Pathogenic strains of V. cholerae O1 and O139 possess two key virulence factors – cholera toxin (CT) and the toxin co-regulated pilus (TCP). TCP is a surface pilus that aggregates organisms together on the surface of the small intestine [33]. CT is a prototypical AB subunit toxin. The B subunit binds the toxin to gangliosides on the surface of epithelial cells, which allows for the enzymatically active A subunit to be translocated into the cell [34]. Once inside the cell, the A subunit increases cyclic AMP activity, leading to chloride secretion at the apical surface. Concurrent losses of sodium and water lead to the massive fluid and electrolyte efflux that is the hallmark of cholera.