cpn, and stress causes it to generate of Heat Shock Protein (HSP60). HSP60 is many times more inflammatory than LPS endotoxin. LPS endotoxin is the one that causes the fever and chills and is released mostly when RB's are killed and lyse, or when EB's are killed. The inflammation of plaques in cardiovascular disease has been associated specifically with Cpn HSP60 and with the persistent (cryptic) form of Cpn. Inflammationi [19] by HSP60 when forcing Cpn into cryptic form may in fact, in Dr. Stratton's current view, be the major cause of so-called die-off reactions. "So-called" because HSP60 is induced not by the bacteria dying off, as the release of LPS is, but rather by the Cpn surviving in a stressed, cryptic form.
Additionally, ongoing disease and tissue damage may be occurring as much from the cryptic form, this is apparently so in heart and lung disease, as it is occurring from replication and sub-optimal cell functioning by infected cells. Autoimmune diseases, for example, also exhibit antibodies to HSP.
Some additional observations have collected together to add to this shift in viewpoint. A medical colleague who has treated Cpn through IV treatments using all the agents for all.
So this new approach is based on inducing existing persistent/cryptic Cpn to convert back to RB form and limit the conversion into persistent/cryptic form by the threat of antibiotic.
Paul Griffith, a non-medical friend researching this whole area, found that supplementing pyruvate might do the trick. Pyruvate may also have other beneficial effects. Basically, this approach uses 6 grams of calcium pyruvate one hour before taking the antibiotics, and an additional 6 grams if needed later for reactions when the antibiotics exert their effect. In theory the first dose of pyruvate encourages the cryptic/persistent form of Cpn to convert back into RB (replicating) form by supplying it with a ready source for generating cellular energy.
In RB form it is:
a) Susceptible to the regular antibiotics and,
b) Can be killed when it is not in "stress" so it is not stimulated into producing and releasing so much the highly inflammatory HSP60.
In essence, you are feeding it until it is comfy and sprawling in its chair at the dining table, and then whacking it upside the head before it can spew its hot sauce at you. I know, a terrible metaphor, but it's the best I could do. You get the point?
In theory this approach should limit turning Cpn into cryptic form by the treatment and make it more directly susceptible to the protein synthase inhibitors (like doxycycline and azithromycin).
In theory, it should also winnow down the cryptic load one has acquired, along with its inflammatory affects, without needing to kill it directly with flagyl. Flagyl would be used to "clean up" persistent/cryptic forms not gotten to by this approach.
Also in theory, the second dose of pyruvate for reactions to the antibiotics should supply the fundamental cellular energy needed to help lower the generation of porphyrins.
Dr. Stratton outlines below the experimental protocol that they have found, in a small subset of cases, to offer less difficult and faster treatment of Cpn. Please remember that this is experimental, and has not been clinically used with a wide array of Cpn related diseases yet, so should not be engaged in without a knowledgeable clinician to monitor treatment.
From Dr. Charles Strattoni [20], 4/24/08
My thoughts on the current Stratton Protocol is that this is a work in
progress, but given what we know now, it would be the following:
NACi [21] 600 mg one a day to test "Chlamydial Load."
If no reaction, go to 1,200 mg twice a day.
If a severe reaction ("Flu-Like" reaction), use low dose prednisone (5 mg per day) for the first few weeks of therapy.
The next step would be two weeks of a macrolide (clarithromycin preferred because of higher levels obtained, roxithromycin, or azithromycin) with 6 grams of pyruvate given 1 hour prior to the antibiotic dose. In addition, 400 mg of Ibuprofen should be taken twice a day along with 1,200 mg of NAC twice a day. For those with severe reaction, low dose prednisone 5 mg per day. For those who get a severe reaction with the pyruvate/macrolide, 3-4 days of low dose prednisone could be tried. Also, using additional pyruvate (3-6 grams) for reaction should be tried.
For those that have a major side effect on the pyruvate/macrolide alone, I'd continue to treat with the macrolide alone until the side effects are manageable. For those that don't, I'd add doxycycline 100 mg twice a day with 6 grams of pyruvate 1 hour before. Continue the NAC and Ibuprofen.
After two weeks of doxycycline if all went well, I'd add metronidazolei [22] 500mg twice a day with 6 grams of pyruvate before that. If a reaction is seen.
To the metronidazole, I'd then pulse it until the reactions were manageable.
If minimal reactions, I'd continue therapy for at least 1 year and then recheck titers. If titers were low, I'd add rifampin or rifabutin (preferably), using the rifamycin with pyruvate taken 1 hour before the rifamycin. If no reactions to this, I'd consider the therapy to be complete.
I would continue to monitor titers every several years. If the titers increased, I'd retreat with 6 months of clarithromycin or roxithromycin plus rifabutin plus pyruvate and ibuprofen. I'd continue the NAC for life.
For people on the existing CAP who are being switched:
For those on the current Doxycycline, Azithromycin, Metronidazole, and NAC protocol, my thoughts are that they should first switch from Azithromycin 250 MWF to Clarithromycin 500 mg twice a day (or Roxithromycin) and then add pyruvate
Dr. Stratton adds that Levaquin may be used instead of Clarithromycin for a short period (one month) as it has excellent activity for a short period of time. Clarithromycin = higher levels. Levoquin Both when combined with pyruvate theoretically will provide better killing.
Severe neutropenia among healthy volunteers given rifabutin in clinical trials
Glen Apseloff, MD, Clinical Pharmacology & Therapeutics, December 2003
This is probably why those "big" studies of 6 months of azithromycin showed no lowering of risk of heart disease---it's not caused by the replicating form of Cpn and the idiots never asked a microbiologist about what might kill cryptic Cpn!
Heat shock protein 60 from Chlamydia pneumoniae elicits an unusual set of inflammatory responses via Toll-like receptor 2 and 4 in vivo.
Da Costa CU, Wantia N, Kirschning CJ, Busch DH, Rodriguez N, Wagner H, Miethke T.
Institute of Medical Microbiology, Immunology and Hygiene, Technical University of Munich, Munich, Germany. Eur J Immunol. 2004 Oct;34(10):2874
Effects of Repeated Chlamydia pneumoniae Inoculations on Aortic Lipid Accumulation and Inflammatory Response in C57BL/6J Mice†
Liisa Tormakangas, et al
INFECTION AND IMMUNITY, Oct. 2005, p. 6458-6466 Vol. 73, No. 10
Worsened MRI Findings During the Early Period of Treatment with Penicillin in a Patient with General Paresis.
Zhang SQ, Wan B, Ma XL, Zheng HM.
J Neuroimaging. 2007 Nov 6
Role of Heat Shock Proteins in Protection from and Pathogenesis of Infectious Diseasesi [5]
Ulrich Zugel and Stefan H.E. Kaufmann
Microbiology Reviews, Jan. 1999, p. 19-39 Vol. 12, No. 1
Ethyl pyruvate: a novel anti-inflammatory agent
M. P. Fink
2007 Blackwell Publishing Ltd Journal of Internal Medicine 261; 349-362
Dr. Charles Stratton writes:
As far as the ideal Cpni [2] Antimicrobial Regimen is concerned, my thoughts (as of 2/06) are as follows:
First, as a general rule, the sicker a patient is, the slower they should go. This is why our protocol started out with only one antibiotic and one dose, and then gradually adding the next dose/antibiotic as the reactions to each dose/antibiotic become apparent. These reactions, as you know, can be delayed by days to weeks.
I still think that all patients should start with supplementsi [23]/vitamins before they start any antibioticsi [24]. Baseline lab studies, including liver function studies, should be done and these parameters followed every 3-4 months, more frequently when INHi [8] is added. Our initial protocol, as you know, recommended this.
I would add NACi [21] to the supplementsi [25]. We used amoxicillini [26] in our regimen as an anti-elementary bodyi [15] agent, but NAC seems to work equally well and may offer additional benefits in boosting the immunei [27] system and protecting the liver. As far as supplements/vitamins are concerned, I think David's supplement/vitamin suggestions are very complete and should be the bench mark.
Once antibiotics are ready to be started, I would start with a macrolide. We like azithromycin because it is easy to give and has become somewhat cheaper since it went off patent. I would still give just one 250 mg azithromycin tablet and then wait two weeks to see if there is any reaction to it. Then I would give two tablets, one on Monday and one on Wednesday. Once again I would wait two weeks.
I'd continue in this way, adding each dose until the patient was taking 250 mg of azithromycin MWF. If the patient has severe reactions (meaning they can't work - most people are trying to work and take care of a family while they are on this therapy), I'd slow down the process.
After the azithromycin, I'd add doxycycline - again doing this very slowly. Once the patient was taking both azithromycin and doxycycline, I'd start the metronidazolei [22] pulses - again, doing these slowly and working up to a once a month pulse.
Once the patient could do the monthly pulse of metronidazole, I'd add rifampin, 150 mg BID. Once this was tolerated, I would add INH 300 mg QD to the metronidazole pulse, doing so slowly (i.e. pulsing both the metronidazole and INH together, Ed.).
Once a patient could do this regimen without any reactions, I would continue it for at least a year and probably three for MS. It might take a year or two (or longer) to get to the point where there is no reaction to the metronidazole/INH pulse, depending on the chlamydia load, followed by 1-3 years of therapy. This might be a 5 year program, but should allow the patient to continue to work with minimal disruption. They, as you know, should also be gradually improving during this time. The sicker the patient is, the longer the therapy is going to be. There is no shortcut.
With MS patients, due to the possible CNSi [28] damage that might occur by going slowly, I would move more quickly unless there were major reactions. This means compressing what might have taken a year into several months. (Ed note: David Wheldoni [29] has written his concurrence with this, "I think Chuck's update is excellent: it's clear in matters of detail. Where MS is rapidly progressive, and I know from experience that it can progress frighteningly fast, I too would speed things up with the protein-synthesis inhibitors, paying the price of reaction for stopping progression.")
As you can see with Cpnhelp.org, the reactions patient have are varied - some are severe enough that they stop the antibiotics. That, of course, defeats the purpose of the therapy. It is very tricky and each patient needs to learn their own limitations. Cpn.help is very useful in providing support. When we started this, we were thinking of a hotline to answer questions that are now easily and better answered via the internet.
Finally, I don't think this is the only regimen that will work nor do I think it will work better or faster. It is just what I would do in 2006 if I were treating a patient.
Take care,
-Chuck Strattoni [20] MD
As I could not find this in the current Handbook, I thought I'd create it's own page so it is more easy to locate! This is from a treatment handout created by Dr. Stratton in 2005, but the information is still relevant:
II. THERAPEUTIC REGIMEN FOR VITAMIN B12 DEFICIENCY
Many patients with systemic/chronic chlamydial infection appear to have a subtle and unrecognized vitamin B12 deficiency at the cellular level. This functional B12 deficiency can be documented in an individual patient by obtaining both a vitamin B12 level (usually normal or low) and serum homocysteinei [3] and methylmalonate levels (one or both of these metabolites will be elevated). This vitamin B12 deficiency can corrected by high-dose vitamin B12 therapy as follows:
1. Vitamin B12 Therapy Prior to Chlamydial Therapy
Adults normally have approximately 3,000 mcg of vitamin B12 in body stores, mostly in the liver. Initial vitamin B12 therapy before chlamydial therapy includes replacement therapy for any vitamin B12 deficit in these body stores. Therefore, over the first several days of antiporphyrin therapy, 6,000 mcg of parental (intramuscular or subcutaneous) vitamin B12 is given. For each of the next 3 weeks, 6,000 mcg of parental vitamin B12 is given once per week.
2. Vitamin B12 Therapy During Chlamydial Therapy
Chlamydial antimicrobial therapy is associated with increased need for vitamin B12. Therefore, 6,000 mcg of parental vitamin B12 (3,000 mcg in each anterior thigh) is given once per week while the patient is receiving antimicrobial therapy for systemic/chronic chlamydial infection. This is in addition to the 5,000 mcg of sublingual vitamin B12 taken three times each day.
3. Vitamin B12 Therapy Post Chlamydial Therapy
Following the completion of antimicrobial therapy of systemic/chronic chlamydial infection, the vitamin B12 and serum homocysteine/methylmalonate levels should be rechecked. If the methylmalonate level remains elevated, it suggests a continued vitamin B12 deficiency. Oral therapy with 5,000 mcg of sublingual cobalamin three times per day should be continued. After several months, 6,000 mcg of parental vitamin B12 may be given as a therapeutic trial. If the patient’s energy is not increased by the parental dose, continued therapy with sublingual vitamin B12 is probably adequate. Periodic trials of parental vitamin B12 can be used to assess the sublingual therapy.
See the following note and web site for additional information on B12. Sublingual B12 can be obtained from <puritanspride.com>.
Below is an introduction from the article: "Vitamin B12: Surprising New Findings" by Terri Mitchell
The whole article can be found at: http://www.lef.org/magazine/mag2000/dec2000_report_b12_1.html [30]
For years, vitamin B12 languished as the vitamin that cures anemia. Hardly any research was done into what this vitamin could do for non-anemic people. It turns out that it may do a lot. New studies show that the right amount of B12 can protect against dementiai [31], boost immunei [27] function, maintain nerves, regenerate cells and more. B12 is in the news because it lowers homocysteine and protects against atherosclerosis. It's also vital for maintaining methylation reactions that repair DNA and prevent cancer. One of the crucial areas for B12 is the brain. It's not surprising that people with B12 deficiency develop mental disorders. The vitamin is crucial for the synthesis or utilization of important neuroi [32]-factors including monoamines, melatonini [33] and serotonin. In addition, B12 is absolutely critical for the function and maintenance of nerves themselves. B12 is needed for methylation reactions that maintain these cells, and enable them to function. B12 contributes to brain function by lowering homocysteine. Homocysteine is a toxic by-product of methionine metabolism that can damage neurons. Importantly, homocysteine interferes with the methylation reactions critical for brain function. Studies show that people with elevated homocysteine can't think.
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 Cpni [2]. 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 INHi [8] band metronidazolei [22] 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/tinii [34]. Does INH act differently than the other antireplicatives?
* I also understood that we use a dual abxi [24] to prevent developing resistance. Why can we use INH alone without developing resistance?
2. Although doxyi [35]/azith/minoi [36] and the other antireplicatives are not supposed to kill Cpn, only inhibit it's replication, clearly everyone with any kind of bacterial loadi [37] reports a die-off reaction as they start these agents. People commonly note some agents as causing more die-off than others, azith for example seems to create more die-off than doxy. This could, of course, be an inexact measure of immunomodulatory action or it's lack, but azith is definitely immunomodulatory. My experience and others on the site say that it generates more die-off. What do you think this die-off is from? Do the antireplicatives also kill Cpn?
3. About flagyl and energy increase: Although often this agent creates a more challenging die-off reaction, it can also result in a burst of energy and reduction in brain fog. The liberation of energy and brain fog after (sometimes during) pulses suggests to me that the so called "non-metabolizing" or "dormant" image of the cryptic phase is incorrect. If cryptic Cpn wasn't stealing host energy or gumming up the machinery in some way, it should not have such an energizing effect to kill it. After all, flagyl isn't killing the RB's which we know are actively using host ATP.
JimK
Here are some of my thoughts on your questions. First of all, remember that Cpn is able to shift to different phases in its life cycle. In order to eradicate the organism, you have to deal with all three phases and, I believe, you have to deal with them simultaneously. For example, INH alone does not eradicate Cpn from a cell culture, INH plus metronidazole does not eradicate Cpn from a cell culture, but INH plus metronidazole plus penicillamine does eradicate Cpn from a cell culture. (NACi [21] does the same as penicillamine.)
So, Stratton Rule Number One is that the best effect is going to be when all the antibiotics are present. It doesn’t mean that you have no effect if all are not present, just that the best effect is when all are present.
One combination that we tried years ago was INH, Bactrim, and Amoxicillini [26] (i.e., penicillamine). People got better while on the drugs, but relapsed when they were stopped, even after years of therapy. Therefore, Cpn was not eradicated.
My educated guess would be that INH is more potent, but physicians are not happy prescribing INH. By the way, the most potent combination (in the original studies described in the patent materials) was metronidazole, INH, and penicillamine (NAC does the same thing.). My thoughts would be to pulse INH along with the metronidazole, starting slowly (1 pill at a time) so as to reduce the side effects. As long as you are also taking NAC, the metronidazole/INH pulse should root out Cpn very effectively. Again, the average physician is probably unwilling to do this. Because INH is known to have hepatotoxicity and physicians feel uncomfortable using it and thus must obtain monthly liver function tests when using it. This suggests to me that a pulse would be better (less risk of liver toxicity unmonitored), and if the best effect is when the metronidazole is present, that is when the pulse should be done.
Now, on the resistance issue: INH is a prodrug and is converted to the active drug, a free-radical, by catalases/peroxidases – which may be supplied by the pathogen or perhaps by the cell, if the cell is a monocytei [38]/macrophage. Metronidazole is also a prodrug and is converted by electrons to the active drug, a free-radical. Free-radicals damage DNA/RNA and can destroy the pathogen and in some cases the host cell. Although it does happen, resistance to free-radicals is much less likely to occur.
Why the antireplicatives create die-off-
Moreover, Cpn can prevent apoptosis (natural cell deathi [18]), a cell mechanism to deal with intracellulari [39] pathogens. When Cpn is shut down by macrolides or tetracyclines and can’t make the proteins that prevent apoptosis, apoptosis can happen and the cell dies. The more cell death, the more side effects.
Finally, Cpn-infected cells are protected from additional Cpn entering the cell and causing more infection in the same cell. When infected cells are cleared, they can then be re-infected if elementary bodies are nearby. This is why a reducing agent such as NAC is so important as they eliminate the elementary bodies. Re-infection is why we like rifampin, which prevents the re-infection as it targets the DNA-dependant RNA polymerase – elementary bodies need this enzyme to transform to a reticulate or cryptic body.
Also, both the replicating phase and the cryptic phase may be stealing ATP – but the cryptic phase may also have anaerobic metabolism at work and thus be generating ATP as well. It’s all very complicated and much is theoretical. Hope this helps. Take care.
-Chuck Strattoni [20], M.D.
TABLE 11
Serological and PCRi [43] Responses to Combination Antibiotic Therapy
Months of
Combination
Pa- Titer Antibiotic
tient Diagnosisa IgMi [44] IgGi [44] Therapy PCR Status
PH FM 800 800 6 months + Asymptomatic
3200 1600 +
800 200 wk+
BL MSi [45] 2000 500 9 months + Dramatic
400 3200 9 months wk+ Improvement:
MM CFSi [46]/AND 3200 800 1 month.sup. + Improvement;
400 1600 + Relapse
(non-
compliant)
PM CFS 2000 25 6 months + Asymptomatic
400 800 wk+
AM IBD 800 0 6 months wk+ 90%
3200 400 + Improvement
FO MS 800 3200 10 months st+ Improvement
800 800 + in speeds and
400 600 wk+ bowl contin-
400 800 + ence
WM CF 25 25 Pre-illness wk+ Asymptomatic
1000 25 serum <-- st+
50 800 Antibioticsi [47] +
50 1600 start wk+
50 400 -
HM CF 2000 100 6 months + Asymptomatic
3200 3200 +
200 800 wk+
CN CFS 3200 800 8 months + 75%
800 800 wk+ Improvement
AN MS/CFS 400 400 wk+ Strength .uparw.
200 3200 st+ Fatigue .dwnarw.
JS CFS 2000 2000 5 months st+ Asymptomatic
(severe) 2000 2000 +
200 800 -
AG IBD 3200 400 9 months + Improvement
800 400 + in joint Sx
800 800 +
800 400 -
AT CF 3200 3200 9 months + Asymptomatic
1600 1600 +
1600 1600 +
800 800 +
400 400 +
LH RAi [48] 3200 1600 6 months wk+ Improvement
600 400 wk+
200 50 +
HS MS 2000 400 5 months + Improvement
3200 800 +
50 200 -
ST CFS/FM >1000 100 7 months wk+ Asymptomatic
1000 100 wk+
400 100 +
800 3200 +
100 100 +
RV CF 1000 100 10 months + Asymptomatic
400 1600 +
400 400 -
a CF = Chronic Fatigue < 6 months
CFS = Chronic Fatigue Syndromei [49]
FM = Fibromyalgiai [50]
IBD = Inflammatory Bowel Diseasei [51]
MS = Multiple Sclerosisi [45]
AND = Autonomic nervous dysfunction (neural-mediated hypotension)
RA = Rheumatoid Arthritis
IgM >> IgG .fwdarw. immunei [52] tolerance to the antigeni [44]
IgG >> IgM .fwdarw. successful immune control of the antigen
CAPi [1] for Chlamydia pneumonia since 11/04. 25yrs CFS & FMSi [53]i [50]- Currently: 300mg INHi [8]i [54], 200 Doxycyclinei [55], 500mg MWF Azithromycini [56], 1000mg Tinii [34]i [57] daily (Taking a break from continuous protocol)
Even more detailed case descriptions in the latter part of Patent: 6,884,784
Response to Antibiotic Therapy
Table 13(a) illustrates typical responses to combination antibiotic therapy in a variety of patients with diagnostic evidence of an active infection by C. pneumoniae. Unlike typical immunei [52] responses to infection with infectious agents, most of the included patients have not only detectable IgMi [44] titers against the chlamydial genus but in many cases very high IgM titers. With specific therapy over time the IgM titers generally fall, with a rise in IgGi [44] titer (as expected). Current methods of detecting antibodies against C. pneumoniae (Indirect immunofluoresence, MIF) are incapable of accurately identifying high IgM titers against C. pneumoniae. Moreover, current procedures are genus specific and not species specific as are peptide-based ELISAs.
With clearing of the pathogen, the IgG titers fall. Concomitant with combination antibiotic therapy, there is generally an improvement of patient symptoms associated with the specific diagnosis indicative of evidence of an active chlamydial infection.
Table 13(b) describes the course of therapy for a number of individuals treated with a combination of agents and their clinical outcomes.
Table 13(c) describes the detailed case histories of the patients undergoing combination therapy, as reported in Table 13(b).
Table 13(d) provides a listing of drugs and standard dosages for those used herein.
TABLE 13a
Serological and PCRi [43] Responses to Combination Antibiotic Therapy
Pa- Diag- Titer Time on
tient nosisa IgM IgG Therapy PCR Status
PH FM 800 800 6 months + Asymptomatic
3200 1600 +
800 200 wk+
BL MSi [45] 2000 500 9 months + Dramatic
400 3200 wk+ Improvement
MM CFSi [46]/ 3200 800 1 month + Improvement;
AND 400 1600 + Relapse
(non-compliant)
PM CFS 2000 25 6 months + Asymptomatic
400 800 wk+
AM IBD 800 0 6 months wk+ 90% Improvement
3200 400 +
FO MS 800 3200 10 months st+ Improvement in
800 800 + speech and bowel
400 800 wk+ continence
400 800 +
WM CF 25 25 Pre-illness wk+ Asymptomatic
1000 25 serum st+
50 800 <--Anti- +
50 1600 biotics wk+
50 400 start -
HM CF 2000 100 6 months + Asymptomatic
3200 3200 +
200 800 wk+
CN CFS 3200 800 8 months + 75%
800 800 wk+ Improvement
AN MS/ 400 400 wk+ Improved Strength
CFS 200 3200 st+ Fatigue decrease
JS CFS 2000 2000 5 months st+ Asymptomatic
(severe) 2000 2000 +
200 800 -
AG IBD 3200 400 9 months + Improvement
800 400 + in joint Sx
800 800 +
800 400 -
AT CF 3200 3200 9 months + Asymptomatic
1600 1600 +
1600 1600 +
800 800 +
400 400 +
LH RAi [48] 3200 1600 6 months wk+ Improvement
800 400 wk+
200 50 +
HS MS 2000 400 5 months + Improvement
3200 800 +
50 200 -
ST CFS/ >1000 100 7 months wk+ Asymptomatic
FM 1000 100 wk+
400 100 +
800 3200 +
100 100 +
RV CF 1000 100 10 months + Asymptomatic
400 1600 +
400 400 -
a CF = Chronic Fatigue < 6 months, CFS = Chronic Fatigue Syndromei [49],
FM = Fibromyalgiai [50], IBD = Inflammatory Bowel Diseasei [51], MS = Multiple
Sclerosis, AND = Automatic nervous dysfunction (neural-mediated
hypotension), RA = Rheumatoid Arthritis
IgM >> IgG: immune tolerance to the antigeni [44]; IgG >> IgM:
successful immune control of the antigen
TABLE 13b
Treatment Regimens
Treatment Regimen
Phase of Chlamydial Life Cycle
EBi [69] (Extra- or EB->RB Stationary Replicating
RB->EB Duration
Patient Sex Diag Intracellulari [70]) Transition Phase RB RB
Transition Enhancer (months) Comments
BL M MS Rifampin Flagyli [71] Floxin
2
Flagyl Bactrim,
5
Levaquin
-- -- -- -- --
3 Took a break, had relapse
Flagyl Bactrim,
2
Levaquin
Penicillimine Flagyl Bactrim,
Penicillimine 7
Levaquin
Penicillimine Rifampin INHi [54] INH
Penicillimine Probenicid 3
MC M MS Rifampin INH INH
9
Flagyl
Levaquin
6 Probably not compliant
Minocyclinei [72]
-- -- -- -- --
-- Discontinued
JM M MS Flagyl Floxin
7
Bactrim
Minocycline
Amoxicillini [73] Levaquin
Amoxicillin 4
Bactrim
Amoxicillin Levaquin
Amoxicillin Probenicid 3
Bactrim
LL F MS Flagyl Levaquin
15
Minocycline
Penicillimine Levaquin
Penicillimine Probenicid 1
Minocycline
AN F MS Tenitizole Floxin
7 She was given a copy of the
protocol, but ran her own
therapy
FO M MS
Prednizone 0.25 Phased in over several days
to mitigate effect of therapy
Flagyl Biaxin
2
Biaxin
1 Stopped flagyl due to
persistance of side effects
Kemet Biaxin Kemet
0.5
Kemet Flagyl Biaxin Kemet
6 Began phasing Flagyl back
in over a month
Kemet Flagyl Biaxin Kemet
1 Began 2 week switchover to
Amoxicillin
Amoxicillin Amoxicillin
Amoxicillin Flagyl Biaxin
Amoxicillin 2
Amoxicillin Flagyl Biaxin
Amoxicillin Probenicid 6 Began 6 week phase in of
probenicid
JC F MS Amoxicillin
Amoxicillin 1 Phased in over 7 months.
Amoxicillin
Amoxicillin Probenicid 1
Amoxicillin Bactrim
Amoxicillin Probenicid 1
Amoxicillin INH Bactrim
Amoxicillin Probenicid 7
FW M MS Penicillimine Flagyl Doxicycline
Penicillimine 7
Penicillimine INH INH
Penicillimine Probenicid 5
Bactrim
-- -- -- -- --
-- Stopped treatment
LH F RA Penicillimine Flagyl Minocycline
Penicillimine 11
Penicillimine Flagyl Minocycline
Penicillimine Probenicid 3
-- -- -- -- --
-- 3 PCR negative, symptom
free, but titer @ 1:800.
Decided to stop.
Penicillimine Flagyl Minocycline
Penicillimine Probenicid 2 After symptoms flared, PCR
went positive, and titer to
1:1600, restarted therapy
XX F IC Amoxicillin INH INH
Amixicillan Probenicid 4 Symptoms gone after 4
Bactrim
months of treatment
NC F PG Amox INH INH
Amoxicillin 7 Continued improvement
Bactrim
CH M PG Amoxicillin INH INH
Amoxicillin 3
Levaquin
Amoxicillin INH INH
Amoxicillin 2
Bactrim
-- -- -- -- --
-- Discontinued after all ulcers
cleared up except for those
in poorly blood-supplied leg
RI M PG
Missing patient chart
PL M PG Amoxicillin INH INH
Amoxicillin 2 Non-compliant because
Bactrim
could not afford medicines
-- -- -- -- --
-- 1
Amoxicillin INH INH
Amoxicillin 0.5 Would often only take what
Bactrim
he had left.
-- -- -- -- --
-- 2 Off for 2 months, then flared
Amoxicillin INH INH
Amoxicillin 1 No subsequent follow-up
Zithromaxi [56]
TW M PG Flagyl Minocycline
4
Amoxicillin INH INH
Amoxicillin 2
Levaquin
-- -- -- -- --
1
Amoxicillin Levquin
4 No improvement
-- -- -- -- --
Moved to topical antibioticsi [47]
AM M UC Flagyl Biaxin
11
Amoxicillin Flagyl Biaxin
Amoxicillin 2
INH INH
Amoxicillin Flagyl Bactrim
Amoxicillin Probenicid 5 Now doing very well
INH INH
AG F UC Flagyl Doxycyclinei [55]
6
-- -- -- -- --
-- Discontinued after
symptoms resolved.
DM F IBD Flagyl
7
Cupramine1 Flagyl Doxycycline
Cupramine Probenicid 5
-- -- -- -- --
-- Discontinued after doing
well clinically; wanted to
start a family.
RP F UC Flagyl Biaxin
5
-- -- -- -- --
-- Discontinued after impvt
AB F CD Flagyl Doxycycline
7
-- -- -- -- --
-- Non-compliant
EU F UC Flagyl Doxycycline
9
-- -- -- -- --
-- 1 Stopped
Amoxicillin Flagyl Doxycycline
Amoxicillin Probenicid 2 Restarted after symptoms
flared. Now doing well again
RR CD Flagyl Doxycycline
2 Colectomy 2 months prior
Amoxicillin Flagyl Doxycycline
Amoxicillin Probenicid 6 Now doing well; no
evidence of active disease
1 125 mg BID
TABLE 13c
Detailed Case Histories
Patient Diag Test data1 Case History
BL MS Row 2 First symptoms began with numbness of the left arm
and leg which rapidly
progressed to a partial Brown-Sequard syndrome
(i.e.-cord myelitis) with an
associated urinary retention. Despite therapy with
corticosteroids, and Beta
interferon he rapidly progressed over the next
three months with an EDSS - 8.0
(triplegic plus speech and swallowing impairments).
A positive CSF PCR and
culture for C. pneumoniae led to treatment with
combination antibiotics. The
patient improved on all spheres of neurologic
function over the following six
months. HIS EDSS score 9 months later was 3.0 with
return to work and routine
athletic activities (e.g.-jogging). His
neurological status remains stable and he
continues on an anti-chlamydial combination
regimen.
MC MS This patient had a ten year history of MS with
evidence of progressive ataxia and
weakness in the legs. Over 5 months his EDSS score
worsened from 7.0 to 8.0.
His CSF was positive by PCR for C. pneumoniae and
he was placed on
combination antibiotics. Over the next six months
he gradually improved in his
balance, coordination and lower extremity strength.
His most recent EDSS score
was 6.5.
JM MS Initially seen with rapidly progressive paraparesis
secondary to MS. He failed to
response to corticosteroids on two successive
occasions. Five months later, his
EDSS score was 7.5. Following a positive C.
pneumoniae PCR he was placed on
combination antibiotics. He has gradually gained
strength in his lower
extremities and five months later was able to walk
with a walker (EDSS = 6.5)
while being maintained on combination antibiotics.
LL MS Patient with a long history (14 years) of secondary
progressive MS with recent
progressive bulbar symptoms, axtaxia, and
paraplegia (EDSS = 8.5). PCR for the
MOMP gene of C. pneumoniae in the CSF was positive.
She was placed on
combination antibiotics with no further progression
of symptoms for the last six
months.
AN MS Row 10 Long history of MS and wheel chair bound for
approximately ten years. She has
received continuous physical therapy to retain leg
muscle tone. Following
approximately 6 months of combination antibiotics,
she was able to stand
unaided and take several unaided steps. She reports
a significant decrease in
fatigue and cognitive dysfunction. She remains on
combination antibiotics and
other supportive medications.
FO MS Row 6 Wheel chair bound with a long history of MS with a
2-3 year progression of
severe dysarthriae and incontinence. On combination
antibiotics (14 months) he
has had improvement of speech and incontinence.
Speech, ability to open
mouth for dentist, stamina all improved. Can stand
better on his own mid-
transfer. He remains wheel chair bound.
JC MS Diagnosis of MS with development of a foot drop
approximately one year prior
to therapy requiring the use of a cane in walking.
Approximately four months
after initiation of combination antibiotic therapy,
patient reports reversal of foot
drop and no longer requires a cane. She continues
on antibiotic therapy.
FW MS Male executive in late 50s with a year history of
MS. Used a cane for a rolling,
unstable gait. Easily fatigued: After 12 months of
combination antibiotics, was
able to walk without cane or excessive fatigue,
although his gait can still wander.
Can easily make it across the parking lot, which
had previously been a challenge.
Stopped antibiotics even though was still PCR
positive; plans to restart therapy if
he has another flare-up.
LH PA Row 14 Patient LH had an active case of RA which was
moderately debilitating.
Following two months of combination antibiotic
therapy, her RA is in complete
remission.
XX IC She responded to combination antibiotics with
complete remission of symptoms
after one month. Cessation of antibiotics resulted
in a return of IC symptoms.
NC PG PCR + 61 year old man who had had lesions for several
years. Large ulcerated lesions
on feet that resolved on combination antibiotic
therapy. Only residual
hypertrophic scars remain.
CH PG PCP + 75-year-old male diabetic with multiple, large,
severe lesions on both legs,
abdomen, and arms. Lesions first formed in 1993.
Severity of process required
chronic nursing home care at an estimated cost of
$300-400 per day. All lesions
above the knee have resolved on combination
antibiotic therapy: lesions only
remain on right lower leg, where inadequate blood
supply offers poor prognosis.
The patient no longer requires nursing home care.
RI PG PCR + Original severe PG lesions on legs required
bilateral amputation. Lesions now
occurring on arms. Treatment with combination
antibiotics has resulted in
resolution of lesions although not complete to
date. [No update - chart missing]
PL PG PCR + 18 year old female with history of leg ulcers.
Multiple PG lesions completely
healed on combination antibiotic therapy. Patient
then lost his job and could
not afford to maintain drug regimen. Upon
re-flaring of ulcers, re-started
therapy and ulcers improved again.
TW PG Severe PG, initiated after a chemical burn in 1991,
but with PCR negative
serologyi [74]i [75] for C. pneumoniae. Patient did not
initially respond to combination
antibiotic therapy. A positive biopsy culture for
C. pneumoniae resulted in the
recent re-institution of combination antibiotics.
However, after no
improvement, patient went off therapy.
AM IBD Row 5 This is a 35 year old male who first presented as a
prostititisi [76] ten years ago at the
age of 25. This progressed to acute ulcerative
colitis, involving the entire colon,
which was associated with severe arthritis, iritis,
and weight loss. Diagnosis was
biopsy confirmed. Control required high doses of
corticosteroids and azacol.
Attempts to reduce steroids resulted in partial
control of symptoms. Six months
prior to initiation of combination antibiotic
therapy, patient was experiencing
frequency (20-25 times per day), frank bleeding,
and mucus in the stool. Patient
on combination antibiotics for one year. Following
significant stress, patient had
significant increase in symptoms. Alteration of
antibiotic combination has
resulted in normal bowel habits with no mucus and
minimal blood. Associated
neuropsychiatric manifestations of cognitive
dysfunction and depression have
resolved. Steroids have been discontinued.
AG IBD Row 12 This is a 27 year old white female with two month
history of fulminate,
progressive ulcerative colitis which had not
responded to the usual medical
therapy. A total abdominal colectomy with ileostomy
and rectal pouch was
done. The microscopic appearance confirmed
ulcerative colitis. Following the
colectomy, the patient experienced neurologic
symptoms, fatigue, myalgias,
arthralgias, and a acneoform skin rash. Serology
was performed for C.
pneumoniae and was positive with an IgM of 1:3200,
IgG 1:400, and PCR positive.
Therapy with combination antibiotics was initiated.
After six months of
antimicrobial therapy, her serology was IgM 1:800,
IgG 1:400, and PCR positive.
The neurologic symptoms, fatigue, myalgias,
arthralgias, and acneoform rash
resolved completely. There was no further evidence
of inflammatory bowel
disease, and the ileostomy was successfully
anastomised to the rectal stump. The
patient has felt more energetic. Serology after 1
year was PCR negative.
DM IBD This 37 year old female had a six year history of
inflammatory bowel disease
(uncertain CD or UC) associated with painless
rectal bleeding, arthritis, myalgias,
skin ulceration, abdominal cramping/diarrhea, and
rectal fistulas. She had
increasing fatigue which caused her to frequently
miss work as a minor
executive. On combination antibiotic therapy, all
symptoms resolved but
recurred with cessation of antibiotics while on
vacation. Reinstitution of
combination antibiotics resulted in a second
remission of symptoms.
Prior to
combination antibiotic therapy, she had not gone
longer than 3 months without
an anal manifestation of IBD. She has been symptom
free of IBD for over a year.
RP IBD Patient presented with proctocolectomy and
ileostomy due to UC. Following a
flu-like illness in 1993, she became fatigued and
anemic with blood-tinged
diarrhea. Examination of her ileostomy pouch
revealed inflammationi [77] and
ulcerations. Upper GI series/small bowel series
revealed no abnormalities and
no cause of her anemia was diagnosed. On
combination antibiotics her
ileostomy activity was more regular and less
spastic. She claimed to feel better
with higher energy levels and ceased antibiotic
therapy. Six months post-
antibiotic therapy she remained asymptomatic other
than a moderate anemia.
AB IBD Patient with long history of CD involving small
bowel, large bowel, and anus.
She had been treated with a small bowel resection
and fissurectomy. She
continued to suffer from numerous rectal fistulas.
On combination antibiotics
she experience some symptomatic improvement but
failed to completely resolve
her IBD symptoms. She discontinued antibiotics due
to a probable chronic
Herxheimer reaction. Currently she is lost to
follow-up.
EU IBD Colitis with inflamed distal sigmoid colon and
proctitis associated with frequent
loose stools with significant mucus. Following six
weeks of combination
antibiotic therapy with a significant reduction in
symptoms. Shortly after
cessation of antibiotics her symptoms return.
Reinstitution of antibiotics
resulted in a second remission of the majority of
her symptoms with resolution
of her proctitis on visual exam.
NM CFS Vanderbilt University initial patient that resulted
in our first association of C.
pneumoniae, initially complained of the insidious
onset of debilitating fatigue.
This was associated with a severe cognitive
dysfunction that disrupted his ability
to function as the supervisor of a clinical
diagnostic laboratory. Despite six
months of intensive diagnostic efforts by the
Infectious Disease Clinic at
Vanderbilt no definitive or presumptive diagnosis
could be made. A subsequent
high antibody titer against C. pneumoniae led to
standard anti-chlamydial
antibiotic therapy over a three month period with
gradual disappearance of
fatigue and cognition symptoms. On cessation of a
fluroquinolone antibiotic,
symptoms returned within two weeks. He was placed
on combination
antibiotics with complete reversal of symptoms
after six months. He remains
asymptomatic.
JS CFS Row 11 Academic physician with a greater than 10 year
history of CFS. Cognition
problems resulted in his grounding himself as a
private pilot. Initial treatment
with combination antibiotics results in an apparent
Herxheimer reaction with
resolution over a two week period with gradual
improvement in symptoms.
After three months therapy, he piloted a light
aircraft under instruments from
Florida to North Carolina. He remains on
combination antibiotics for over a
year and is asymptomatic.
PM CFS Row 4 Physician with long-standing CFS. Treated with
combination antibiotics with
gradual resolution of symptoms. During course of
treatment developed cardiac
myopathy. Currently asymptomatic from CFS. Cardiac
myopathy resolved over
six month period on combination antibiotics.
MM CFS Row 2 CFS and AD. Resolution of postural tachycardia over
1 month combination
antibiotic therapy. Partial reversal of fatigue
during this period. Patient non-
compliant after one month and lost to follow-up.
PH FM Row 1 Three year history of debilitating FM following the
stress of being a stalking
victim. Patient relatively asymptomatic after nine
months combination
antibiotic therapy.
CN CFS Row 9 Five year history of severe CFS with debilitating
cognitive dysfunction and
depression. Gradual improvement on combination
antibiotics for
approximately nine months. Estimated 75% of normal
function.
PG CFS Ten year history CFS with cognitive dysfunction.
Complete response to
combination antibiotics over a course of one year.
AT CF Row 13 Moderate fatigue and cognitive dysfunction
following acute infectious illness.
Depression was major problem. During one year
course of combination
antibiotics fatigue and cognitive dysfunction
largely reversed. During mid-
course of therapy patient developed acute anxiety
attacks relieved by anti-
porphyrin therapy.
WM CF Row 7 CF following acute stress. Pre-illness serum
negative for anti-Chlamydia
pneumoniae antibodies which peaked six weeks
following stress. Pre-illness PCR
was weak positive that became strongly positive. On
combination antibiotic
therapy at 3 months became asymptomatic. Cessation
of antibiotics resulted in
symptomatic relapses. Currently asymptomatic with
low serum antibodies and
negative PCR.
HM CF Row 8 Medical student with short history of CF and
cognitive dysfunction affecting
studies. Combination antibiotics over a multi-month
course resulted in
complete reversal of symptoms.
ST CFS Row 17 Mother of Patient AT. Three year history of CFS
with FM. Combination
antibiotic therapy has resulted in partial reversal
of symptoms allowing her to
retain a job in jeopardy. Estimated 80-90% normal
function currently.
RV CF History of fatigue although non-incapacitating.
Combination antibiotic therapy
has resulted in 100% return to normal function.
EB CFS Teen-ager with long history of CFS resulting in
home-bound schooling. On
combination antibiotic therapy returned to school
and recently graduated.
Recovery has not been complete probably secondary
to non-compliance in
therapy.
I spoke with a rheumatologist in California, Dr. Michael Powell, who is cautiously using a combination of antibioticsi [24] in conjunction with standard therapeutics for the treatment of nanobacterium (including Cpni [2]) in patients suffering from FM, CFSi [78] 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 [79] for Cpn when other clinical signs lead him to suspect some involvement. Serologic assays for IgGi [80], IgM and IgA are sent to confirm infection prior to treatment. He would like to see a positive serologyi [81] 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 [39] 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 [8] and supplementsi [23] for endotoxinsi [82]-
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 [21] 600 mg twice daily, INH 300 mg once daily before breakfast, and metronidazolei [22] 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 [83] 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 asked Dr. Powell to comment directly on concerns that have been mentioned over time as to whether he uses the CAPi [1] with his new patients. I received his response a number of weeks ago but have had no time to put it together in a cogent context. But continued posts on these questions has mobilized me to get his comments to our readers here. But context is, as we say, everything.
A problem with reading posts on a website such as www.cpnhelp.org [84] is that one does not really have the whole context of that particular person's illness, medical history, the complexity of what is happening in their body as a result of more and more systems being affected by more than one thing going on. While it is perfectly fitting that our site here has it's mission focus of treating Cpn via combined antibiotic (and other relevant antichlamydial agents such as Vitamin Di [4], tocotrienols, etc.), a physician is treating, hopefully, a patient rather than a bacterium.
I'm a clinician myself, although a psychologist rather than a physician. One of the things that becomes clear is that the particular clinical population one sees, the kind of clinical practice you have, shapes your understanding of what's needed in order to help people. If you are curious and growing as a professional, you are always learning from the particular complexity of what you see in your patients: what helps them, what doesn't; how general approaches fit and don't fit; and how you need to go beyond the standard approach to respond to what's real, where the standard prescriptive algorithms "You must always do these things and these things only..." fails utterly to help those you must care for.
A doctor who sees mostly patients with neurological problems related to chronic infection as from Cpn will get attuned to how those conditions respond and to the complex interactions of treatment with the rest of the person's health process. A physician who sees rheumatological patients learns what works well and what doesn't in that population, and the nuances of attuning treatment to the whole spectrum of patients, even to see the difference of patients who have the same disease label.
A physician who sees a lot of complicated cases has two options as a professional. One is to learn to think more broadly and reject the formulaic, in order to account for and encompass, that complexity. The other is to narrow their viewpoint to the accepted practice and say, "Well I do this, I don't know about those other things." The latter is perfectly acceptable to my thinking, as we all need to know our professional limits. But I thank God for those who are willing to grasp the former position, such as Dr. Stratton, Dr. Wheldon, and Dr. Powell amongst others, and dig deeper into things.
You see, I'm one of those complicated-type cases, and it has taken a nuanced and complex approach to get treated properly. I'd been sick so long and with so many different systems affected, and likely not just by Cpn, that it has taken a complex clinician to weed through the layers of debris, gradually clearing the tangled mess my health had become. Cpn and the CAP has been at the center of my treatment, hence my devotion to maintaining this website, but it has not been the only thing in my treatment, nor the only concern of my physician.
Dr. Powell reflects below on the questions and concerns that have evolved for him through many years of treating Cpn and other infectious inflammatory conditions in his rheumatology practice. He was among the first physicians to use Dr. Stratton's protocol actively in his practice, and has a lot of cases under his belt using the CAP. And he found out about Dr. Stratton's work through his own researches and insistent curiosity. No websites were then available to inform him. That should tell you something about his intellect and curiosity. I think his questions are good ones for any of our readers to ask and consider. They might just help us broaden our thinking the way we hope that our physicians will be willing to broaden theirs.
**********************************
Dear Jim,
Thank you for bringing these concerns to my attention. I am not opposed to treating infected people with antimicrobials. But I do think we all need to ask a few important questions before we start CAP. What is it we expect from CAP? What is CAP this month? Can we clear Cpn? Is Cpn like herpes viruses that can not be cleared, only pushed back? If one has an overgrowth of Cpn does that say something about their immunei [27] system? How many other infectionsi [83] does the average Cpn person have? Do you treat the viruses first or second? Could the viruses flare while you are stirring up die off reactions with antibioticsi [24]? Does the oxidative stress of these die off reactions have negative consequences to the immune system, neurological system and key infection opposing nutrient levels? For how long do we want to take antibiotics?
These are reasonable questions to ask.
It is important to understand that:
1.) No one knows which CAP combination is optimal.
2.) No one knows how long to treat. 3 months? 12 months? 3 years? Longer?
3.) No one knows if the infection can be cleared...clearing every elementary body, every cryptic, every reticulocyte form? Is that a realistic expectation?
4.) No one knows how many other infections are present and whether it might be better to begin with those, such as by using antivirals, before starting CAP.
5.) No one knows what impact geneticsi [85] are playing in these infections and few people know how to compensate for genetic predisposing factors (e.g supporting methylation defects helps to oppose infection).
People need to be realistic when they are considering CAP treatment and make sure they are not approaching these infections with the expectation that taking multiple antibiotics for a few months is going to restore their vitality. Please be sure to mention that you and I have seen CAP fail.
I have seen antiviral therapy work tremendously well with some who have failed CAP. That means something. I have seen people recovering faster with sauna, Iodoral and infection-opposing nutrients (weeks rather than months) and that is why I may start with these. When people are done having die off with these measures, they tolerate antivirals and antibiotics better and can get back to working and living full lives faster.
If someone comes to me with a 2/10 ratings of their energy and depleted levels of essential nutrients and hormones, the worst thing I can do is send their energy to 0/10 by increasing the demands on their system through premature initiation of antibiotic therapy. I have patients who say that the T3, Vitamin D and infrared sauna have had the largest impact on their health. Some patients respond best to antiviral medication while others respond best to NACi [21], Zithro, Flagyli [22]. Some patients seem to respond better to NAC, Rifampin, Doxyi [35], Nifedipine. Some patients do very well with IM or IV gammaglobulin if they are hypogammaglobulinemic. Last week I saw a gentleman who failed CAP and antiviral therapy, but he has returned to work feeling better in years after adding niacini [86] therapy. A recent study from Harvard confirms the antibacterial and antiviral properties of niacin, but liver enzymes need to be watched if the dose is increased about the RDA. The doctor can not know in 2008 which modality will work best because we do not know who we are dealing with in terms of these mixed infections and varied genetic mutations.
Starting treatment by restoring depleted nutrient levels before starting antibiotics is not a bad idea. Running into battle with your nutritional levels around your ankles is short sighted and likely to cost you more in than preparing properly and building a strong defense before going for the antibiotics and antivirals. I would be surprised if most of the people who dropped out after I recommended sauna actually tried sauna twice daily for 20 minutes as recommended. I have had so many patients swear by this benign method and I have seen recovery occur much faster for those who do daily sauna. Seriously, people tend to respond in weeks rather than months if they are doing daily sauna therapy.
In summary, there is no proof that even 3 years of CAP will clear Cpn in humans. I have seen CAP work wonders for those whose illness is linked to Cpn or other polymorphic bacterial infections, which is why I continue to recommend this important therapy. It is wise to minimize antibiotic exposure as much as possible and most patients want to transition from antibiotics to infection opposing supplementsi [23] as soon as possible. There is no test that can prove to the patient or the physician that Cpn or any other chronic infection is eradicated, so we are forced to use clinical symptoms as a guide. Herpes viruses persist forever, but when herpes is in remission people do not feel the infection. It may be that this is also true for Cpn.
We believe the best way to address these infections and restore health is to begin by strengthening the immune system rather than stress the patient's system in the initial stages of treatment. We have tried it both ways and we have better results by starting treatment with measures that support methylation, restore depleted nutrients, increase body temperature and WBC function. Then when the die off from these measures has subsided, antivirals and antibiotics are discussed and can be started more safely. I can't say this enough times, there is no proof that you can ever clear these infections or even know how many different organisms are involved. Check the websites for Lyme, Mycoplasma and other occult infections...relapse is very common. That is why we think it is essential to build one's defenses and improve immune function as the primary focus of therapy. It is wishful thinking to presume that 6-12 months of CAP will restore health in most fatigued patients. If only it were that simple.
Best regards,
Michael Powell, D.O.
Note: In a few cases these expert comments may have been superceded by updates to the particular protocolsi [87] mentioned. Please use the CAPi [1]'s descriptions in the Cpn Handbook [88] as the most up to date versions of the protocol's using these Expert comments as useful sidebar information where they differ from current practice.
Comments by physicians treating various diseasesi [5] with a Cpn protocol and by scientis