S.typhimurium

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Classification

Bacteria; Domain; Proteobacteria; Gammaproteobacteria

Species

Salmonella choleraesuis serotype typhimurium; Salmonella typhi-murium; Bacillus typhimurium

Description and Significance

S.typhimurium is a genus of rod-shaped, Gram-negative, nonspore forming,and motile enterobacteria with diameters around 0.7 to 1.5 µm, lengths from 2 to 5 µm, and flagella that grade in all directions[5]. They are chemoorganotrophs, obtaining their energy from oxidation and reduction reactions using organic sources, and are facultative anaerobes. Most species produce hydrogen sulfide, which can be detected by growing them on media containing ferrous sulfate, like TSI[5]. Most isolates exist in two phases: a motile phase I and a nonmotile phase II. Cultures that are nonmotile upon primary culture may be switched to the motile phase using a Cragie tube[2].

Genome Structure

The genome structure of Salmonella typhimurium has a chromosome that is 4,857 kilobases long and a virulence plasmid that is 94 kilobases long[2].

Cell Structure, Metabolism and Life Cycle

S. typhimurium can secrete small signaling molecules called autoinducers. The LuxS gene is responsible for initiating the phosphate transfer reactions that produce this molecule and allow for cell to cell communication[4]. Sugar compounds like glucose activate LuxS and the autoinducer concentration increases with the bacterial concentration until the substrate is done. At this point the autoinducer is degraded and can be recycled by the bacterial cell. This quorum sensing allows cells to determine the metabolic potential of the environment[4].

Ecology and Pathogenesis

S. typhimurium infects when it comes into direct contact with nonphagocytic cells. This induces the formation of appendages on the bacterial cell surface[4]. The appendages formed are shorter than flagella but thicker than both flagella and pili[4]. They cause the host cytoskeleton to rearrange and that allows the bacteria to enter the cell. This membrane system is due to 14 genes on the S. typhimurium chromosome. The inv genes are responsible for the assemblage and withdrawal of these appendages[4]. All of the inv genes must be intact for this system to work[4]. S. typhimurium causes gastroenteritis in humans. When the bacterial cells enter epithelial cells lining the intestine they cause host cell ruffling which temporarily damages the microvilli on the surface of the cell. This causes a rush of white blood cells into the mucosa, which throws off the ratios between absorption and secretion, and leads to diarrhea[4].

References

[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.

Author

Page authored by Nacole Lilly, student of Prof. Doreen Cunningham at Saint Augustine's College.