: Mycobacterium avium spp. paratuberculosis (MAP) is the causative agent for Johne’s disease, an incurable, chronic, infectious enteritis of ruminants, which results in diarrhoea, weight loss and, ultimately, death. Because of the similar pathology of Johne’s and Crohn’s disease in humans, MAP has also been proposed as the aetiological agent of Crohns’ disease. The latter is a chronic inflammatory disease that most commonly affects the distal ileum and colon, but it can occur in any part of the gastrointestinal tract. The organism has been isolated from the large intestine of patients suffering from Crohn’s disease and antibodies to MAP proteins can be isolated from sera of sufferers. However, evidence against MAP being the cause of Crohn’s disease has also been amassed. These opponents to the role of MAP as the cause of Crohn’s point to a large trial conducted in Australia, which concluded that there was no prolonged remission of disease when antimycobacterial drugs were administered. MAP has been isolated from raw and pasteurized milk and this led to the conclusion that the organism could survive pasteurization. There have been many studies to determine the accuracy of this statement but definitive experiments conducted in New Zealand indicate that the organism is unable to survive HTST pasteurization. Because the organism is difficult to cultivate, there has been an interest in the development of rapid diagnostic tests. These involve immunological and molecular approaches, both of which have advantages and disadvantages. Several approaches have been adopted to control the bacterium, including vaccination, but the most effective approach involves culling calves of infected cows, early culling of suspect cows and test reactors along with animals that have been in contact with these cattle. In conclusion, a causal link between MAP and Crohn’s disease has yet to be established but the precautionary principle approach has been advocated until the role of the organism has been definitively recognized. However, elements of the disease appear to consist of genetic predisposition, immune-mediated tissue damage and enteric factors such as intestinal microbial flora and so it is unlikely that a single aetiological agent is responsible.