ABSTRACT
The infl ammatory bowel diseases, Crohn’s disease and ulcerative colitis, are distinct and heterogeneous syndromes. However, a consensus of evidence suggests that most cases of infl ammatory bowel disease (IBD) represent the outcome of complex interplay among genetic susceptibility risk factors, environmental triggers, and disturbed immune responses to the enteric microbiota. Genetic risk factors appear to code for proteins involved in sensing or regulating the host response to the microbiota or in maintenance of mucosal barrier function (Jostins et al. 2012). Given the underpinning disturbance of host-microbe interactions, and the degree of mucosal tissue injury in both Crohn’s disease and ulcerative colitis, it is remarkable that opportunistic infections are not more common than has been evident to date. This may be about to change as increasing concern is voiced in relation to the increasing use of immunosuppressive and immunomodulatory drugs and the persistent, albeit diminishing, concomitant use of corticosteroids.
