Ulcerative colitis (UC) is a chronic inflammatory condition of the large bowel of unknown aetiology, characterised by the presence of bloody diarrhoea and mucus associated with a negative stool culture for bacteria, ova, or parasites.

This definition finds its historical rationale in the first supposed description of the disease by Wilks and Moxon more than one century ago (1875)1; they reported a case of bloody colitis that was apparently not caused by dysenteric pathogens. Later, Sir William Hale-White reported upon occasional patients with severe ulceration of the colon not due to tuberculosis, typhoid fever, or malignant disease. The origin remained obscure, however, and he felt this condition should not be confused with bacillary dysentery.2

Since these first descriptions, are there now data supporting a non-bacterial origin of the disease as suggested, or have we found evidence to support a bacterial role in the onset of symptoms?

In the last decade, the dogma that no bacteria could grow in the acid milieu of the stomach has been systematically destroyed by the evidence that an infective agent, Helicobacter pylori, is responsible for gastric/duodenal disease.3 If only a few thousand bacteria can cause gastritis, can we be so sure that among the billions of bacteria living within the colon some strains are not responsible for the onset of intestinal inflammation or for its perpetuation?

During the period 1938–1954, the only drug available for treatment of UC was sulphasalazine (SASP). Nanna Svartz used SASP, which is composed of a sulphonamide-sulphapyridine and a salicylate-5-aminosalicylic acid (5-ASA). Because of its anti-bacterial activity, it was postulated that the onset of UC might have some linkage with bacteria.4Though we know today that 5-ASA is the active part of SASP,5 a recent meta-analysis showed a trend towards a superior efficacy of …