Clostridium a new trigger of MS?

Has a new trigger been identified for MS? #MSBlog #MSResearch

“This is an interesting study identifying a novel exposure to a bacterium that lives in the gut of people. The authors then study exposure to this bacterium in a larger group of MSers and propose it as being a potential MS trigger. It appears that MSers may have a greater exposure to this particular bacterium than controls. Clearly this work will need to be repeated to make sure it is not a one off finding and then the temporal sequence of events will need to be studied. Causation is a complex subject and needs to be carefully considered.”

“I have posted before on causation theory. If you are interested I would recommend reading my previous post I did in relation to CCSVI.”

16 Oct 2012
Why are we wasting our time with this two bit theory (CCVSI)? I come on this blog to learn about B cells, EBV, Vit D… CCSVI ruined another MS website I used to visit and I can it happening here – the followers treat it as a 
Clostridium bacterium: source Wikipedia

Rumah et al. Isolation of Clostridium perfringens Type B in an Individual at First Clinical Presentation of Multiple Sclerosis Provides Clues for Environmental Triggers of the Disease. PLoS One. 2013 Oct 16;8(10):e76359.

These investigators have isolated Clostridium perfringens type B, an epsilon toxin-secreting bacillus, from a young woman at clinical presentation of  MS 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 barrier (BBB) and binding to oligodendrocytes/myelin makes it a provocative candidate for nascent lesion formation in MS. They  examined a well-characterized population of MSers 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. The examined sera and CSF obtained from two tissue banks and found that immunoreactivity to ETX was 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 death in the absence of an adaptive immune infiltrate.

WikipediaClostridum perfringens is ever present in nature and can be found as a normal component of decaying vegetation, marine sediment, the intestinal tract of humans and other vertebrates, insects, and soil. There are five types of C. perfringens (A, B, C, D and E), which are identified by the main types of toxins they produce (alpha, beta, iota, epsilon and theta). Type A produces alpha toxin, type B produces alpha, beta, epsilon toxins, type C produces beta toxin, Type D produces alpha and epsilon toxin and type E can produce alpha and iota toxin. C. perfringens Type A is the most common C. perfringens type. This dietary bacteria can cause food poisoning and a condition known as gas gangrene in extreme cases.

About the author

Prof G

Professor of Neurology, Barts & The London. MS & Preventive Neurology thinker, blogger, runner, vegetable gardener, husband, father, cook and wine & food lover.


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  • I read this and assume this has something to do with the leaky gut theory.What I don't understand is why all MSers get offered the same treatment, aimed at the effect rather than the cause. I have MS and had the usual scans/LP but surely question 1 should have been what has caused this ie viral/bacterial. Extensive blood tests should be routine with more targeted treatment. I know the argument is that you cant treat all viruses, but isn't that where all the research should be aimed. I have the JC virus, and who knows what others but I will never get better until the cause is attacked and this isn't happening. I could not work out why nobody ever got better from MS, I think it is because it is being approached from the wrong point. I have no medical training, I am just an observer who has MS and see many others in the same boat all of us heading down the EDSS scale.

    • Let's see if the Charct project has any success, This aims to get at a cuase, is it the right target? Are the drugs good enough to get at the target? We will have to wait and see

  • Causation is the key. Why are all MSers given the same treatment? I was diagnosed following scans/LP but no focus on the cause. I know I have the JC virus, and maybe other viruses, surely the cause will vary from person to person, where only the effect is treated. This explains why nobody ever gets better. Just an opinion from someone with MS but no medical training, and very little hope!.

    • When I was in the process of being diagnosed for the cause of a dodgy sensory nerve 27 years ago, I had a spinal fluid examination which showed a virus was present. I was never told which virus, just that the virus might be temporary, and I would improve when it went away. No such luck, and 4 years later MS was confirmed.

      I recently had a positive test for the JC virus, which I think I caught 40years ago (from a girl with glandular fever). So I feel that a virus might have been a trigger for my MS, but that several other factors were also probably involved. The cases in the Orkney Islands may have a viral effect, as might the slightly different MS around Sardinia.

      Because several factors may be involved, with perhaps a virus as one trigger, it must be virtually impossible to identify a cause of MS, which is why we are hanging around so long for an answer. We all seem to have different symptoms from the MS, and respond to different drugs, which suggests our genes are involved too.

      A cure would be lovely, but at least we are seeing several symptom remedies now, and I am sure more are in the pipeline.

    • Remember Clostridium is a bacteria and the virus associated with glandular fever is Epstein Barr virus. There have been lots of electron microscopy studies in MS where i the fixation is good enough then it has t power to see structures smaller than a cell and bacteria should not be that hard to spot

    • It just needs some one to do the study again and if the toxin is the problem it would not be seen in the electron microscope. To repeat this it just needs a bank of serum/CSF and a few days/weeks if you have the detection assay sorted. However it has to be said that the toxin was not detected in the majority of MSers s the causality for most people is lacking is 1 toxin positive verses 99 negative (control) and 12 verses 106 (MSers) really that different? Although the authors suggest these figures could be a gross under estimate.

      The paper suggests that B tpye bacteria is a problem of cattle but it is interesting tonote that an company interested in MS has a treatment for cows.

  • Well, they reached statistical significance on the percentage of MSers showing immunoreactivity against the ETX (Epsilon Toxin produced by the Clostridium Perfringens type B bacteria) at serum levels compared to controls (10% vs. 1% on 118 patients and 100 controls). P-value (Chi-square test) was 0.0044.
    This is not the first study of this kind published. 3 years ago, in Munich university (and Max Planck institute), they found that mice depleted of all microbiome in their guts did not develop EAE ( Now they are trying to find identical twins (one with MS and the other without) in order to compare their gut microbiomes.
    From my point of view, this theory could explain the pathogenesis for a subset of us MSers (most probably not for all of us).
    The way you compare this study to the CCSVI theory would mean there is no scientific base on this theory from your perspective?

    • Can some check the stats?

      This is the "first time" is a few words to up the importance of a paper that people use. If the referees do their job they may note it is not the first time, however an abstract or partial web post is not currently considered as the first report. It is the full paper that counts, as an abstract may fail to stand up to the rigor of peer-review. Thus a study on microbiome could be found to be just SH1 🙂

      However, I am aware of these studies they were also presented at ECTRIMS 2013,you can check out the abstract presented by Prof Wekerle.

      "They way you compare CCSVI…your perspective?"

      Whilst I have my views on this.There is really a lot of scientific interest in the microbiome (Gut bacteria) at the moment. However, I believe this has the potential to become the next fad outside neurology, just as CCSVI became.


      Because you do not need a neurologist to change your microbiome. There are already clinics springing up to change your gut microbiota. You pay for a holiday in a clinic where they feed you SH1 and charge you for it. This bit of biology is being championed by some eminent scientists but can so easily be hijacked by the scammers.

      All we say is "Don't pay for unproven treatments"

  • Having recently been diagnosed, I can't help but agree with this possibility. 1 year ago exactly I began having acute bowel problems literally overnight following some questionable food… I still have these everyday having had doctors pass it off as IBS. 4 months after these symptoms began I had my first MS relapse. Maybe the biome theories floating around at the moment purported by T J Barody and his ilk may hold some promise yet???

  • Obviously association does not equal causation but the paper was interesting in providing a mechanism of BBB disruption by ETX. Authors also point out that retinal blood barrier is compromised with retinal vascular scarring in the absence of myelin. It seems BBB compromise is the important initiating event and leads to causation.

By Prof G



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