Development of antibiotic resistance in Chlamydia pneumoniae

I'm quite frequently asked whether the development of antimicrobial resistance in C. pneumoniae is likely, particularly when starting with one antibiotic or when adding metronidazolei intermittently. To be honest I think the emergence of antibiotic resistance is unlikely, given that the organism in not actively replicating while in the cryptic formi. I've put a new page on my website which discusses this: http://www.davidwheldon.co.uk/resistance.html< Do forward comments and criticisms.

(Editor's note: I've attached this post to the Handbook as-is so that readers may see Dr. Wheldon's article directly on his site through the provided link as well as the discussion here at www.cpnhelp.org< . That way readers will have access to the most up-to-date version should he edit it on his site. Jim K) 

Thank you darling: easily understood, so should put many people's minds at rest.  I'll go and add it to ThisisMS..............Sarah
An Itinerary in Light and Shadow  
Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still slowly improving and no exacerbation since starting. EDSSi was 7, now 2, less on a good day.
Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Thanks as always DW, for the very easy to read and understand explanation.

One thing I've been kind of confused by recently is discussion about few EBs in chronic infectionsi. I've always thought that the RBs were pumping them out in spades, even in chronic infections.

So, assuming that chronic infections are behind diseasesi like CFSi, MSi, Asthmai, etc, how did Cpni infect the local tissues? Is it likely mostly by this transmigration of the RB from the blood monocytes?

I always thought that Cpn infected blood monocytes showed up in the area, possibly due to some injury, etc and started producing tons of EBs that infected the local tissues.

Could you explain this area a bit further for the extremely curious?

Thanks again...

On Combined Antibiotic Protocol for Cpn in Rosaceai 01/06 - 07/07, On Vit D3 + NACi since 07/07 and daily FIRi Sauna since 08/07

Treatment for Rosaceai<

  • CAPi:  01/06-07/07
  • High-Dose Vit D3, NACi:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-
Thank-you very much as I can take this into my next appointment as it is seems this is my doctors main concern. On Wheldon protocol for MS since April, 2006.  doxyi 200 mgs daily, zithromax 250 mgs 3x/ week , Flagyli Pulses start end Sept., LDNi 2004. Gad-enhanced MRI of brain and spine shows NO NEW DISEASE ACTIVITY and one lesion diminishing in size on 9/30.

5oo mgs Ceftin 2 x/day, 500 mgs Zithromax, 500 mgs 2 x tinii pulses,100 mg diflucan, 4.5 ldni; Wheldon protocol for MSi April, 2006 to May 2008. 2008 MRI shows NO NEW DISEASE ACTIVITY, 2012 MRI no new disease activity.

Hi, Wiggy, I'm glad to be of help: I hope you're successful. Hi, Red - EBs are turned out in vast numbers in acute infection, and seed themselves throughout the body. However, as host defences are mounted, the organism goes into a different mode, relying wholly on host ATP and producing few EBs. (One of the reasons why there is so much argument about C. pneumoniae and MS is that few EBs find their way into the CSF and may even be intermittent.) So, early spread is by seeding with EBs; in chronic infection the spread is much more likely to be transmigration from cell to cell and the stimulation of infected host cells to divide (interestingly, other intracellulari pathogens can do this.) You can see this in atheroma: it starts off in childhood as fatty streaks involving the endothelial layer. Later on, these expand, foam cells appear and the structure becomes disorganised, with increased and rather choatic smooth muscle. On doing an autopsy on someone with bad arteriopathy you find that most of the atheromatous lesions are of the same age (and quite ancient: calcification is common.) You tend not to find 'young' and 'old' lesions in the same person. I had always wondered why this was; it was this early 'seeded' appearance which made my path teacher, Oliver Cromwell Lloyd (his real name) suspect infection when everyone else was looking at cholesteroli. (Gosh, you have got me thinking about O. C. Lloyd, now. He was a spelaeologist, a cave diver, a musician, a specialist in skin pathology, an archeologist and a Punch and Judy Professor. (All children's entertainers who run a Punch and Judy show are called 'Professor'. O. C. Lloyd's Punch and Judy was very traditional, with no pandering to political correctness. Each and every character who encountered Punch was grimly despatched, meeting a grisly fate usually connected with his trade. For instance, when Punch is sentenced to death he ascends the scaffold where Jack the Hangman is waiting. Punch affects not to understand the principle of the thing, and asks Jack to demonstrate. Jack puts his own head through the noose, and Punch pulls the other end of the rope, shouting 'That's the way to do it!' in his rasping voice - his voice being produced by a schwazzle, an artificial vocal cord held between tongue and palate.) D W - [Myalgia and hypertension">i (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now; just supplementsi and IR sauna. Morning BP typically 110/75]
D W - [Myalgia and hypertension">i (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now. Morning BP typically 110/75]

Ah, the old light bulb finally switched on with this explanation DW.   Thanks!

And your path teacher, O.C. Lloyd appears to have been quite an amazing character, with extremely varied interests.    I imagine he must have given some very interesting lectures!

Thanks again... 

On Combined Antibiotic Protocol for Cpni in Rosaceai 01/06 - 07/07, On Vit D3 + NACi since 07/07 and daily FIRi Sauna since 08/07

Treatment for Rosaceai<

  • CAPi:  01/06-07/07
  • High-Dose Vit D3, NACi:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Thank you David, I have bookmarked this for the information of those who might require it in the future.   I'm of the trusting follower type so I have not had a moment's worry about following the protocol, but I know others do.

Michele (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse. Zoo keeper for Ella, RRMSi, At worse EDSSi 9, 3 months later 7 now 5.5 Wheldon CAP 16th March 2006

Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse.

 David- Thanks for this cogent and accessible explanation. I think the proper accolade on your side of the water is "Brilliant!"

Many people approaching the CAPi, especially physicians, have concerns about this issue but don't have enough grasp of the particulars. The dictum of "antibiotic overuse creates resistance" is a useful rule of thumb for busy doctors in their practices, but doesn't say enough about how resistance is formed and in what kind of usage to give the intellect something to reason out the problem with a particular organism or protocol. I'll add this page right to the Handbook with your link intact so that users can always have access to the most up to date version, along with whatever commentary and discussion takes place here.

CAP for Chlamydia pneumonia since 11/04. 25yrs CFSi & FMSi- Currently: 200 Doxycycline, 500mg MWF Azithromycin, Tinii pulses.

 

CAPi for Cpni 11/04. Dxi: 25+yrs CFSi & FMSi. Currently: 250 aithromycin mwf, doxycycline 100mg BIDi, restarted Tinii pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Thank you, David, for the explanation.
I knew that the resistance was unlikely, but like others, I pictured the dynamics of the infection very differently.
Barbara

Multiple sclerosis, on the intrmittent Wheldon protocol since March 2006, EDSSi 0 for over 4 years

Cured of multiple sclerosisi, stopped the Wheldon's protocol in Nov,2008. Use only LDNi.

DW           

Thanks for the explanation of resistance and how/when it can emerge.  I've wondered about it myself from time to time.  This raises the question about the recent outbreak of resistent staph infectionsi which seem to becoming increasingly common.  Is this a case of the bacteria being resistant to one antibiotic or is it more complex than that?

Also, in your page you mentioned that production of infectious EBs in the chronic stage to be rare.  That surprises me, I think that most would have expected the opposite.  Why would it be rare, wouldn't there be more RBs pumping out EBs in that stage?

all my best

John

RRMSi/EDSSi was 4.5, now 4.??? on Wheldon Protocol (naci, doxycycline, azithromycin, metronidazolei) since 04/12/2006. Added Rifampin 2x150mg/daily on 08/19/2007

best, John

RRMSi/EDSSi was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
naci 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazolei 3x400mg/day then 3x500mg/day

David,

I have a more specific question relating to your post that has been really worrying me for awhile, and I wonder if you would be willing share your opinion or wisdom with regards to the following:  Can cycling any of the first two antibiotics (not flagyli or any other abxi added later) increase the probability of the development of resistance or of a poorer treatment outcome? 

 My doctor is fine with giving the abxi, but is of the opinion that abx have inherent dangers, kind of like chemotherapy does.  He also said that he has read that cycling abx does not increase resistance.  Therefore, he started giving me doxy and Biaxin in a cycle of 3 days off and 2 days on, and after 5 weeks I am supposed to take 2 weeks off abx.  I am on NACi all the time. 

I did this for about 6 weeks, but then, of my own accord, I went on abx straight for a month because I was afraid of being off abx so frequently.  I was afraid cycling might promote resistance AND even more so, I was afraid that if I didn't keep a steady or high enough amount of abx in my system, the treatment wouldn't be effective.  

On the other hand, I am wondering if one can take occasional time off from abx (for reasons such as yeast or extreme diarrhea or a short illness, or just to give the body a short break) without worrying that might have screwed up the treatment.  Is it ever beneficial to take a short break, and if so, when?

Anybody, please feel free to give me your ideas, but I am mostly very much looking for strong evidence/research/statistics or experienced opinions that will definitely help me make a good judgement call on this.  As I'm sure you would all agree, deciding how to carry out this treatment and whether to depart, in even any small way, from the standard treatment protocol (or how to make mild adjustments) can be a very serious and scary task.  

On the other hand, I don't want to ignore my doctor's advice without really having a good reason for it.  My doctor has been instrumental in helping me find this treatment and he is quite knowledgeable in general, so I don't want to brush off his opinions or ideas.  On the other hand, I know that even the best doctors sometimes find their long held opinions changing on occasion, and my doctor is always willing to rethink something and make a change.  I just need to arm myself with more facts so that I can feel comfortable that I am making the right decision and feel that I can discuss this with him in an intelligent fashion, and right now I am not armed with that information.  My doctor's view is so unique that I'm just not sure where to find information to either confirm it or intelligently question it.

I am very afraid of making a huge mistake in my treatment, yet I am not exactly sure what to do.  I would greatly appreciate any insight that you might be able to provide me.

Reve' 

Memphis,TN - FM, IBSi, rhinitis, depres ~20 yrs. CF, intestine, bladder, pelvic inflam., red itchy skin, anxiety ~5 yrs. CPni titer 1:256.  CAPi 6-07 Current NAC 2400 mg; doxy 100 mg x 2 and Biaxin 250 mg with 3 days on 2 off cycle and holiday wks 6,7

Memphis,TN - FMSi, IBSi, rhinitis, depres (~20 yrs) CFSi, intestine, bladder, pelvic inflam., red itchy skin, anxiety (~5 yrs). CPni titer 1:256.  CAPi 6-07 Current NACi 2400mg; doxyi 100mg x2, Biaxin 500mg x2, supplementsi, 1st pulse Flagy

Reve, coming from someone who has had to quit the abxi twice now for a number of months due to liver enzymes . I can tell you that stopping for any length of time just sets you back that much further . Every time you start again you go through symptoms that occured in the beginning. I had hypertention, dizzy spells, muscle fasculations,gaul bladder pain,bowel and bladder troubles to mention a few , all act up again. I dont recommend stopping and starting ! ........chuck treating reiters syndrome, cronic fatigue, heart symptoms, myalgia symptoms, started with doxcycline 200mg and rifampin 300mg in jan 15/05. switched to doxyi 200mg and azithromycin 250mg m.w.f in sept 06. after being on abxi for two years now doctors dont think I have reiters syndrome
treating reiters syndrome, cronic fatigue, heart symptoms, myalgia symptoms, started with doxcycline 200mg and rifampin 300mg in jan 15/05. switched to doxyi 200mg and azithromycin 250mg m.w.f in sept 06. after being on abxi for two years now doctors dont t

Reve,
I wouldn't intentionally cycle antibioticsi as part of a schedule, though sometimes you have to reduce doses because of unpleasant die-off reactions. I've seen some people with MSi who have taken intermittent treatment and lost ground.

John,
The virtual stopping of the production of EBs in chronic C. pneumoniae infection is due to the organism altering its metabolic strategy (a 'stringent response') as a result of host denial of various important factors. The organism goes into 'tickover' mode, running on the idling jet. There is probably an input from the likely evolutionary history of C. pneumoniae, where chronic infection in man is a dead end. More on this later.

Red,
O. C. Lloyd was indeed a most unusual man with very idiosyncratic views. He was not at all amusing in his lectures, but drily informative. He had been a scholar of Classical Greek before reading Medicine, and clearly felt that if you use a word you should know what it means. Medicine is full of Greek and Latin words of which few know the root: OCL would cover the blackboard with Greek symbols to explain the roots of histological words. I recall 'hamartoma' being one such. As an academic he was reputed to be utterly ruthless in the pursuit of what he thought was right. He was much liked by the students, though. His teaching was one of the main reasons I went into pathology. He died in 1985.

D W - [Myalgia and hypertension">i (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now; just supplementsi and IR sauna. Morning BP typically 110/75]

D W - [Myalgia and hypertension">i (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now. Morning BP typically 110/75]

So far, I follow the protocol to the letter.

Some of my die off symptoms from flagyl pulsing are pretty serious -sudden rage & aggressiveness.  I need to take it slow!

CFIDSi/ME 25yrs, FMSi, IBSi, EBVi, Cpni, (insomnia - melatonin">i, GABA, tarazadone, temazepam, novocyclopine, allergy formula, 2 gm tryptophan), Natural HRT peri-M, NACi 2.5 gm, 6-07 Doxy 200 mg day pm, Azith 375 mg M/W/Fday, 9-30-07 2nd pulse 1 X 250 mg Metroi<

CFIDSi/ME, FMSi, MCS, IBSi, EBVi, CMV, Cpni, H1, chronic insomnia, Chronic Lyme, HME, Babesia, Natural HRT-menopause, NAC 2.4 gm,Full CAP 6-2-07, all supplementsi+Iodorol, Inositol-depression, ultra Chitosan, L lysine Pulse#27 04-19-10 1gm Flagyli/day-5 days<

Thank you all very much for your input.  David, thank you very much for your answer.  I appreciate it very much.  I will definitely bring this to my doctor's attention at my next appointment.

Reve' 

Memphis,TN - FM, IBSi, rhinitis, depres ~20 yrs. CF, intestine, bladder, pelvic inflam., red itchy skin, anxiety ~5 yrs. CPni titer 1:256.  CAPi 6-07 Current NAC 2400 mg; doxyi 100 mg x 2 and Biaxin 250 mg with 3 days on 2 off cycle and holiday wks 6,7

Memphis,TN - FMSi, IBSi, rhinitis, depres (~20 yrs) CFSi, intestine, bladder, pelvic inflam., red itchy skin, anxiety (~5 yrs). CPni titer 1:256.  CAPi 6-07 Current NACi 2400mg; doxyi 100mg x2, Biaxin 500mg x2, supplementsi, 1st pulse Flagy

Hi chuck,

I know your post is seven years old but...

I was browsing when i saw a reference to Reiter Syndrome. I am 58 and had Reiters when i was 21 - Uvitis, Arthritic swelling, Urethritis - 3 weeks as in patient. No apparent relapses, but have had prostatitis three times and - my reason for finally finding this site - Asthmai. Thing is, i always understood reiters to be a classic chlamydial infection; is there any conncetion with Cpni as far as you are aware?

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