SUMMARY The faecal flora of 21 patients with proctocolitis and five patients with Crohn's disease of the large bowel was examined both while sulphasalazine was being administered and during control periods. Patients with proctocolitis and Crohn's disease who were not receiving sulphasalazine had a similar flora which did not differ in any way from the normal. The effect of sulphasalazine was to decrease the numbers of opalescent-negative clostridia, enterobacteria, and total non-sporing anaerobes. It is suggested that this antibacterial effect of sulphasalazine, which has not been previously demonstrated, may be related to the beneficial effects of this drug in proctocolitis and should be investigated further.Sulphasalazine (salicyl-azo-sulphapyridine, SASP) has been shown to be effective in the treatment of mild proctocolitis (Baron, Connell, Lennard-Jones, and Avery Jones, 1962;Dick, Grayson, Carpenter, and Petrie, 1964), and, more importantly, in the prevention of relapses of this disease (Misiewicz, Lennard-Jones, Connell, Baron, and Avery Jones, 1965;Dissanayake and Truelove, 1973). The metabolic pathways involved in SASP metabolism are now well established (fig 1) but the mechanism of the beneficial action remains unexplained. After ingestion, a proportion of the drug is absorbed and reexcreted unchanged in the bile and also partly in the urine; the major step in metabolism is reductive cleavage of the azo-link releasing 5-amino-salicylic acid (5-ASA) and sulphapyridine (SP) which is a sulphonamide. The latter is absorbed almost completely from the colon and excreted in the urine after a variety of conjugation processes, while the 5-ASA is only partly absorbed and excreted in the urine after acetylation (Hanngren, Hansson, Svartz, and Ullberg, 1963;Schroder and Campbell, 1972). These metabolic pathways are essentially similar both in healthy subjects and in proctocolitis patients (Das, Eastwood, McManus, and Sircus, 1973).Experiments with germ-free animals have shown that the initial azo-link reduction takes place in the colon and depends on the presence of colonic bacteria (Peppercorn and Goldman, 1972; Schroder and Gustaffson, 1973), a finding supported by observations in ileostomized subjects (Schroder, Lewkonia, 'Requests for reprints should be sent to Dr R. Lendrum,