Isolation of Clostridium perfringens Type B in an Individual at First Clinical Presentation of Multiple Sclerosis Provides Clues

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0076359<

Abstract

We have isolated Clostridium perfringens type B, an epsilon toxin-secreting bacillus, from a young woman at clinical presentation of Multiple Sclerosis (MSi) with actively enhancing lesions on brain MRI. This finding represents the first time that C. perfringens type B has been detected in a human. Epsilon toxin’s tropism for the blood-brain barrieri (BBBi) and binding to oligodendrocytes/myelini makes it a provocative candidate for nascent lesion formation in MS. We examined a well-characterized population of MS patients and healthy controls for carriage of C. perfringens toxinotypes in the gastrointestinal tract. The human commensal Clostridium perfringens type A was present in approximately 50% of healthy human controls compared to only 23% in MS patients. We examined sera and CSF obtained from two tissue banks and found that immunoreactivity to ETX is 10 times more prevalent in people with MS than in healthy controls, indicating prior exposure to ETX in the MS population. C. perfringens epsilon toxin fits mechanistically with nascent MS lesion formation since these lesions are characterized by BBB permeability and oligodendrocyte cell deathi in the absence of an adaptive immunei infiltrate.


This is a fascinating study which provides an alternative hypthoesis for the initiation of MS via infection with Clostridium perfringens type B. A discussion on the merrits of the idea would be appreciated.

This seems related:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC352052/

It's about antibioticsi tested on that bug.  From a very brief review of the article you posted beyond the abstract - it appears that the team of researchers involved steered the individual with the infection towards a standard MS treatment, though I'm not sure of that.  I would hope that they would consider a course of antibiotics - such as the Stratton or Wheldon protocolsi

The article above suggests that the germ could be treated with such a protocol.  There was a recent article about some other bug found in dirt - it seems that there are now several infectious bacterial candidates as causes of MS. 

Another question - I'm curious if the germ isolated in this case has a similarly complex lifecyle.  I'm still astonished the original French / Le Gac study from the 1960's was dismissed, ignored, or lost in the noise.... (see http://www.davidwheldon.co.uk/le-gac.html< - towards the last part a story of 30 folks with what they identified as "neo- and para-rickettsias.")

Best & Highest Regards,

Tom


Proud Parent of Rick - R started CAPi in Nov. 13. Small measurable improvements as of 7/14, more by 10/14.  Holding Steady in early 2017.  "I will leave no stone unturned, no theory unexamined, to help my son." Tommi

http://www.msdiscovery.org/news/new_findings/8472-new-pathogen-linked-ms<

 

This is a decent review of the article. But basically it's the toxin that the bacteria generates which causes the damage. The epsilon toxin has an affinity for white matter and for retinal vessels, which makes it a plausible candidate for causing MS-like sympthoms and damage.

 

With respect to treating patients with antibioticsi, this may not even be necessary if the proposed hypothesis is correct. It was found that healthy controls were more likely to harbour the relativly harmless sub-type A which also had a protective effect against colonization with sub-type B. So it may be possible to treat the patients by giving them a probiotic with the sub-type A. Alternativly, giving patients antibiotcs may do the trick as well by changing the gut microbe composition and/or targeting the bacteria as well; however, we have to realize that the gut contains biofilms which may provide a safe-harbour for the sub-type B which may render the antibiotics useful only if administered on a continous basis.

 

In any case, I will have to look into the lifecycle of Clostridium perfringens type B a bit more to get a better understanding of it.

 

I am aware of the Le Gac study, which makes a strong case for the use of antibiotics. However, I am not sure what to make of their observations about the rickettsias organisms observed. Just what exactly are the antibiotics killing?

 

You may be thinking of Mycobacterium avium subsp. paratuberculosis as the other soil bacteria.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0018482<


In any case, I am confident that Chlamydia pneumonia also plays a role in MS and similar yet to be explained diseasesi. The million dollar question is to what degree in a given patient.

Rad, Are you an MSi patient?

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

Not MSi, but MS-like.

Good question.

One thing I found on this site that makes sense - is on this page:

http://cpnhelp.org/simple<

"If you have any of the diseasesi in which Cpn has been implicated, it may be worth trying an “empirical” (based on symptoms alone) combination antibiotic protocol (Link)." 

(my son has MS and is starting the capi protocol soon - while I am considering it for a pernicious case of chronic bronchitis - the bronchitis is currently being treated and "under control" - but I believe for a variety of reasons that it's possibly caused by cpn).

Given a bacterial infectious agent - cpn or other - it seems likely the combinations suggested in the protocolsi mentioned on this site (Stratton, Wheldon) - would have some positive effect on a broad variety of bacteria.  It could be a different bacteria could require a different set of antibioticsi.

It could be one disease many causes.  I bet in the not too distant future that there is some sort of Point of Care Rapid and Inexpensive Diagnostic test that will screen for a variety of different infectionsi that could be causing MS and the other illnesses that CPN (and other germs) are implicated in.

Best & Highest Regards,

Tom

 

 

Proud Parent of Rick - R started CAPi in Nov. 13. Small measurable improvements as of 7/14, more by 10/14.  Holding Steady in early 2017.  "I will leave no stone unturned, no theory unexamined, to help my son." Tommi

What pray, is an MSi-like patient?  You haven't really answered Mac's question.............Sarah

A Journey through Light and Shadow

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.

I read this basically as a negative study: they found C. perfringens type B in their first patient, but then when they looked for it in stool samples from other patients they didn't find it: instead they found less of type A of the bacteria, which doesn't produce the toxin (epsilon toxin) that they think is guilty.  This means little, especially as the numbers aren't dramatic (50% versus 23%).  In another experiment, they find that antibodies to epsilon toxin are present in ten times as many MSi patients as controls, but that means 10% rather than 1%.  They say that they "rigorously excluded the likelihood of false positives", but although that sentence sounds brave, it has a loophole, namely the words "the likelihood of": they didn't actually rigorously exclude false positives, and indeed there's plenty of room to wonder whether that's just cross-reactivity: the "positive" western blot that they show has just one band, not a distinctive pattern of bands.

They try hard to make this toxin sound like a likely culprit, but other descriptions of the symptoms that result from it don't sound at all like MS.  For instance, the paper

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC108230/<

says:

"Clinical signs, such as retraction of the head, opisthotonus, convulsions, agonal struggling, hazard roaming, and head pressing, are often observed during the chronically progressive course of the enterotoxemia. Characteristic neurologic features have also been reported for an experimental animal model: muscular incoordination, tremor, and pleurothotonos developed after the toxin was injected intravenously (i.v.) into a mouse. Pathological changes caused by the toxin were observed mainly in the brain. Liquefactive necrotic foci are formed in the brains of affected animals, and epsilon-toxin intoxication is characterized by the occurrence of focal-to-diffuse necrotic brain lesions..."

That is, animals who are being poisoned by the toxin (the above is from animal experiences, since few humans get this germ) act like they're being poisoned, unlike people in MS attacks.  And the brain lesions that result are "necrotic", which is worse than what usually goes on in MS lesions, namely an apoptotic demyelinationi.

Of course their ambitions are rather modest: they are only looking for the "trigger" of the disease, not its lock, stock, and barrel.  And as such, there's no difficulty granting them their point: what would otherwise be a mild and scarcely observable episode of poisoning perhaps could trigger an MS attack in a patient already prone to such attacks.

I didn't know I had to. I'd rather not go too much into my own personal details. Never-the-less my reasons for asking the questions don't have any malice involved. I am just trying to understand certain things better.

@Tom Clark

Thanks for the insights.

Thank you Norman, as always clear, concise and incisive. I don't think that what happens in the mouse model is too relevant to me or anyone else who HAS MSi.

speedbird

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