ESR2 and infection: The inverse kinetics of the requirements for rpoS and esrB support a model where rpoS is required early in infection to activate genes required for adaptation to host-derived stresses (e.g. rpoS, cadA1, cadB1, cadB3, uspB, cspA, cspG, cspH, cspI, speAB, speG, trxC, dps, phoR, csrA); later, presumably at the point when the pathogen begins to occupy the niche where T3/T6SS enable growth, rpoS becomes dispensable, because its repression of esrB inhibits production of these secretion systems.