Precise excision of the large pathogenicity island, SPI7, in Salmonella enterica serovar Typhi

Area of Science:

• Microbiology
• Genetics
• Bacterial Pathogenesis

Background:

• The Salmonella pathogenicity island 7 (SPI7) is a large DNA segment in Salmonella enterica serovar Typhi, encoding the viaB operon essential for Vi antigen synthesis.
• SPI7 is flanked by direct repeats and contains numerous open reading frames, contributing to the pathogen's virulence.
• Some clinical isolates exhibit spontaneous excision of SPI7, resulting in significant phenotypic changes.

Purpose of the Study:

• To investigate the characteristics and consequences of SPI7 excision in Salmonella enterica serovar Typhi.
• To understand the genetic instability of SPI7 and its implications for bacterial evolution and pathogenicity.

Main Methods:

• Analysis of SPI7 structure, including flanking direct repeats and open reading frames.
• Observation of spontaneous SPI7 excision in laboratory-grown clinical isolates.
• Phenotypic characterization of strains with and without SPI7, including Vi antigen production, phage resistance, and cellular invasion assays.

Main Results:

• SPI7 excision is precise, occurring at the pheU gene locus and leaving an intact gene copy.
• Excision results in the loss of Vi antigen production and resistance to phage Vi-II.
• Strains lacking SPI7 demonstrate more rapid invasion of human epithelial cells.
• SPI7 exhibits instability, undergoing spontaneous excision in vitro.

Conclusions:

• SPI7 is an unstable genetic element in Salmonella enterica serovar Typhi, prone to precise excision.
• Excision of SPI7 significantly alters bacterial phenotype, impacting virulence and host cell interaction.
• The instability of SPI7 suggests its role as an intermediate in the lateral transfer of pathogenicity islands among bacteria.