Many microbial pathogens and toxins exhibit elaborate mechanisms of engagement with mammalian cell structure and cell biochemistry. For instance, some toxins gain entrance into cells using exquisite secretory devices and, once inside cells, interact in very specific ways with intracellular membrane trafficking factors and cell signaling components. Because many microbial pathogens and their associated toxins appear to be created to interact with human cells, they are difficult to explain within the context of a “good creation.” In this paper, we examine the pathogenic role of V. cholerae, the cholera toxin (CT) and other associated virulence factors, and their origin in the context of the creation model. We examine the literature and use methods of genomic comparison to investigate the origin of CT and the corresponding origin of cholera. Our results are consistent with a model of nonpathogenic function for CT prior and even after the Fall. We suggest that the originally beneficial function of CT has been subsequently modified by the presence of phages and mobile genetic elements.
