**2.2 Aetiology**

The aetiology is unknown but evidence suggests an immune dysfunction which is triggered by an environmental factor in a genetically susceptible individual (Cho, 2008) leading to chronic inflammation and injury to the gastrointestinal tract. Many of the susceptibility genes identified in recent studies have been shown to have important roles in immune regulation but there is increasing evidence that these genes pertain to the innate immune system and are involved in the sensing or intracellular processing of bacteria (Packey and Sartor, 2008). Potential microbial triggers which have been studied include a form of enteroadherent *Escherichia coli* and *Mycobacterium paratuberculosis,* but more recent investigation suggests that a disturbance of normal enteric microflora may play a role in aetiology (Sartor, 2008). Additionally, a number of other potential environmental factors have also been studied including diet, smoking, appendiceal inflammation, certain drugs and stress but causality has remained difficult to establish (Bernstein, 2010). The particular combination of susceptible genes and environmental triggers probably varies between individuals with IBD and leads to different patterns and severity of disease.

Ulcerative colitis causes a continuous mucosal inflammation of the colorectum, whereas Crohn's disease can affect any part of the GI tract, characteristically with skip lesions and transmural inflammation. Additionally, chronic inflammation in Crohn's disease can lead to fistulising and stricturing disease behaviours (Satsangi et al., 2006).
