This Is MS Multiple Sclerosis Knowledge & Support Community

See this link... May be relevant to those who are looking in to CPn and ABX..



<shortened url>

I don't quite see the relevance because people are only looking into CPn and antibiotics once they have the disease. Penicillin is not effective against CPn once you have it. I had only been given antibiotics twice before: penicillin for scarlet fever when I was seven and something else for an infected insect bite when I was in my late twenties. I developed MS when I was 24.

Sarah

Well whatever.. No offense, but I am not going to go through a really long winded response to explain why I posted that, and why that could be relevant.

-B

Fair enough, but if you don't, we won't know why you think it relevant.

For those that don't want to click through, the study finds:

"Overall antibiotic use or use of antibiotics against C. pneumoniae was not associated with multiple sclerosis risk. However, use of penicillins in the 3 years before the index date decreased the risk of developing a first attack of multiple sclerosis (odds ratio = 0.5, 95% confidence interval: 0.3, 0.9 for those who used penicillins for >/=15 days compared with no use). In conclusion, use of antibiotics active against C. pneumoniae was not associated with a decreased risk of short-term multiple sclerosis. The observed lower risk of multiple sclerosis for penicillin users needs to be confirmed in other populations."

They used a retrospective analysis of what prescriptions people had taken and when. Caveats galore (retrospective studies are notorious for not being able to draw firm conclusions), but an interesting data point.

Arron, yes, I read it already, but I still don't see the relevance for someone who already has MS who is maybe thinking about trying certain antibiotics. If Viper is meaning that one would be better to try penicillin, then that is completely wrong, so he should explain what he means.

Sarah

Hi!
In the paper posted by Viper the researchers looked at a whole lot of medical records of people who had MS to see if treatment with CPn effective abx in their pre- MS diagnosis days was less then those who did not get MS. In otherwords they seemed to presume if MS is caused by CPn then people who were treated by abx should not get MS, or would have less prevalence. On the surface this might seem reasonable but not really there are some problems

To understand this the reader must understand that there is not much information in the MS world connecting MS to CPn, though there is some. However there is a lot of it asociated with other diseases esp atherosclerosis and heart disease, and reading and learning from them one learns a lot about how it works in the body. Papers like the one quoted here are frustrating because they ignore well known facts about CPn, in this case that abx that are helpful for CPn may induce persistence, an uncultureable state that yet remains inflammatory(which is why CPn is considered an emerging pathogen in atheroscleerosis). In the following paper found here <shortened url>
we see that abx therapy does not kill all CPn......(there are numerous papers on persistence of CPn caused by abx, not just this one)

Chlamydia pneumoniae-specific DNA was found in 10 of 11 GO (gingivitis overgrowth)tissue samples pre-treatment. Azithromycin therapy effectively reduced GO and C. pneumoniae IgM titres. In residual GO, C. pneumoniae-specific DNA remained detectable after 1 year in all GO tissue samples despite azithromycin treatment. The C.pneumoniae IgM titres correlated with GO scores. CONCLUSION: Chlamydia pneumoniae infection is highly prevalent in CsA-induced GO. The infection can persist over a long period in residual GO despite short-term azithromycin therapy. The results indicate that CsA immunosuppression enhances C. pneumoniae infection rates in non-cardiovascular tissue.

Antibiotics deemed effective against CPn can in fact induce persistence
in this paper here <shortened url>

First-choice antibiotics at subinhibitory concentrations induce persistence of Chlamydia pneumoniae.

Gieffers J, Rupp J, Gebert A, Solbach W, Klinger M.

Institute of Medical Microbiology and Hygiene, University of Lubeck, 23538 Luebeck, Germany. Jens.Gieffer@hygiene.ukl.mu-luebeck.de

Persistent growth forms of Chlamydia pneumoniae have been associated with chronic infections in vivo. We investigated the effects of first-line therapeutics on the induction of persistence by monitoring recoverable organisms, gene expression of membrane proteins, and morphology. We found that all of the antibiotics tested have distinct and subinhibitory concentrations at which they induce persistence.

PMID: 15047553 [PubMed - indexed for MEDLINE

A short course of abx such as is used for a bladder infection for example would be subinhibitory.

And in this paper we see Margaret Hammerschlag MD saying that persistent infection, though it can cause chronic illlness we had not thought before was infective, is not culturable, and she essentially concludes we can't know therefore if our treatments work. Found here
<shortened url>

Chronic, persistent infection with Chlamydia pneumoniae has been implicated in the pathogenesis of several chronic diseases initially not thought to be infectious, including asthma, arthritis and atherosclerosis.

and this

Persistence of the organism does not appear to be due to the development of antibiotic resistance. However, one cannot extrapolate from this experience to the treatment of chronic C. pneumoniae infection, especially cardiovascular disease. As there are no reliable serologic markers for chronic or persistent C. pneumoniae infection, it cannot be determined who is infected and who is not, which means that it cannot be assumed that any effect seen is due to successful treatment or eradication of C. pneumoniae.

Please note that arthritis is listed here as a disease not thought to be infectious but which is now being increasingly found to be possibly caused by CPn. RA is considered by most to be "autoimmune" just like MS. The woman who wrote this paper is a lead MD researcher for the US Centers for Disease Control. Steroids reduce symptoms of RA. So do NSAIDS. So do immunosuppressive therapies like Enbrel, all becasue it knocks back the immune system and thus symptoms. Hmmm sound familiar?
It is not proven that RA is caused by CPn (nor was it ever proven to be autoimmune in spite of decadess of treating it that way) but there is enough evidence for it to be considered a strong possibility, and as such you see it mentioned in this paper.

In particular I'd like to point out the fact that serologic markers are not possible to detect according to Dr Hammerschlag. Notice that she does not say that the disease is not caused by the organism, in fact she acknowledges that it has been implicated (though not yet proven: the CDC calls CPn an emerging pathogen in atherosclerosis). What she says is that though it may be causing the diseases, we cannot culture it. This is important as it may explain why we often get people saying We cultured MS CFS and did not find any CPn present. when others say they do find(vanderbilt university) ie Dr Sriram.
What does it mean if an organism that goes into an unculturable state is NOT cultured from a certain diseased organ? What if that organism in the unculturable state also can cause the same kinds of inflammation that the diseased organ has? Is the fact of the negative culture meaningful? This is an academic argument which science is just now in the process of answering. That is why we still get some papers on both sides of this argument.The scientific answer is not in yet. We are still mid debate.

So how does this relate to the article at the top of this thread?. What I am saying is this, that paper is meaningless. It is obvious that persistent infection in fact can be triggered by abx in subinhibitory levels, so saying these people were treated for unrelated things like bladder infections etc for a week or 10 days a few times in the years before they got MS doesn't in any way prove MS is not a CPn disease. Besides that if you take an abx this month does it stop you from having a bladder infection next month? Of course not!

The theory that MS might be caused by CPn is theoretical. But it is not without basis. There are good reasons why microbiologists Wheldon, Stratton and Mitchell and Neurologist Sriram are interested in it as a possible cause, and it is work like the above, which ignores well known facts of the germ and perhaps was done by non microbiologists and non pathologists that muddies the waters needlessly. It means nothing. I repeat if you had abx for a bladder infxn this month you are notprotected next month. It is also known that haveing cpn and being treated does not prevent future infections, so why would being treated for an unrelated infection prevent this?

If CPn were in a brain and if it were persistent it would be undetectible, would cause demyelination identical to MS demyelination (they use LPS to induce a lab version to study MS), would cause upregulation of nitric oxide, would cause apoptosis, and overall would look very similar the cytokine profile we see in MS brains. THAT'S why people think it is a plausible possibility. and I edit to add "though it is unproven".
Marie

Great post Marie! I only wish I knew as much about all of this as you. Thank you for the clarification and adendum to my original post.

Brock

Oh thanks I'm glad it was helpful
marie

it was indeed helpful...

Hi Marie

I too found your summary helpful. You know hormones are only a breath away. I've never gotten to that DHEA post, but since you mentioned the LPS, here's some info about DHEA and LPS.

AED and DHEA protect mice against lethal bacterial infections and LPS toxicity

the 88% mortality rate seen in LPS challenge was reduced to 17% and 8.5%, by treatment with DHEA and AED, respectively. The protective influences of both steroids were shown not to be directly antibacterial, but primarily an indirect antitoxin reaction.....The data suggest that both DHEA and AED may have a role in the neuro-endocrine regulation of antibacterial immune resistance.

It's interesting a hormone usually low in people with MS offers some protection against bacterial infections and the LPS toxicity you referenced (at least in mice.) And, as you noted, it has been proposed as one model to study MS.

Of course, DHEA, in animals, also shows some protection against a Japanese form of viral encephalitis in animals.

Dehydroepiandrosterone (DHEA), an adrenal-derived steroid, has been implicated in protection against neurotoxicity and protection of animals from viral-induced encephalitis, resulting in an increased survival rate of the animals.

Sharon

hi here's my first impression re: dhea

-manufactured in adrenal glands
-healthy adrenals synthesize cholesterol to make it (and use vitamin b5)
-adrenals fatigued by stress/excess cortisol can't effectively make the dhea - cortisol production hogs the goodies required

SO, i would think stress reduction and vitamin b5 supplementation (from unprocessed food sources, or supplements) might be beneficial. oh and look at that, vitamin b5 helps with stress reduction!

ok is it just me, or is this going in circles?! lol! i'll do some deep breathing and eat some kale anyway

Thanks Sharon and JImmylegs for the input. Interesting articles and thoughts. THere is such a thing as adrenal fatigue. ANd low levels of DHEA can result. On pubmed if you look there are many articles associating DHEA with infection, so it can tie in to chronic infection also.
You need DHEA to fight infection. In one study people who got sepsis (a severe infection all over essentialy in the blood) all started out with the same levels of DHEA, but the ones who died of the infection had levels drop toward the end.. Did those people die becasue of adrenal exhaustion and the subsequent drop in DHEA allowed the infection to go unchecked? why were they different than the survivors? It's clear they did not get it in the first place becasue of low levels as they were all the same at the start, the decrease was secondary and spelled disaster for the person in whom it occured.

Could this be why people with "MS" get it vs their neighbor? One guy gets CPn and recovers no sweat, but the MS patient somehow has inadequate DHEA so the infection goes chronic? Is it becasue that person is stressed and has some level of adrenal fatigue to begin with, therefore it just gets the upper hand? It's an interesting possibility. MS is really complex at this point becasue we are looking at a million and one physical reactions in the body and trying to see if the reactions are a cause or an effect. The autoimmune folks are on the cause side of it. If you evaluate these things from an effect standpoint as in can infection cause *this* whatever this is, often we see it can. I spend mostof my time reading research on CPn and how it reacts in the body. There are about 4 papers a week coming out through pubmed on it. It is an active area of research.

By the way to the reader note that in my firt post above I coipied research that indicates RA is likely a CPn disease. I have RA and MS. IMHO I'd be a fool to not try abx.
marie

i agree marie, i'm trying the herbal abx route myself, for now. don't think i'm necessarily in the cpn subset, but i was definitely stressed when the shite hit the fan. that said i will try to relax and help my bod make that handy dhea! and everything else it needs