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Phenotypic and molecular characterization of Salmonella enterica serovar Sofia, an avirulent species in Australian poultry
Author(s) -
Emily Gan,
Fiona J. Baird,
Peter J. Coloe,
Peter M. Smooker
Publication year - 2011
Publication title -
microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.352
H-Index - 35
eISSN - 1465-2080
pISSN - 1350-0872
DOI - 10.1099/mic.0.047001-0
Subject(s) - serotype , salmonella enterica , salmonella , biology , phenotype , microbiology and biotechnology , virology , genetics , bacteria , gene
Salmonella enterica serovar Sofia (S. Sofia) is often isolated from chickens in Australia. However, despite its high frequency of isolation from chicken and chicken meat products, S. Sofia is rarely associated with animal or human salmonellosis, presumably because this serovar is avirulent in nature. The objective of this work was to investigate the phenotypic and molecular properties of S. Sofia in order to assess its pathogenic potential. Our in vivo studies support the observation that this serovar can colonize tissues, but does not cause disease in chickens. This was further confirmed with tissue culture assays, which showed that the ability of S. Sofia to adhere, invade and survive intracellularly is significantly diminished compared with the pathogenic Salmonella enterica serovar Typhimurium (S. Typhimurium) 82/6915. Molecular analysis of Salmonella pathogenicity islands (SPIs) showed that most of the differences observed in SPI1 to SPI5 of S. Sofia could be attributed to minor changes in the sequences, as indicated by a loss or gain of restriction cleavage sites within these regions. Sequence analysis demonstrated that the majority of virulence genes identified were predicted to encode proteins sharing a high identity (75-100 %) with corresponding proteins from S. Typhimurium. However, a number of virulence genes in S. Sofia have accumulated mutations predicted to affect transcription and/or translation. The avirulence of this serovar is probably not the result of a single genetic change but rather of a series of alterations in a large number of virulence-associated genes. The acquisition of any single virulence gene will almost certainly not be sufficient to restore S. Sofia virulence.

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