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Chapter 29 : Evolution of Salmonella and Salmonella Infections

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Evolution of Salmonella and Salmonella Infections, Page 1 of 2

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Abstract:

Human disease is mainly caused by Salmonella serotypes belonging to subspecies I. Salmonella is capable of causing a variety of disease syndromes: typhoid (enteric) fever, gastroenteritis, septicemia, and focal infections, depending on the serotype and the host susceptibility. Speciation of the genus Salmonella are correlated with the acquisition of virulence genes, mainly by horizontal transfer. Acquisition of SPI-1 is believed to be an essential event for the separation of the Escherichia and Salmonella genera and permitted the latter to invade intestinal epithelial cells. The invasion step in which the enzymatic activity of SigD is essential is the biogenesis of the Salmonella-containing vacuole (SCV) after membrane ruffling. A new step in the evolution of Salmonella could be gained by acquisition of the pathogenicity island SPI-2, a region of 40 kb composed of at least two distinct elements. Several of them are involved in the control of trafficking and evolution of these vesicles, but details about their function are still scarce. The evolution of all these, relatively recent, serotypes has involved acquisition and loss of a substantial number of genes. The nature of many pseudogenes and some phenotypic traits is different in the two serotypes, indicating an independent evolution pathway. Currently, ceftriaxone is considered the most effective antimicrobial agent for Salmonella infections, and the fluoroquinolones are an alternative option.

Citation: Rotger R. 2008. Evolution of Salmonella and Salmonella Infections, p 349-359. In Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J (ed), Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC. doi: 10.1128/9781555815639.ch29
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Figures

Image of Figure 1.
Figure 1.

Phylogenetic groups of Salmonella. Acquisition of pathogenicity islands (SPI) and other genes during speciation is indicated (↓); in parentheses, the estimated number of acquired genes. 1 Genetically defined group belonging to subsp. IV. *Monophasic salmonellae. **Diphasic salmonellae. SPV: Salmonella virulence plasmid. Based on data from Baumler, 1997; Boyd et al., 1996; Groisman and Ochman, 1997; and Porwollik et al., 2002.

Citation: Rotger R. 2008. Evolution of Salmonella and Salmonella Infections, p 349-359. In Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J (ed), Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC. doi: 10.1128/9781555815639.ch29
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Image of Figure 2.
Figure 2.

Location in centisomes (in parentheses) of Salmonella pathogenicity islands (SPI) and other virulence genes in the chromosome of serotype Typhimurium LT2 (except for those marked with “*” that correspond to the chromosome of serotype Typhi). The site of insertion is indicated in brackets. (Based on data from Hensel, 2004; Mirold et al., 2001.)

Citation: Rotger R. 2008. Evolution of Salmonella and Salmonella Infections, p 349-359. In Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J (ed), Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC. doi: 10.1128/9781555815639.ch29
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Image of Figure 3.
Figure 3.

Schematic representation of the Salmonella invasion of epithelial cells. Bacterial effectors are represented in ovals, and those of host cells in rectangles. SCV: Salmonella-containing vesicle; EEA1: Early endosomal antigen-1.

Citation: Rotger R. 2008. Evolution of Salmonella and Salmonella Infections, p 349-359. In Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J (ed), Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC. doi: 10.1128/9781555815639.ch29
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Tables

Generic image for table
Table 1.

Diseases caused by some Salmonella subspecies and I serotypes in humans and higher vertebrates a

Citation: Rotger R. 2008. Evolution of Salmonella and Salmonella Infections, p 349-359. In Baquero F, Nombela C, Cassell G, Gutiérrez-Fuentes J (ed), Evolutionary Biology of Bacterial and Fungal Pathogens. ASM Press, Washington, DC. doi: 10.1128/9781555815639.ch29

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