Similarities between chronic idio-pathic granulomatous ileocolitis and mycobacterial infections have been noted since the original descriptions of the clinical syndrome now called Crohn’s disease. 1–4 Interest in a possible infectious origin of this disorder was renewed in 1989 when Chiodini et al cultured apparently identical Mycobacterium avium subspecies paratuberculosis (MAP) from three patients with Crohn’s disease. 5 This controversy increased in intensity following the detection of the specific DNA insertion sequence, IS900, of MAP in relatively high numbers of patients with Crohn’s disease relative to ulcerative colitis and normal controls, 6 and is now raging as several different groups have detected this organism in the food chain7 and water supply, 8 proposed maternal-fetal transmission in human milk, 9 reported long term responses to antimycobacterial antibiotic combinations, 10 and even cultured viable M paratuberculosis in blood samples of Crohn’s disease patients. 11

Additional data to support an association of MAP with Crohn’s disease is provided by Autschbach and colleagues12 in this issue of Gut (see page 944). This carefully performed and well controlled study used nested polymerase chain reaction (PCR) to detect the IS900 insertion element of MAP in 52% of Crohn’s disease resected tissues versus 2% of ulcerative colitis and 5% of mostly non-inflammatory control tissues. This study provides novel data regarding the prevalence of MAP in various phenotypes of Crohn’s disease by showing slightly higher detection of IS900 DNA in colonic (66.7%) compared with distal ileal (40.5%) tissues and decreased detection rates with corticosteroid use. In addition, these authors reported weak associations with perianal involvement and a shorter duration of disease but no correlation with patient sex, age at diagnosis, stricturing versus penetrating phenotype, or presence of granulomas.