One study showed that two-thirds of tissue samples from those with Crohn's had evidence of the bacterium, but only 5 per cent of those with ulcerative colitis did (Gut, 1992; 33: 890-6).

Professor John Hermon-Taylor at St George's Medical School in London has been investigating the condition for many years (Appl Environ Microbiol, 1996; 62: 3446-52).

According to his research, M paratuberculosis was found in up to one in four samples of whole pasteurized milk randomly obtained from retail outlets, suggesting that it cannot be wholly destroyed by the pasteurizing process.

Another study confirms the findings that pasteurization process does not completely destroy M paratuberculosis (App Environ Microbiol, 1996; 62: 631-6). Its presence in Crohn's patients may explain in part why Crohn's sufferers can react so badly to milk and other dairy products

It is further claimed that if M paratuberculosis is responsible for intestinal disease, filing the whole range of disorders under the banner of Crohn's may be misleading. Intestinal tuberculosis, also a mycobacterial disease, is very similar to Crohn's (J Gastroenterol Hepatol. 1996; 11: 183-6; BMJ, 1975; 4: 395-7), but the treatment of the two conditions is very different.

For instance, corticosteroids a mainstay of Crohn's treatment may make intestinal tuberculosis worse (J Gastroenterol Hepatol, 1996; 11: 532-4).

That said, the cause of Crohn's remains elusive, and other researchers claim that the link between Mycobacterium, while strong, is not convincingly established (Scand J Gastroenterol, 1990; 175 (Suppl): 93-6). Mycobacterium can be difficult to culture in the laboratory, and some still doubt that it plays a part in causing Crohn's (Gut, 1995; 37: 660-7).

Dr Andrew Wakefield at the Royal Free Hospital, London, has been conducting research into Crohn's for many years. Recently, he suggested that, instead of being an ulcerative disease, Crohn's may be caused by restricted blood flow in the blood vessels which feed the lining of the gut.

What causes the constriction in the first place is not known. It could be that small tumours, or granulomas, form within the walls of the blood vessels causing vascular injury (Gastroenterol, 1991; 100: 1279-87). But Wakefield's belief is that the missing link between granulomas and vascular constriction is a persistent measles virus (Gastroenterol, 1995; 108: 911-6; J Med Virol, 1997; 51: 90-100; J Med Virol, 1993; 39: 345-53).

According to his research, exposure to the measles virus in the womb or shortly after birth greatly increases the risk of contracting Crohn's later in life (Lancet, 1996; 348: 515-17). In a review of four counties' health records in Sweden, Wakefield and his colleagues identified all those who were born between 1945 and 1954 who had Crohn's diagnosed before the age of 30 (Lancet, 1994; 344: 580-10). Yearly reports showed that five measles epidemics had affected all four counties over the trial period. The number of cases of Crohn's significantly exceeded the researchers' expectations: 57 versus 39. For those with ulcerative colitis the actual number, 42, was close to what they expected: 47.

According to Wakefield it could be the measles vaccine and not the circulating virus which may be responsible for the rising rates of Crohn's in children. When a large study in Scotland looked at data from 1968 to 1983, it discovered that cases of Crohn's in children have risen by more than seven times from four per million to 29 per million (Gut, 1989; 30: 618-22). Other studies point to the fact that during that time, although cases of live measles dropped drastically, the measles vaccine was introduced and widely used (Lancet, 1995; 345: 1071-73).