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Diseases in which Chlamydia Pneumoiae has been implicated

Infections and asthma

Infectionsi and asthma.Martin RJ.
National Jewish Medical and Research Center, University of Colorado, 1400 Jackson Street, Office J206, Denver, CO 80206, USA. martinr@njc.org

A new paradigm is developing in regard to the interaction between infection and asthma. This paradigm comprises the acute exacerbations seen in asthma and also asthma chronicity. Viral infections have been commonly evaluated in acute exacerbations, but findings suggest viral-allergen and viral-bacterial interactions are important for chronicity. Most recently, studies are also invoking atypical bacterial infections, Mycoplasma pneumoniae and Chlamydia pneumoniae, as factors in both acute exacerbation and chronic asthma.

PMID: 16543054 [PubMed - indexed for MEDLINE]

Being sick, in general: Dealing with loss

Jim mentioned a forum like this when we met a few weeks back. I don't know quite where to go with it, since it's not C.Pn. specific. However, I think that it has a place here.

Anyway, my daughter sent me this link< from "ButYouDontLookSick.com". I don't think I could have expressed it any better. 



Another two diseases for the list?

A lady I know has dermatomyositis, an inflammatory muscle disease that is usually fatal within 10 years of diagnosis. She developed it relatively rapidly after or during her fifth pregnancy. She simultaneously developed the face and body changes that I now associate with C. Pn.

So, I started googling.

First, I find a scary incident:

Acute thrombotic thrombocytopenic purpura following doxycycline treatment of Chlamydia pneumoniae infection in a patient with dermatomyositis

Authors: Knox-Macaulay H.H.M.1<; Adil S.N.1<; Ahmed E.M.E.2<

Doing quite well at the moment!

I just thought I would annonce that I am doing quite well at the moment.

I am currently taking Lamisil and Fungizone (orally) which are both antifungals.

I have been taking these for about 4 months, and I am noticing improvments all the time.

I am sure now that much of what has been holding me back has been fungi. This is not too surprising considering the battle against bacteria I have had, and considering all the abxi that I have consumed.

My gut feeling is that everyone who has been through these wars, should also consider a trial of antifungals. To see if this is a factor for them too. I killed the bulk of the bacteria that caused ReA around 2001-2 but I have limped on since then, mostly with a comprimised immunei system I suspect due to fungi. No diet or lifestyle changes seemed to be able to resolve this alone.

Diseases associated with Cpn: the exhaustive list

I have culled from Mitchell & Stratton patent #6,884,784 an exhaustive list of diseasesi where Cpni has been implicated as a possible cause or co-factor (reference: Mitchell & Stratton patent #6,884,784):

Diseases where an association has been discovered between chronic Chlamydia infection of body fluids and/or tissues with several disease syndromes of previously unknown etiology in humans which respond to unique antichlamydial regimens include:

Editorial comment: Strong findings from their research. If you have any of these it suggests to me that at least an empirical course of the combination antibiotic therapy is strongly indicated, with or without serologyi.

Multiple Sclerosis (MSi)
Rheumatoid Arthritis (RA)
Inflammatory Bowel Diseasei (IBD)
Interstitial Cystitisi (IC)
Fibromyalgiai (FM)
Autonomic nervous dysfunction (AND neural-mediated hypotension);
Pyoderma Gangrenosum (PG)
Chronic Fatigue (CF) and Chronic Fatigue Syndromei (CFSi).

Early Peri-menopause??

I know a lady who is 36 years old, and who has been suffering hot flashes for several years. I suspect that she may have some variation on the CPni theme -- swelling of the neck, low B12, IBSi, uterine fibroidsi, fasciculationsi, brain fog, numb patches, etc. -- but I wondered specifically about this early onset of perimenopause.

If anyone here cares to contribute even anecdotal information, I would be grateful. Has anyone noticed hot flashes occuring earlier than normal in women with CPn? Please, if you don't feel comfortable posting to this forum, respond with a private message to me, and I can remove anything that identifies you specifically and put the resulting "abstract" on the forum.


The Basics Page

Hello and Welcome!

This site is focused on treatment of chronic disease like Multiple Sclerosis (MSi) Chronic Fatigue Syndromei (CFSi) and Fibromyalgia (FMSi) an many other diseases with antibioticsi. Recent research indicates that Chlamydia Pneumoniae (CPni) plays a role in these diseases.

Here are the basics that make it easier for people new to the site to get going (if your brain isn't ready for even this much right now-- we've all been there-- read Cpn Simple< first):

Is this a sexually transmitted disease? No. this is chlamydia pneumoniae, a bacteria that can cause pneumonia. It may soon be called chlamydiophilia (meaning in the family of).

Is chlamydia pneumoniae (CPn) rare?

Is Science Overlooking the Role of Pthogens in Chronic Illness?

Here< is an article written by a researcher that makes the case that science is biased against finding bacterial causes to chronic illness. This is focused on the considerable work that Alzheimers is in fact tied to CPn infection, and the reluctance of the general medical community to accept this theory as plausible in spite of the quality and quantity of the available research. A wonderful overview of the state of science in general in regards to infectious cause of chronic illness.

The Role of CPn in disease

I have to say as I read the Stratton stuff the actual citation is very enlightening vs the abstract. If you are thinking about using antibiotics for MSi or CFSi, then take the time to get and read the actual citations. ( we will be linking these here...look for that in the next weeks, though some may need to be purchased by you if you want the whole thing)

The VU people are not saying necessarily that CPn causes MS alone. They mention all kinds of possible mechanisms, not least of which is that the CPn causes auto immunity in mice. It is mild auto immunity but it does exist.

Another interesting thing is that Experimental animal encephalomyelitis (EAE) is vastly worse with chlamydia pneumoniae (CPn) infection being triggered ahead of time by researchers. It almost suggests that MS might be mild or benign without CPn getting in. As an aside, did you know that EAE is curable and self limiting? The idea that CPn turns it from a fairly benign disease to one that is disabling is intriguing. Like an evil cofactor. Interesting. And the fact that CPn triggers autoimmunity in mice answers the question "how can it be that there is all this autoimmune stuff and research out there?" "How can it be that if we treat people with steroids for example they get seem to get somewhat better?" ( see topic on steroids)

Comments by David Wheldon MD on treating MS with Cpn protocal:

Edited from post on http://www.thisisms.com/modules.php?name=Forums&file=viewforum&f=28

I've learnt a lot in the last year through treating a number of patients with MSi. As a patient goes through RRMSi, he or she tends to accrue progressive deficits; this is often unnoticed at first, but seems to equate with rising bacterial load. It's almost as though there were two parallel components to the disease, an idea which is supported by studies of sequential MRI data. I've recently seen two patients with early RRMS who have had no reactions on starting antibiotics. Both are improving, and have lost many of their accrued deficits. In the case of one patient, the deficits were so slight that the patient noticed them only when they started to go. In later RRMS and in early SP disease the reactions are often more severe; one assumes that this is because the bacterial load has grown. As the disease progresses ever deeper the immune system usually gains the upper hand and destroys the organism. It's a hard-won victory, and there may be immense collateral damage. At this stage there is little or no reaction to antibiotics, and little benefit from treatment. But a trial is worthwhile.

These acute reactions on starting doxycycline/minocycline are probably due to a freezing of bacterial protein synthesis. The organisms are intracellulari; one of the host-cell defences against intracellular infections is host-cell suicide; this releases bacterial antigen so that antibodies can be raised against it. In an amazing evolutionary strategy, Chlamydia pneumoniae can prevent host-cell suicide. This, however, requires continuous synthesis of a specific protein. (It is now known that Chlamydia pneumoniae in the CSF of MS patients actively makes this protein; furthermore, persons with MS have antibodies to the same protein.) So the infected host cells are now free to die, releasing their bacteria; these cannot survive in their current state and die also. Their death releases endotoxins, which are a component of the bacterial cell wall. (In an interesting parallel, another chlamydia with a similar strategy is associated with a very rare periocular lymphoma which shrinks when treated with tetracycline.) Unfortunately, a lot of bacteria remain in other cell-lines, and need to be actively killed.

Roxithromycin is a powerful immunomodulator, and partially suppresses the immune system, allowing the toxins to be flushed away rather than evoking an inflammatory response. Both doxycycline and minocycline are immunomodulatory too.

The risk of the emergence of a resistant mutant is, as you say, an unpleasant thought. Workers have tried to do produce resistance in the laboratory with negative results. I suspect the risk of resistance emerging is actually minimal. Resistant mutants usually emerge in rapidly growing cultures treated with minimally inhibitory concentrations of antibiotic; this gives the right evolutionary drive to produce resistance. The organism is in 'tickover' mode in chronic infections like MS and some of the evolutionary pressure is removed. Using two antibiotics which act synergically certainly reduces any risk.

So I should be in no hurry to start metronidazolei. Long-term minocycline is likely to be effective, with roxithromycin if this can be obtained, together with full supplementation - I'd allow three months before metronidazole is considered; and it should be started gently. Having witnessed a bad reaction to minocycline it would be beneficial to 'waste' as many organisms as possible before starting the killing phase.

One interesting rider. Serologyi is usually negative in MS, but this is not always the case. I've just seen a man with early PPMSi (18 months), retinal vasculitisi and follicular conjunctivitis. He has raised antibodies to Chlamydia pneumoniae, with an MIF of 1:1024 and high Chlamydia pneumoniae-specific IgA. (This is a fairly reliable indicator of persistent infection.) It's early days, but his carer reports good early improvement. His neurologist was very dismissive (rudely so), so I must write to him and tell him the serology results.

MS is multifactorial. A number of genesi seems to play a part in the expression of the disease. I have recently seen a patient with a multisystem disorder including retinal vasculitis and Crohn's disease. She had grossly elevated Chlamydia pneumoniae serology. An MRI scan showed typical white-matter hyperintensities which transected the long motor tracts in several places. However, she had no focal neurological signs. Presumably she was fortunate in her genetic make-up.

Work has been done in many different disciplines, in microbiology, immunohistology, cellular biochemistry and neuroimmunology. The science is all there, but not many people have yet joined up the dots.

And you are right; treating someone close to you for a large-load Chlamydia pneumoniae infection of the brain is an emotional roller-coaster.

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