Human genetic defects and misinterpreted pharmacological data indicate that Crohn disease is consequent to a mycobacterial infection.

Abstract

For more than a century, there has been controversy whether Crohn’s disease is a cryptic zoonotic mycobacterial infection. In this manuscript we address two, usually ignored, critical elements that suggest that this concern is probably correct. First: human genetic defects identified in Crohn’s disease are associated with increased susceptibility to mycobacterial infections. Second: multiple pharmaceutical agents that are used in Crohn’s disease are misnamed. Many “anti-inflammatories” and “immune modulator” medications have dose dependent inhibition of mycobacteria in culture. Accordingly, their primary mechanism of action are as antimycobacterial antibiotics. Failure to incorporate these data renders all previous antibiotic studies in Crohn’s disease irrevocably flawed. Finally, incorporating these genetic and antibiotic data, we suggest the necessary clinical studies to address the hypothesis that Crohn’s diseases is a zoonotic infection.