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The ability of Salmonella typhimurium to synthesize enterochelin (enterobactin; ENT) affects its capacity to grow both in vivo and in vitro. An ENT mutant (96-1), blocked in the conversion of chorismate to 2,3-dihydroxybenzoate, was derived from SR-11, a strain of high mouse virulence. This mutant was unchanged in the other characteristics tested: colonial, biochemical, antigenic, and cellular. In contrast to SR-11, growth of this mutant in complement-inactivated human serum was strongly inhibited. However, addition of 5 muM ENT to the cultures relieved their inhibition. Viable counts of bacteria injected into the mouse peritoneal cavity showed that without ENT, growth of 96-1 was inhibited markedly; with ENT, the apparent growth rate of 96-1 exceeded that of SR-11. The 50% lethal dose (LD50) of 96-1 was 2 to 3 log units higher than that of SR-11. When ENT was injected, the ENT- mutant exhibited an ENT-dose-related decrease in its LD50. A single injection of 300 micrograms of ENT per mouse with the inoculum reduced the LD50 of 96-1 to that of the wild-type strain. These findings support the contention that ENT is a virulence factor for S. typhimurium.
Yancey et al. (Sun,) studied this question.