ArticleApplied and environmental microbiology2012
Virulence and metabolic characteristics of Salmonella enterica serovar enteritidis strains with different sefD variants in hens.
Article in Applied and environmental microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Molecular Epidemiology and Virulence of Non-TyphoidalInternational journal of molecular sciences · 2022Article
- Through the Looking Glass: Genome, Phenome, and Interactome ofPathogens (Basel, Switzerland) · 2022Review
- AT Homopolymer Strings inMicroorganisms · 2021Article
- Reduction of Salmonella Enteritidis in the spleens of hens by bacterins that vary in fimbrial protein SefD.Foodborne pathogens and disease · 2015Article
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Salmonella enterica serovar Enteritidis is one of a few Salmonella enterica serotypes that has SEF14 fimbriae encoded by the sef operon, which consists of 4 cotranscribed genes, sefABCD, regulated by sefR. A parental strain was used to construct a sefD mutant and its complement, and all 3 strains were compared for gene expression, metabolic properties, and virulence characteristics in hens. Transcription of sefD by wild type was suppressed at 42°C and absent for the mutant under conditions where the complemented mutant had 10(3) times higher transcription. Growth of the complemented mutant was restricted in comparison to that of the mutant and wild type. Hens infected with the wild type and mutant showed decreased blood calcium and egg production, but infection with the complemented mutant did not. Thus, the absence of sefD correlated with increased metabolic capacity and enhanced virulence of the pathogen. These results suggest that any contribution that sefD makes to egg contamination is either unknown or would be limited to early transmission from the environment to the host. Absence of sefD, either through mutation or by suppression of transcription at the body temperature of the host, may contribute to the virulence of Salmonella enterica by facilitating growth on a wide range of metabolites.
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