David Wheldon

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British physician who has created a combination antibiotic protocol for Cpn based on Vanderbilt/Stratton work.

Sarah's Unillustrated Blog

Please read this very carefully.

I mentioned in my first blog  http://www.cpnhelp.org/?q=sarahs_illustrated_blog#comment< that there was much I didn't remember about the early days of my treatment.  I have never been a terribly good record keeper, but I did start out keeping a journal.  For a few days I even added to this daily, but soon I could go for a couple of weeks without adding anything.  This period rapidly became longer and then eventually I ditched it all, probably in a fit of pique.  I had no intention then of taking part in anything like ThisisMS or this site.  If I had I might have been more circumspect.  In one way it is good that I even now only remember something when someone experiences a similar reaction themselves, because if I had a list of absolutely everything and had put it all down, then I might have risked putting ideas into someone's head.  It is better if someone new to the treatment suddenly comments about various things  -  I'm going carefully here lest I say something that hasn't been mentioned yet!  Let's take one of the most recent comments on the board about a desire for hot food: if someone has not experienced that at all, they might feel that they are not succeeding!  Then there are Karen's blue toes, or my early experience of putting my feet down to the ground when I got out of bed when the weather first turned wintry and feeling the cold floorboards, one toe turning blue and the toe nail actually coming off.  It has grown back perfectly now, by the way!
A very important thing that I want to mention here, though, is something that I only realised a few days ago when talking to someone who started antibioticsi this year, back in Early August, nearly exactly on the same date as me two years previously.  This person is just about to start his third pulse of tinidazole, timed to finish on December 25th and yet I have been saying that my only really severe reaction was during my third pulse.  It can't have been because I didn't experience it until February, so it must have been at least the fifth.  I think it is important to say this because many people are almost looking forward to feeling that something is happening yet will never experience the agonies that other people do and so might just think that they are failing somehow with the treatment, like with the ubiquitous Marshall Protocol, where if you don't go through purgatory and back several times over, you are made to feel like you failing.  Its not like that, if you don't have a build up of CPn in your limbs, you won't feel it there.  I felt nothing in the first pulse: I had already gone through the true herxheimer "almost going down with 'flu"  feeling when starting on the doxycline. It was shortly after this that I nearly gave up the treatment because we both thought it wasn't working.  Remember I was David's first chronic CPn patient.

Coming up for the 15th time

The usual blinding fog has not descended and I am in the middle of day 4 of 5,  No.15 Flagyli pulse.  But my walking has held, my mental acuity also, and the worse-every-night unpleasant "shimmering, glowing sense in my legs" is almost gone.  (That is why I began this Flagyl 1 week early)  Today I will go for LFT and will after that take my Avonex which will be 8 days.  In the past I was on an ever-declining slope of physical capabiliy, wishing earlier and earlier that I could have my interferon so that I could be a little less tired and walk a little better (with cane or walker) for a few more hours-  after the reaction of at least 20 hours had passed, of course.

 This morning  I did the test for myself that neurologists love: the shin test.  All of us who can stand are familiar with that: you stand, holding on of course, and run the heel of your bad leg down the other shin.   In the past  I could not get within 3 or 4 inches except when I hit it by accident on the way from here to somewhere else.  As a matter of fact, at some point I could not even lift my foor from the floor.  This morning I ran my right heel (the bad one) down my left shin and then again and again.  Not only could I run it up and down, it goes without saying that I could PICK UP my foot to do this.  I just  now stood up to do it again this minute and did it without holding on to ANYTHING.  Perfect, or close enough!  Where is Marie????  Remember, this is 8 days after weekly Avonex on day 4 of Flagyl!  Stay with it, guys.   Requirements are  lots of patience, choking down lots of pills,  and the knowledge that you may not be what you were before this nightmare but I bet you will be better than your worst!  None of us expected to get better so this is miraculous.   And I have two strikes against me.  I am an "older patient"  (I am 66 going on 35) and I am PPMSi.  We are supposedly limited in our recovery in either case.   If this is "limited" I definitely say "GO FOR IT!

Roxithromycin anyone?

Hi, any roxithromycin users out there?  Help!!! ........I recently started taking Rulid instead of the generic version I'd been taking for about three months and I feel awful.......more pain, worse nausea and sooooo miserable!

Does anyone think that Rulid really is more effective than the generics, both in terms of immediate response and also in long term results, or is it just co-incidence and I'm going through (yet another) bad patch?

I am taking it along with doxyi as part of the Wheldon protocol so I'm also taking the supplementsi to help with die-off etc. Thanks for any thoughts on this.


The rhythm of our days

A Flagyli rhythm is  emerging.  Maybe I was not mentally clear enough to see it before or maybe it was not there.  Maybe it is the stage of recovery or the addition of Azithromycin and NACi a couple of months ago.  My 14th pulse of Flagyl ended 13 days ago but my body is telling me to do it again.  I have become aware the last few months of not a tingling but a "shimmeriing, glowing" after about 12 days post Flagyl.  I feel REALLY good after the fog wears off (about 4 or 5 days after finishing Flagyl) then there is a buildup, very subtle at first, now clamoring, of -what?.  I woke at 5 am wondering if I could take 1 dose of Flagyl of 500mg. (in the US we have 250 and 500mg)  per day every day or if I might just begin a week early.  My walking is not as good either- not bad, but it was better than ever 12 days ago. 

Maybe I could run (walk) the Iditarod

Here I am at  Day 5, post Flagyli the 14th.  My mind is clear, it is winter (NC  version. That is why we are here- it is like Texas with trees).  I am walking really well and yesterday walked 1/2 mile over rough ground because I could.  I had admirers with me-  our 4 dogs.  They thought it was a great idea!


The most amazing thing is that I am not only not freezing, I am comfortable and it can be in the 40s F.  For a number of years I have worn as standard outside clothing below 50 F.: t-shirt, turtleneck. sweatshirt, snowsuit, down jacket.  It has been in the 30s F. and I have  worn only t-shirt, turtleneck, and sweatshirt, at times removing the sweatshirt in the barn.  Only twice have I worn a jacket because it was raining.  We have a down comforter that goes to  -20  and it is still put away.

Sarah's Illustrated Blog......................

Nov. 17th 2005  -  A New Life for 2006
To start my blog, I thought I would add three pictures, so that people can see I am a real person and not just a figment of someone's imagination.  The first two little black and white ones are the only ones that remain of a horrible period of my life, dating from 1999 until late 2003.  I destroyed all the others.  By the second one, taken a few months before my diagnosis, I was looking particularly ill.  This was when my memory was starting to go but I was convinced I was getting better.  The colour one, me and two recently finished watercolours  was taken today.


Addendum to MS is not for Wimps Ch 2

These are symptoms that are ongoing and in view of the bigger picture did not even come to mind earlier today but I see that they are fairly common. I have had ringing in the ear several to many times, the last three fimgers beginning with the middle one, are somewhat to almost totally numb, I have had iritis for 18 years with two lens replacements (both eyes)for steroid-induced cataracts- not systemic steroids. Iritis was not part of the MS picture but I now have a count of 9 prisms (everything is double). That probably was caused by MS and half my hair fell out after onset of MS 10 years ago. Sounds worse than it is but easily dismissed when I think of where I was headed shortly and the fact that now I can walk, turn around, get up from a chair (or even the floor), climb a fence and go a

MS is not for Wimps- Chapter 2

Happiness may be the realization that you don't need a cape to fly (if you are Superman) or that you don't need Avonex to walk (if you have MSi). One week before I take up the Flagyli thing for the 13th time. Now that it is not just on faith that I will someday see improvement but can actually expect it makes my heart sing. The hardest part may be behind me. Those are words I never thought I would say. Maybe I will call that neurologist because he may say "Let's do an MRI." Boy, would I like that. I don't think it is a delusion that I walk, talk, and think better than I ever thought I would again during the very dark, dismal days of 2003 and 2004. I only wish I could relieve my friends on these sites of even some of their anxiety and say "LOOK, friends, no hands, no walls, no canes." But we each have to make our own ways.

Comparing the Antibiotic Regimens

As people get into more of the information about the combination antibiotic (abxi) protocolsi on this site, confusion can arise about what medications are used with which protocol, and even which version. In the interests of clarity, I will try to summarize and compare the 7th Stratton/Vanderbilt protocol (published on this site), the most recent version of it represented by the interview with Dr. A, and David Wheldon's most current regimen. Drs. Stratton and Wheldon have graciously replied with their overviews of protocol variations.

Wheldon Regimen:

  1. Doxycycline 200mg once a day (working up to this dose as the patient can manage)
  2. Then adding Roxithromycin (not avail in USA) 150mg twice a day OR Rifamcini 300mg twice per day OR Azithromycin 250mg three times per week (working up to this dose as the patient can manage)
  3. After 2-3 months or when the patient experiences little reaction from this dual abxi combo metronidazolei (Flagyl) is added (tinidazole may also be used if better tolerated). First a single 400mg (it comes in 500mg in the USA) is tried for the first pulse. Then every 3-6 weeks depending on tolerance a pulse of this is done working up over time to 400mg three times a day for 5 days.

When metronidazole pulses yeild no further reactions or improvements, the goal is to do 2 week courses of the abx, with days 5-9 being also Flagyl pulses. 

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

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

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

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

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

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

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

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

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

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

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

Expert Comments

Note: In a few cases these expert comments may have been superceded by updates to the particular protocolsi mentioned. Please use the CAPi's descriptions in the Cpn Handbook< 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 with a Cpn protocol and by scientists and researchers studying Cpn.

Comments by David Wheldon

Comments by David Wheldon on antibiotics in his protocal and the Vanderbilt protocal<

Comments by David Wheldon MD on treating MS with Cpn protocal"<

Wheldon Protocol

David Wheldoni MB CHB, FRCPath (Fellow of the Royal College of Pathology) Cpni Protocol

Dr. Wheldon's <site< has an excellent summary of Cpn and it's implication in disease, especially MS, and a much more complete description of the Cpn and of his treatment protocal than is given here. David updates his site regularly, and it has the best up-to-date information on supplementsi for Cpn treatment as well. Make sure you consult it for the latest information.

Dr. Wheldon is a consulting medical microbiologist in England whose wife, Sarah, was diagnosed with Multiple Sclerosis. When her worsening condition and lack of useful treatment from conventional medical resources occured, Dr. Wheldon explored the emerging evidense for bacterial causation. Although Sarah did not show any serological results for Cpn, he used the Vanderbilt (Stratton and colleagues) work and his own microbiology knowledge to formulate his own protocol.

His protocol calls for the use of two bacteriostatic agents continuously, both of which can cross the blood-brain barrieri and thus are particularly geared to MS, and short pulses of Flagyl (metronidazolei) an anearobic bacteriacide.

Sarah, as well as others he has treated, has shown both symptomatic reversal and clear reduction of brain lesions shown by radiological study.

We recommend you read his site in detail and download his treatment pdf< before initiating any treatment.

The following is extracted from his website (as of 02/07/06) and may not be complete or up to date. His website is updated frequently with new material and should be read thoroughly by anyone using a CAPi for Cpn.

Wheldon Regime

Why doxycycline and roxithromycin (or azithromycin)?

Both are oral, both are active against Chlamydia pneumoniae, both are relatively inexpensive. They are relatively risk-free. They act synergically against test strains of the organism; giving both together would be the equivalent of giving a four-fold increase of each drug were it to be given alone. The drugs work on different steps in the bacterial protein synthesis pathway. Combination therapy reduces the chance of the emergence of resistance. Both drugs pass into the brain. Both reach good levels inside cells. This is very important. Both are well tolerated. Azithromycin is an alternative to roxithromycin. They deplete the organisms slowly: this is very important, as the release of bacterial endotoxinsi should not be sudden.

Rifampicin may also be considered. It, too, is synergic with doxycycline, penetrates the brain and is active intracellularly. It is not suitable for intermittent use. It is highly active, and, in patients with a large bacterial loadi, it may give rise to intense reactions.

Why are later short courses of metronidazole to be taken together with these antimicrobials?

Chlamydiae are complex organisms. Long ago their ancestors must once have been free-living bacteria which possessed their own energy-generating pathways. The transformation from EB to RB is an active change, and an active change implies the retention of at least some of these pathways. The ones with the most utility for this purpose would be anaerobic, and thus susceptible to metronidazole.

Doxycycline and roxithromycin block the replicating phase by inhibiting protein synthesis and may be expected to force the organism to maintain itself by using its own primitive anaerobic respiratory mechanisms. In this suspended state it would be susceptible to anti-anaerobic agents such as metronidazole.

This is borne out by clinical evidence. The administration of metronidazole after doxycycline in a patient with likely high-load Chl pneumoniae infection causes a bacteriolytic reaction more severe than that following the original administration of doxycycline.

However, there is a difference: in this leg of treatment there is no risk of the emergence of resistance, for the organism is unable to replicate. Metronidazole need thus be given in courses only as long as can be tolerated.

Five-day courses of metronidazole at three-week intervals, during continuous treatment with doxycycline and roxithromycin, would seem reasonable; at first, metronidazole may be limited to one or two doses on one or two days to judge the severity of reaction.

The eventual aim would be to give all three agents intermittently. This, the final leg of treatment, would entail a 14 day course of doxycycline and roxithromycin, with metronidazole given from day five for five days. (The reason for continuing doxycycline and roxithromycin for a few days after the metronidazole has been stopped is because these drugs both possess anti-inflammatory activity which may prevent a reaction to the organisms killed by metronidazole.) This course would be given once a month. After several months the intervals between the antibioticsi would be cautiously extended.

Why this complex antibiotic regime?

The literature is filled with instances of treatment-failure in serologically-proven chronic Chl pneumoniae infectionsi of non-CNSi systems, whether macrolides, tetracyclines or rifampicin have been used. When the drug is stopped, even after months of treatment, serologyi rises, and the patient relapses.

The intensive cyclical regime of combined antimicrobials outlined here corrals the pathogen, initially halting replication, then eliminating stalled intracellular forms. Extracellular forms may be depleted by giving N-acetyl cysteine (see below.)

No single antimicrobial agent can be expected to achieve this effectiveness against every phase of the organism's life.

What are the expected reactions to the antibiotics?

There seems to be two components to the reactions experienced on taking the antibiotics.

The first is caused by elimination of bacterial fragments — endotoxins — and is characterised by shivering, influenzal symptoms and general malaise.

The second is caused by the release of metabolic toxins; waves of giddiness and feelings of unreality are quite common. They are alarming if not known about and understood. The strength and duration of these reactions depends largely on the bacterial load. In MS, particularly early relapsing-remitting MS, the bacterial load is likely to be small, and the reaction brief. In other conditions, particularly those with multi-system involvement, the bacterial load may be large and the reaction to antibiotics unpleasant and prolonged.

It may seem unlikely that doxycycline, roxithromycin and rifampicin can kill chlamydiae; they are, after all, considered to be bacteriostatic agents — normally they inhibit rather than kill bacteria. However, intracellular Chlamydia pneumoniae must continuously elaborate proteins to ensure its own survival within the host-cell.

The reaction to the metronidazole component of treatment is particularly severe as at this stage numerous bacteria are being killed. For this reason it may be best to give an initial course of one single day, followed by review. Prochlorperazine, 10mg orally, may be useful.

The patient can be reassured that a reaction to the antimicrobials are evidence of bacterial destruction and that they will end. And, too, the morale induced by physical improvement has to be set against them.

Isn’t giving antibiotics for a long time is a bad thing?

That depends on the illness. Long-term doxycycline is used fairly routinely for certain kinds of gum disease and for acne. Doxycycline is also used long-term in malaria prophylaxis.

Long-term use of these antibiotics engenders no real risk of an increase of resistance in other bacteria within the wider community.

What might a schedule of treatment comprise?<


What might a schedule of treatment comprise?<

200mg once daily with plenty of water.
Roxithromycin 150mg twice daily or Azithromycin 250mg three times a week.
These are maintained without a break for at least six months.

N-acetyl cysteine 600mg - 1,200mg twice a day, should be taken continuously. This is a commonly-taken dietary supplement, available at health-food stores. It is an acetylated sulphur-containing amino-acid, and may be expected to cause chlamydial EBs to open prematurely, exposing them to starvation; more on this and other benefits here<.

Two or three months into the treatment regimen, or when the patient is experiencing few problems with reactions, three-weekly cycles of intermittent oral Metronidazole are added. During the first cycle metronidazole is given only for the first day. If problems with reactions are found, the period of administration is kept short. When metronidazole is well tolerated the period of administration in each cycle is increased to five days.

The dosage of metronidazole is 400mg three times a day. If it is suspected that a patient may have a heavy chlamydial load a smaller daily dose may be given.

The eventual aim is to give all three agents intermittently so that the patient has a respite from antibiotics. This, the final leg of treatment, may entail a 14 day course of doxycycline and roxithromycin, with a five day course of metronidazole in the middle. This course is given once a month. After several months the intervals between the antibiotics may be cautiously extended.

Rifampicin is not suitable for intermittent use, and azithromycin may be given instead.


The brain has extraordinary powers of repair, but must be provided with the building-blocks by which to do it. This infection is intracellular; the organism interferes with mitochondria, the cells' powerhouses. Many of the symptoms of the disease - particularly the fatigue - may be due to mitochondrial exhaustion. Toxins known as free radicals are released as various synthetic pathways are disrupted. If this oxidative stress continues unchecked for too long irreversible mitochondrial damage may occur. A combined dietary supplementation of antioxidants is strongly recommended. (See Syburra C, Passi S. Oxidative stress in patients with multiple sclerosis. Ukr Biokhim Zh. 1999 May-Jun;71(3):112-5.)

Vitamin C 1G daily
E 800iu daily
Omega 3 fish oil daily
Evening primrose oil 1G daily
Acetyl L-Carnitine 500mg daily
Alpha Lipoic acid 150mg daily
Ubiquinone (Coenzyme Q10) 200mg daily
Selenium 200 micrograms daily.
N-acetyl cysteine 600mg twice daily
melatonin">i 1.5mg at night may be considered.

This may seem like polypharmacy, but there are good reasons to consider these agents. This is because the mitochondrial membrane is the bottle-neck for numerous key cellular reactions, and it is exactly here that chlamydiae hover as they control the host cell and steal its vital molecules via tiny projections. These agents are available at health food stores and are obtainable on-line.

<More details on how antioxidants can act synergistically to enhance their effects, and to regenerate each other can be found on this page.

<Apart from mitochondrial support, Vitamin Di is needed. There is evidence that a relative Vitamin D deficiency is common in MS, and may allow the disease process to begin. High dose supplementation - 4000iu is recommended. (less may be needed in infections other than MS) A page on this is given here.<

In addition, B complex, Magnesium, 300mg and Calcium 500mg supplementsi in the evening (remote from the time of taking doxycycline) daily.

Vitamin B12 injections once weekly for 3 months, then monthly for the duration of continuous treatment; B12, (together with B6 and folate">i) counteracts the hyperhomocysteinaemia which accompanies chronic Chl pneumoniae infection and which is thought to cause connective tissue damage. (There is now evidence that oral B12 is satisfactorily absorbed, except in patients with pernicious anaemia. High dose supplementation is recommended.)

Regular Lactobacillus acidophilus, daily, either as a supplement or in capsules. This is to maintain bowel flora in the face of antibiotic treatment. Tablets of Lactobacillus sporogenes spores may be considered. These have the advantage of getting into the small bowel in large numbers.

It would be wise to avoid foods containing artificial trans-fats. These are hard fats made from unsaturated oils which, after heating under pressure, are hydrogenated in the presence of a catalyst. They are widely used because they have a long shelf life and are inexpensive. With certain exceptions hydrogenated fats are not found in nature, and are metabolized with difficulty in the body. They alter cell and mitochondrial membrane functions. Two studies in animal models have found that artificial trans-fats affect mitochondrial efficiency as measured by a reduction of ATP synthesis. [Blomstrand R, Svensson L. The effects of partially hydrogenated marine oils on the mitochondrial function and membrane phospholipid fatty acids in rat heart. Lipids. 1983 Mar;18(3):151-70; De Schrijver R, Privett OS. Energetic efficiency and mitochondrial function in rats fed trans fatty acids. J Nutr. 1984 Jul;114(7):1183-91.] Dietary intake of trans-fats increases systemic inflammatory markers in humans. [Mozaffarian D, Pischon T, Hankinson SE, et al. Dietary intake of trans-fatty acids and systemic inflammationi in women. Am J Clin Nutr. 2004;79:606–12.; Baer DJ, Judd JT, Clevidence BA, Tracy RP. Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study. Am J Clin Nutr. 2004;79:969–73.] If the words 'hydrogenated oil' or 'partially hydrogenated oil' appear in a list of ingredients then trans-fats are likely to be present. (It may be noted that dairy products and animal fats also contain a small proportion of trans-fats, but these naturally occurring trans-fats are digestible and were beneficial in animal studies; evidence is less clear-cut in humans. [reviewed by Wang Y, Jones PJ. Dietary conjugated linoleic acid and body composition. Am J Clin Nutr. 2004 Jun; 79(6 Suppl): 1153S - 1158S.])

Turmeric, the yellow spice used in Indian cooking, may be very useful. The active ingredient, curcumin, moderates the pro-inflammatory effects of bacterial endotoxin, probably by restraining the activation of nuclear factor-kappa B. 'Nuclear factor kappa B has been implicated in autoimmune and inflammatory diseasesi, infection, cell survival, and cell transformation with subsequent promotion of cancer.' [Reviewed by Holmes-McNary M. Nuclear factor kappa B signaling in catabolic disorders. Curr Opin Clin Nutr Metab Care. 2002 May;5(3):255-63.]


Why this complex antibiotic regime?

The literature is filled with instances of treatment-failure in serologically-proven chronic Chlamydia pneumoniae infections of non-CNS systems, whether macrolides, tetracyclines or rifampicin have been used. When the drug is stopped, even after months of treatment, serologyi rises, and the patient relapses. The intensive cyclical regime of combined antimicrobials outlined here corrals the pathogen, initially halting replication, then eliminating stalled intracellular forms. Over a number of cycles it is expected that the load of extracellular forms will be reduced to negligible levels. There is evidence that in persistent infections the extracellular forms are scarce. No single antimicrobial agent can be expected to achieve this.

What are the expected reactions to the antibiotics?

There seems to be two components to the reactions experienced on taking the antibiotics.

The first is caused by elimination of bacterial fragments — endotoxins — and is characterised by shivering, influenzal symptoms and general malaise. The second is caused by the release of metabolic toxins; waves of giddiness and feelings of unreality are quite common. They are alarming if not known about and understood. The strength and duration of these reactions depends largely on the bacterial load. In MS, particularly early relapsing-remitting MS, the bacterial load is likely to be small, and the reaction brief. In other conditions, particularly those with multi-system involvement, the bacterial load may be large and the reaction to antibiotics unpleasant and prolonged.

The early bacteriolytic (Herxheimer) reaction can be alarming. And, as Sarah found, as-yet unorganised repair can cause function to worsen in the short term. This could easily lead to an early impression that antibiotics were unhelpful or even harmful and could have led to their discontinuance.

Rolling back secondary progressive MS using anti-chlamydials

This link is to Sarah Wheldon's quite eloquent story< of treating for Cpni and her recovery from MS via the protocal developed by her husband, David Wheldoni MD.

This segment written August 2005 for ThisIsMS

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