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EcoSal Plus

Domain 8:

Pathogenesis

Epidemiology and Pathogenesis in Food-Producing Animals

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  • Authors: Timothy S. Wallis1, and Paul A. Barrow2
  • Editor: Michael S. Donnenberg3
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Division of Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire RG20 7NN, United Kingdom; 2: Division of Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire RG20 7NN, United Kingdom; 3: University of Maryland, School of Medicine, Baltimore, MD
  • Received 02 February 2005 Accepted 13 May 2005 Published 25 July 2005
  • Address correspondence to Paul A. Barrow paul.barrow@bbsrc.ac.uk
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  • Abstract:

    This review reviews the pathogenesis of different phases of infections. The nature of infections in several domesticated animal species is described to highlight differences in the epidemiology and pathogenesis of salmonellosis in different hosts. The biology of serovar host specificity is discussed in the context of our current understanding of the molecular basis of pathogenesis and the potential impact of different virulence determinants on natural history. The ability to colonize the intestine, as evidenced by the shedding of relatively large numbers of bacteria in the feces over a long period, is shared unequally by serovars. Studies probing the molecular basis of intestinal colonization have been carried out by screening random transposon mutant banks of serovar Typhimurium in a range of avian and mammalian species. It is becoming increasingly clear that pathogenicity island 2 (SPI2) is a major virulence factor during infection of food-producing animals, including cattle and poultry. The prevalence of serovars in domestic fowl varies in different countries and with time. Although chickens are the natural hosts of serovars Gallinarum and Pullorum, natural outbreaks caused by these serovars in turkeys, guinea fowl, and other avian species have been described. There are two possible explanations to account for the apparent host specificity of certain serovars. Environmental factors may increase exposure of particular animal species to certain serovars. Alternatively, there are genetic differences between these serovars, which allow them to survive and/or grow in specific niches only found within ruminants or pigs.

  • Citation: Wallis T, Barrow P. 2005. Epidemiology and Pathogenesis in Food-Producing Animals, EcoSal Plus 2005; doi:10.1128/ecosalplus.8.6.2.1

Key Concept Ranking

Tumor Necrosis Factor alpha
0.44486016
Type III Secretion System
0.4097361
Bacterial Pathogenesis
0.35884908
Salmonella enterica
0.33501816
0.44486016

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ecosalplus.8.6.2.1.citations
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/content/journal/ecosalplus/10.1128/ecosalplus.8.6.2.1
2005-07-25
2017-07-21

Abstract:

This review reviews the pathogenesis of different phases of infections. The nature of infections in several domesticated animal species is described to highlight differences in the epidemiology and pathogenesis of salmonellosis in different hosts. The biology of serovar host specificity is discussed in the context of our current understanding of the molecular basis of pathogenesis and the potential impact of different virulence determinants on natural history. The ability to colonize the intestine, as evidenced by the shedding of relatively large numbers of bacteria in the feces over a long period, is shared unequally by serovars. Studies probing the molecular basis of intestinal colonization have been carried out by screening random transposon mutant banks of serovar Typhimurium in a range of avian and mammalian species. It is becoming increasingly clear that pathogenicity island 2 (SPI2) is a major virulence factor during infection of food-producing animals, including cattle and poultry. The prevalence of serovars in domestic fowl varies in different countries and with time. Although chickens are the natural hosts of serovars Gallinarum and Pullorum, natural outbreaks caused by these serovars in turkeys, guinea fowl, and other avian species have been described. There are two possible explanations to account for the apparent host specificity of certain serovars. Environmental factors may increase exposure of particular animal species to certain serovars. Alternatively, there are genetic differences between these serovars, which allow them to survive and/or grow in specific niches only found within ruminants or pigs.

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