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Probiotics & Clostridium difficile

C. difficile bacteria under microscopic inspection

What is Clostridium difficile?

Clostridium difficile (C. difficile or C. diff) is a species of bacteria that is present naturally in the gut of around 60% of children under the age of 1 years old and 3% of adults.[1],[2] C. difficile does not cause any problems in healthy people with a well balanced gut microbiota. However, antibiotics that are used to treat other health conditions can cause dysbiosis, a condition where the normal gut microbiota is disrupted; compromising a vital part of our immune system and allowing C. difficile to multiply.

Pathogenic strains of C. difficile produce two large protein exotoxins; known simply as toxin A and toxin B.[3] These toxins can induce intestinal inflammation, fluid secretion and mucosal injury.[4],[5] This can result in conditions such as C. difficile-associated diarrhoea (CDAD) and, in more serious cases, colonic damage and pseudomembranous colitis.[6]

Who is at risk?

C. difficile cases occur most commonly in healthcare environments such as hospitals or care homes where patient populations are at higher risk of infection. In the hospital environment, C. difficile is the biggest known cause of infectious diarrhoea in the developed world.[7]


C. difficile infections are most commonly treated with metronidazole or vancomycin antibiotics. Whilst this treatment is effective for most, the disease does recur after therapy in 20% of the outpatient population.[8] In these cases, multiple recurrences are common and can be difficult to treat.[9] Pioneering techniques such as faecal transplants, whereby a healthy donor’s faecal matter is transplanted into a C. diff sufferer’s intestinal tract, have shown initial success in those with multiple recurrences of the disease. (Read our news piece on faecal transplants).

Scientific research on probiotics and C. difficile

A number of studies show that Saccharomyces boulardii, the probiotic found in For bowel calm, may protect against infection and gastrointestinal inflammation induced by C. difficile.[10],[11] ,[12] One randomised, placebo controlled study revealed that S. boulardii, in combination with a standard oral antibiotic, may be more effective in decreasing the likelihood of C. difficile recurrences than standard therapy alone. The efficacy of S. boulardii was significant with a recurrence rate of just 34.6%, compared with 64.7% on placebo.[13] In-depth research has also elucidated the mechanism of action of S. boulardii against C. difficile. Studies have shown that S. boulardii may interfere with the pathogenic process of C. difficile by releasing a 54kDa protease; which may inactivate C. difficile toxins A and B and lyse colonic receptors.[14],[15] Furthermore, Saccharomyces boulardii is also known to stimulate the host’s intestinal mucosal immune response, by stimulating an increase in secretory IgA.[16],[17]

Read more about Saccharomyces boulardii.


[1] NHS Statistics 17/03/2010

[2] McFarland, L.V. (1999) Possible role of cross-transmission between neonates and mothers with recurrent Clostridium difficile infections. Am J Infect Control. 27: 3:301-303

[3] Pothoulakis, C. (1996) Pathogenesis of Clostridium difficile-associated diarrhoea. Eur. J. Gastroenterol. Hepatol. 8:1041-1047

[4] Dove, C. H. et al. (1990) Molecular characterization of the Clostridium difficile toxin A gene. Infect. Immun. 58:480-488

[5] Just, I. et al (1995) The enterotoxin from Clostridium difficile (ToxA) monoglucosylates the Rho proteins. J. Biol. Chem. 270: 11074-11078

[6] Riegler, M. et al. (1995) Clostridium difficile toxin B is more potent that toxin A in damaging human colonic epithelium in vitro. J. Clin. Investig. 95:2004-2011

[7] Fekety, R. (1997) Guidelines for the diagnosis and management of Clostridium difficile-associated diarrhea and colitis. American College of Gastroenterology, Practice Parameters Committee. Am. J. Gastroenterol. 92: 739-750

[8] Fekety, B. et al (1989) Treatment of antibiotic-associated Clostridium difficile colitis with oral vancomycin: comparison of two dosage regimens. Am J Med. 86:15-19

[9] Surawicz, C. M. (2003) Probiotics, antibiotic-associated diarrhoea and Clostridium difficile diarrhoea in humans. Best Practice & Research Clinical Gastroenterology; 17: 5; 775-783

[10] Castex, F. et al (1990) Prevention of Clostridium difficile-induced experimental pseudomembranous colitis by Saccharomyces boulardii: a scanning electron microscopic and microbiological study. J. Gen. Microbiol. 136: 1085-1089

[11] Corthier, G. et al (1986) Prevention of Clostridium difficile induced mortality in gnotobiotic mice by Saccharomyces boulardii. Can. J. Microbiol. 32: 894-896

[12] Corthier, G et al (1992) Effect of oral Saccharomyces boulardii treatment on the activity of Clostridium difficile-toxins in mouse digestive tract. Toxicon 30: 1583-1589

[13] McFarland, L. V. et al (1994) A randomised placebo-controlled trial of Saccharomyces boulardii in combination with standard antibiotics for Clostridium difficile disease. Journal of the American Medical Association. 271: 1913-1918

[14] Castagliuolo, I. et al (1999) Saccharomyces boulardii protease inhibits the effects of Clostridium difficile toxins A and B in human colonic mucosa. Infect. Immun. 67: 302-7

[15] McFarland, L. V. et al (1994) A randomised placebo-controlled trial of Saccharomyces boulardii in combination with standard antibiotics for Clostridium difficile disease. Journal of the American Medical Association. 271: 1913-1918

[16] Arnheim, K. (1994) Intestine-associated immune system stimulation. Saccharomyces boulardii – mechanism of action. Fortschr. Med. 112: 52-53. (In German)

[17] Elmer, G. W. (1996) Biotherapeutic agents. A neglected modality for the treatment and prevention of selected intestinal and vaginal infections. JAMA 275: 870-876



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