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Salmonella Derby from animals

ABSTRACT: Phylogenetic and antibiotic resistance comparison of Salmonella Derby from humans and animals

PROVIDER: PRJEB26879 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2594960_1.fastq.gz	Fastqsanger.gz
	ERR2594960_2.fastq.gz	Fastqsanger.gz
	ERR2594970_1.fastq.gz	Fastqsanger.gz
	ERR2594970_2.fastq.gz	Fastqsanger.gz
	ERR2594980_1.fastq.gz	Fastqsanger.gz

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A single missense mutation in hilD is responsible for further adaptation of a Salmonella Derby lineage to swine and reduced risk to human health

Project description:Salmonella enterica variants exhibit diverse host adaptation, outcome of infection, and associated risk to humans. Analysis of 6,335 Salmonella isolates recovered from integrated human-animal surveillance in Emilia Romagna region, Northern Italy, (human population ca 4,500,000), from 2012 to 2017 showed that Salmonella enterica serovar Derby constitutes a swine associated serovar in this epidemiological context while representing also a significant causative agent of human infections. Comparison of the distribution of subtypes of Salmonella Derby from human and swine identified isolates with a distinct PFGE profile that were significantly less isolated in human infections than in swine infections compared to all other subtypes. Here we show that isolates with this PFGE profile form a distinct phylogenetic sub-clade within Salmonella Derby and exhibit a marked reduction in invasion and replication in human epithelial cells but a relatively small reduction in swine epithelial cells, in line with the epidemiological evidence. A single missense mutation in hilD, that encodes the master-regulator of the Salmonella Pathogenicity Island 1 (SPI-1), was identified in this lineage of Salmonella Derby. Since SPI-1 encodes for a primary system of Salmonella invasion into epithelial cells, we investigated the role of the observed mutation in detail. We demonstrated that the missense mutation results in a loss of function of HilD that accounts for the reduced invasion and replication in human epithelial cells while showing a relatively small impact on the interaction with swine cells. This finding is suggestive of a mechanism of invasion alternative to SPI-1 in the Salmonella-swine combination

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