Although Crohn's disease (CD) is considered to be autoimmune, there is increasing evidence that its etiology is infectious. The most plausible candidate is Mycobacterium avium ssp. paratuberculosis (MAP). Compellingly, Koch's postulates have been fulfilled for MAP and CD, even though they still have not been met for M. leprae and leprosy. In animals MAP causes Johne's disease a chronic wasting intestinal diarrheal disease evocative of CD. Johne's disease occurs in wild, agricultural and domestic animals, including dairy herds. Viable MAP is found in human and cow milk, and is not reliable killed by standard pasteurization. Pathogenic in humans, MAP is found ubiquitously in the environment including potable water. Since cell wall deficient MAP cannot be identified by Ziehl-Neelsen staining, in man identifying MAP requires detection of its DNA, RNA or by culture. Reminiscent of H. pylori and stomach ulcers, if infectious CD should be curable with appropriate antibiotics. Multiple studies arguing against an etiological role for MAP in CD employed antibiotics that are inactive against MAP. Recent data, from trials including macrolides indicate that a cure of CD is possible. The necessary length of therapy remains to be determined. Mycobacterial diseases have protean clinical manifestations, as does CD. The necessity of stratifying CD into two clinical manifestations (perforating and non-perforating) when interpreting the results of antibiotic therapy is discussed. Apparent paradoxes, such as the effect of immune-modulation and the discovery of a "Crohn's related gene", are addressed. Rational studies to evaluate appropriate therapies to cure CD are proposed.