For two decades, Crohn’s disease has been presented to physicians as an autoimmune disease whose mechanism of action was the induction of inflammation and whose therapy focused on disrupting the immune system’s pro-inflammatory response. Strictures, fistula, loop-to-loop anastomosis, and bowel perforations that occurred were attributed to inadequate drug therapy.
Dr. Gilles R. G. Monif argues in his book “The Prevention and Therapy of Crohn’s Disease that Crohn’s disease is an immune-mediated disease whose mechanism of action involves the creation of a persisting, dysfunctional immune response to Mycobacterium avium subspecies paratuberculosis at its points of attachment to the gastrointestinal tract. Eventually, antigen concentration and repeated antigen challenges focally outstrip the regenerative capacity of the gastrointestinal mucosa. Bacteria within the gut flora gain can then access the submucosa and, if unchecked, initiate the anaerobic progression. Strictures, bowel penetration, or fistula that occur in individuals who have Crohn’s disease are not due to inflammation. They are the consequences of untreated or under-treatment of the penetrating gastrointestinal microbiota and its use of anaerobic progression to achieve bowel perforation.