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Colitis is inflammation of the bowel that can be acute or chronic. Acute inflammatory changes are usually self-resolving and are caused by specific infections such as shigella, salmonella, amoebae or Campylobacter jejuni to give few examples. These do not require any treatment with human probiotics since they are self-limiting or can be treated with specific antibiotics. Chronic inflammation can also be caused by chronic infections eg C difficile, Dientamoeba fragilis, and E. histolytica.26

In patients with chronic colitis of unknown origin various subdivisions of the condition have been made. Patients can have a microscopic colitis, which presents as chronic diarrhoea and cramping but colonoscopically there are no areas of inflammation until one takes a biopsy and then typical inflammatory cells are visible under the microscope. Other patients have classic distal where colonoscopically inflammatory changes begin at the rectum and can extend to a variable distance up the bowel. In some patients the entire bowel is involved in colitis and this is called pan-colitis. Crohn's and collagenous colitis make up other subdivisions.

The treatment of colitis has been generally standardised throughout the world and usually requires anti-inflammatory drugs such as corticosteroids (eg. prednisone), 5-aminosalicylic acid (5-ASA) compounds (eg. sulfasalazine, olsalazine, mesalazine), azathioprine, 6-mercaptopurine, cyclosporin, and antibiotics such as metronidazole, ciprofloxacin and vancomycin. Most of these agents, except for prednisone, also have anti-microbial actions, which points to the fact that colitis is almost certainly a chronic infection with a hitherto undescribed pathogen or pathogens. Among theories on causation of colitis it is generally thought that a passing bowel infection initiates an ongoing autoimmune response. The basis for this is - in part - the observation that we cannot find a pathogenic organism that causes colitis, and that it appears to respond to immunity-modifying drugs. Yet colitis may also follow an acute bowel infection-like episode. Other chronic infections such as Helicobacter pylori, hepatitis B or C, bronchiectasis, or fungal infections of the skin do not set up an ongoing 'autoimmune' condition. Hence, from the observation of other infections in the body it is highly unlikely that colitis is anything more than a chronic infection causing chronic inflammation and the infection has simply not been found. A similar situation has been operating in Crohn's disease where an immune reaction to an unknown pathogen has been invoked as the mechanism. It is now unlikely that this is the mechanism operating but rather that Mycobacterium avium ssp. paratuberculosis (Map) is the ongoing infection that starts up and maintains the inflammation. ( www.crohns.org )

From these simple observations it is likely that ulcerative colitis, along with microscopic colitis, represents the visible effects of a chronic infection of the gut flora which science has not yet identified. It is likely that this infection through the release of various cytokines produces the clinical picture we call colitis. Although FMT has been successful in reversing colitis24, 25 this treatment is less successful in colitis than it is in C. difficile diarrhoea and pseudomembranous colitis. The reason for this is unclear but we may be dealing with a pathogen or pathogens which are not as easily destroyed by the influx of normal human bacterial flora. Furthermore, in C. difficile diarrhoea and in patients with diarrhoea-predominant IBS the bowel is generally not inflamed and this may allow for easier implantation of a new bacteria onto the bowel mucosa than it is in colitis. In chronic colitis the implantation of the flora may be less likely on the inflamed tissues. We have noticed that if patients are given standard anti-inflammatory therapy until their bowel wall is completely healed, FMT can achieve long term reversal of colitis in more than 50% of patients in our experience, but the result is still unpredictable in the individual case. In addition if C. difficile co-exists in patients with chronic ulcerative colitis FMT can eradicate C. difficile and reduce the severity of the condition in such patients. Furthermore, the removal of associated parasites, especially D. fragilis which in itself can cause colitis,26 27 can also reduce the severity of colitis. We have patients who have had co-existing D. fragilis, Blastocystis hominis and C. difficile and whose severity of ulcerative colitis could be dramatically improved simply by removing the co-existing pathogens by either specific anti-parasitic agents or by FMT. C. difficile is typically 'impossible' to remove by the use of vancomycin, metronidazole or rifampicin in patients with chronic colitis.