Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2013 Dec;77(4):582-607.
doi: 10.1128/MMBR.00015-13.

Salmonella pathogenicity and host adaptation in chicken-associated serovars

Affiliations
Review

Salmonella pathogenicity and host adaptation in chicken-associated serovars

Steven L Foley et al. Microbiol Mol Biol Rev. 2013 Dec.

Abstract

Enteric pathogens such as Salmonella enterica cause significant morbidity and mortality. S. enterica serovars are a diverse group of pathogens that have evolved to survive in a wide range of environments and across multiple hosts. S. enterica serovars such as S. Typhi, S. Dublin, and S. Gallinarum have a restricted host range, in which they are typically associated with one or a few host species, while S. Enteritidis and S. Typhimurium have broad host ranges. This review examines how S. enterica has evolved through adaptation to different host environments, especially as related to the chicken host, and continues to be an important human pathogen. Several factors impact host range, and these include the acquisition of genes via horizontal gene transfer with plasmids, transposons, and phages, which can potentially expand host range, and the loss of genes or their function, which would reduce the range of hosts that the organism can infect. S. Gallinarum, with a limited host range, has a large number of pseudogenes in its genome compared to broader-host-range serovars. S. enterica serovars such as S. Kentucky and S. Heidelberg also often have plasmids that may help them colonize poultry more efficiently. The ability to colonize different hosts also involves interactions with the host's immune system and commensal organisms that are present. Thus, the factors that impact the ability of Salmonella to colonize a particular host species, such as chickens, are complex and multifactorial, involving the host, the pathogen, and extrinsic pressures. It is the interplay of these factors which leads to the differences in host ranges that we observe today.

PubMed Disclaimer

Figures

Fig 1
Fig 1
Evolutionary history of Salmonella virulence plasmids inferred by using the maximum likelihood method, based on the Hasegawa-Kishino-Yano method. The bootstrap consensus tree was inferred from 100 bootstrap replicates. Analysis was based on 441 SNPs identified from the conserved sequences of 22 plasmids. Analysis was conducted with MEGA5 (403).
None
None
None
None

References

    1. Donnenberg MS. 2000. Pathogenic strategies of enteric bacteria. Nature 406:768–774 - PubMed
    1. Tsolis RM, Young GM, Solnick JV, Baumler AJ. 2008. From bench to bedside: stealth of enteroinvasive pathogens. Nat. Rev. Microbiol. 6:883–892 - PubMed
    1. Guerrant RL, Steiner TS. 2005. Principles and syndromes of enteric infections, p 1215–1230 In Mandell GL, Bennett JE, Dolin R. (ed), Principles and practice of infectious diseases, 6th ed, vol 1 Elsevier Churchill Livingstone, Philadelphia, PA
    1. Herrington DA, Hall RH, Losonsky G, Mekalanos JJ, Taylor RK, Levine MM. 1988. Toxin, toxin-coregulated pili, and the toxR regulon are essential for Vibrio cholerae pathogenesis in humans. J. Exp. Med. 168:1487–1492 - PMC - PubMed
    1. Nataro JP, Kaper JB. 1998. Diarrheagenic Escherichia coli. Clin. Microbiol. Rev. 11:142–201 - PMC - PubMed