Abstract

The establishment of a phylogenetic tree is a prerequisite for studying the evolution of virulence. The current nomenclature of the genus Salmonella is based on this phylogenetic tree and distinguishes only two species: Salmonella enterica and Salmonella bongori. If acquisition of SPI-1 introduced a virulence factor required for the pathogenesis of diarrheal disease, then mutational inactivation of this determinant should attenuate Salmonella serotypes in animal models of gastroenteritis. The contribution of the invasion-associated type III secretion system to serotype Typhimurium pathogenesis in this animal model has recently been investigated using strains carrying mutations in hilA and prgH. The majority of antibodies elicited by immunization with heat-killed serotype Typhimurium or with a live-attenuated serotype Typhimurium aroA vaccine is directed against the immunodominant O-antigen. Mathematical models predict that in this between-serotype competition, the serotype with higher transmissibility will dominate and eventually eliminate its competitor. The generation of O-antigen polymorphism through horizontal gene transfer was therefore a likely mechanism that allowed Salmonella serotypes to adapt to the enhanced immune memory encountered in warm-blooded hosts. The fljB gene is present in biphasic S. enterica subspecies but absent from monophasic S. enterica subspecies and Escherichia coli, suggesting its acquisition by horizontal gene transfer. A primary pathogen can be defined as an organism capable of entering a host and finding a unique niche to multiply and avoid or subvert the host defenses, the outcome of which may be clinical disease manifestations.

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