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Interesting.....http://weill.cornell.edu/news/releases/ ... 6_13.shtml

marcopolo wrote:Interesting.....http://weill.cornell.edu/news/releases/ ... 6_13.shtml

Interesting indeed. Can you imagine if a certain bacteria is the trigger of MS and using a particular anti-biotic becomes the treatment. Big pharma who makes the DMDs certainly won't be happy. Wonder how long it will take them to publish a study to discredit this initial find?

From the article, it appears a probiotic would be the cure. Also, the article mentions that animals infected with this bacteria appear to suffer the MS like symptoms when fed a carbohydrate-rich diet. Perhaps, for humans infected with the same bug, a high-carb diet is also a bad idea.

I haven't read the article or more on the bacteria, but in my mind, I would of thought most bacteria would be affected by antibiotics; for a quick win, not long term management.

and here is the original article from which the news is sourced. You can download a PDF as well.
http://www.plosone.org/article/info%3Ad ... ne.0076359

The right bacteria would prevent the wrong bacteria from getting a foothold (proper gut flora). Antibiotics can wreak havoc with our gut, hence the migration towards such treatments as fecal transplants and "poop pills."

doesn't seem likely considering huntergathering tribes eat the intestines and the stomach of animals they kill which contain this said pathogen. So all hunter gatherers would have it, I don't know we'll see how it unfolds. seems more like a commonality more so than a cause.

I think we all absorb pathogens everyday. The root cause could not be the bacteria itself, but the lack of good bacteria to eradicate the bad one.
MSers have gut dysbiosis, lack of lactobacillus or certain types of bifidobacteria. Many Msers also have candida overgrowth, due to this lack of beneficial bacteria.
Poor diet, lack of vitamine D, too much stress, are all factors that cause gut dysbiosis, and MS.
People who have had an appendectomy are more likely to develop MS, as well as Clostriduim difficile infection. And this organ attached to the colon is now known to be a safe house for beneficial bacteria in case of infection.
It has recently been proved that fecal transplant is much more effective than antibiotics to treat C. diff infection. With 95% success. So it should be a good solution to treat C. perfrigen infection too,… and MS.

This pathogen, Clostridium perfringens, has been associated with a lack of protease in animals. For instance, in the following study low trypsin (trypsin is a protease) was listed as a predisposing factor in the development of Clostridium perfringens infections in animals.

J Vet Med B Infect Dis Vet Public Health. 2004 Dec;51(10):423-6.
Significance of beta 2-toxigenic clostridium perfringens infections in animals and their predisposing factors--a review.
Schotte U, Truyen U, Neubauer H.


"The novel beta 2-toxin of Clostridium perfringens has recently been described as the cause of enteric diseases in animals. The biological activity of beta 2-toxin is similar to that of the beta1-toxin with a possibly weaker cytotoxic activity. However, the production of beta 2-toxin in vitro is not seen in all beta 2-toxin-gene (cpb2)-positive C. perfringens strains, and to deduce a clinical importance solely from the detection of cpb2 is difficult. Detection of cpb2-positive C. perfringens from various animal species with and without enteric diseases demonstrates the wide distribution of cpb2 in nature, and the presence of cpb2 gene is therefore not considered a risk by itself. Predisposing factors like low trypsin activity in the intestinal tract, antibiotic and/or antiphlogistic treatment or changes in diet can result in the selection of beta 2-toxigenic C. perfringens which may lead to enteritis or enterotoxaemia.




The following information from the Merck Manual states: "This toxin is sensitive to proteolytic enzymes, and disease is associated with an inhibition of proteolysis in the intestine". In addition, it states that colostrum, which contains a trypsin inhibitor has been suggested as a factor for increasing the disease susceptibility of young piglets.


Enterotoxemia Caused by Clostridium perfringens Types B and C

"Infection with Clostridium perfringens types B and C causes severe enteritis, dysentery, toxemia, and high mortality in young lambs, calves, pigs, and foals (see Clostridial Diseases: Enterotoxemia Caused by Clostridium perfringens Types B and C). Types B and C both produce the highly necrotizing and lethal beta toxin that is responsible for severe intestinal damage. This toxin is sensitive to proteolytic enzymes, and disease is associated with inhibition of proteolysis in the intestine. Sow colostrum, which contains a trypsin inhibitor, has been suggested as a factor increasing the susceptibility of young piglets. Type C also causes enterotoxemia in adult cattle, sheep, and goats."
http://www.merckmanuals.com/vet/general ... emias.html



The following information from Wiki states that trypsin shortages in the digestive system of experimental animals has been used to "induce" Clostridium perfringens type C.


"Clostridium perfringens beta toxin one of the four major lethal toxins produced by Clostridium perfringens Type B and Type C strains...C. perfringens beta toxin is susceptible to breakdown by proteolytic enzymes, particularly trypsin. Beta toxin is therefore highly lethal to infant mammals because of trypsin inhibitors present in the colostrum...It is primarily fatal to animals 1–3 days old, whose digestive enzymes may not be sufficiently active to break down beta toxin. It has been experimentally shown that trypsin may normally break down beta toxin and trypsin shortages in the digestive system of experimental animals has been used to induce type C disease."
http://en.wikipedia.org/wiki/Clostridiu ... beta_toxin




In the following information it states that ingestion of a protein-rich diet in a protease-deficient intestinal tract allows for "rapid growth" of Clostridium perfringens organisms.


Managing Clostridial Diseases in Cattle
Sheila M. McGuirk, DVM, PhD


"Possible risk factors for calves
o Ingestion of C. perfringens in the first few days of colostrum feeding
o Ingestion of protein-rich diet in a protease-deficient intestinal tract allows rapid growth of C. perfringens organisms"
http://www.vetmed.wisc.edu/dms/fapm/fap ... ridial.pdf


The following information states that the digestive enzyme trypsin is a "Clostridium-destroying" digestive enzyme.

Perfringens Type C usually occurs in newborns, as they have a low population of protective normal gut flora and their diet is colostrum, which contains an inhibitor of the Clostridium-destroying digestive enzyme trypsin.

http://vads.vetmed.vt.edu/demos/Educati ... PerfFS.htm


I have been making some posts under the thread "Some Interesting Connections" on how protease and another digestive enzyme called DNase 1 is involved in the MS disease process.

Very interesting thread. I think this finding is interesting too!!

The absence of an inflammatory infiltrate in nascent lesions argues against MS beginning as an autoimmune phenomenon and instead favors a toxin or viral etiology. We reasoned that the environmental trigger for initial lesion formation in MS might be a soluble toxin based on the histopathologic features of the nascent lesion.

http://www.plosone.org/article/info:doi ... ne.0076359


edit: Or this part of the study

The epsilon toxin travels through the blood to the brain, where it damages brain blood vessels and myelin, the insulation protecting neurons, resulting in MS-like symptoms in the animals. While the D subtype has only been found in two people, based on prior studies by other investigators, the B subtype had never been found in humans.

How does CCSVI come into play..??? Seems to me more evidence CCSVI is the effect of MS and not the cause and should be treated!!

This bacteria was already analyzed 1000 years ago, why they suspect it to be root cause now?

some more information:
http://www.direct-ms.org/sites/default/ ... Review.pdf

"One such toxin which breaks down the blood-brain barrier and causes ataxia
and blindness in sheep is the epsilon toxin of Clostridia Perfringens type
D"

Is there any lab test to detect this bacteria or to measure epsilon toxin level?

leonardo wrote:Is there any lab test to detect this bacteria or to measure epsilon toxin level?

Its been a while since I read the article, but i am pretty sure it described their methods to test for the bacteria; and confirmation. l though it did not sound like a standard test you could ask yr dr for.

grandsons4 wrote:The right bacteria would prevent the wrong bacteria from getting a foothold (proper gut flora). Antibiotics can wreak havoc with our gut, hence the migration towards such treatments as fecal transplants and "poop pills."

CureOrBust wrote:...for a quick win, not long term management.

I tried to be clear that I only mean as a quick attempt to see the effects, not long term management. The "havoc with our gut" would hopefully include the die off of this bad bacteria.

I decided to try some probiotic.

After reading this study I bought one with lactobactillus plantarum:

http://www.ncbi.nlm.nih.gov/pubmed/23471038

In vitro inhibition of Clostridium difficile and Clostridium perfringens by commercial probiotic strains.

I'm currently looking into growing kefir, and eating fermented foods grown at home. Apparently good sources of probiotics.

LR1234 wrote:I'm currently looking into growing kefir, and eating fermented foods grown at home. Apparently good sources of probiotics.

Kombucha is a high probiotic beverage made from fermented tea. Very easy to make at home once you get a starter culture (scoby). Tastes like a tangy, bubbly cider.

http://www.thekitchn.com/how-to-make-ko ... ome-173858