Long-term colonisation–inhibition studies to protect broilers against colonisation with Salmonella Enteritidis, using Salmonella Pathogenicity Island 1 and 2 mutants

Bohez, Lotte; Ducatelle, Richard; Pasmans, Frank; Haesebrouck, Freddy; Immerseel, Filip Van

doi:10.1016/j.vaccine.2007.02.082

Cited by 30 publications

(15 citation statements)

References 37 publications

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“…Those authors concluded that the HilA regulatory protein was required for continued cecal colonization and long-term shedding (268). Subsequent studies by these researchers demonstrated that the initial colonization by the S. Enteritidis hilA mutant was sufficient to prevent long-term fecal shedding and cecal and internal organ colonization by the respective S. Enteritidis wild-type strain (264,269). This linkage of hilA with systemic infection is supported by the general trends of increased liver, spleen, and ovary colonization observed in adult laying hens when S. Enteritidis hilA expression levels were increased (270).…”

Section: The Salmonella-chicken Host Interactionmentioning

confidence: 99%

Salmonella Pathogenicity and Host Adaptation in Chicken-Associated Serovars

Foley

Johnson

Ricke

et al. 2013

Microbiol Mol Biol Rev

270

218

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SUMMARY 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.

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Section: The Salmonella-chicken Host Interactionmentioning

confidence: 99%

Salmonella Pathogenicity and Host Adaptation in Chicken-Associated Serovars

Foley

Johnson

Ricke

et al. 2013

Microbiol Mol Biol Rev

270

218

View full text Add to dashboard Cite

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“…Because the infection of adult hens by S. Enteritidis is asymptomatic, the contamination of eggs due to the colonization of the oviduct is hard to detect and prevent (38). To avoid poultry stock infection by this pathogen, some approaches have been addressed to design vaccines for laying hens using live, attenuated mutants (11,16,57) or bacteria killed by chemical agents or heat (6,11,21). None of these vaccines have been shown to significantly diminish the intestinal colonization or the shedding of the pathogen in the depositions.…”

mentioning

confidence: 99%

Infection of Mice by Salmonella enterica Serovar Enteritidis Involves Additional Genes That Are Absent in the Genome of Serovar Typhimurium

et al. 2012

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Salmonella enterica serovar Enteritidis causes a systemic, typhoid-like infection in newly hatched poultry and mice. In the present study, a library of 54,000 transposon mutants of S. Enteritidis phage type 4 (PT4) strain P125109 was screened for mutants deficient in the in vivo colonization of the BALB/c mouse model using a microarray-based negative-selection screening. Mutants in genes known to contribute to systemic infection (e.g., Salmonella pathogenicity island 2 [SPI-2], aro, rfa, rfb, phoP, and phoQ) and enteric infection (e.g., SPI-1 and SPI-5) in this and other Salmonella serovars displayed colonization defects in our assay. In addition, a strong attenuation was observed for mutants in genes and genomic islands that are not present in S. Typhimurium or in most other Salmonella serovars. These genes include a type I restriction/modification system (SEN4290 to SEN4292), the peg fimbrial operon (SEN2144A to SEN2145B), a putative pathogenicity island (SEN1970 to SEN1999), and a type VI secretion system remnant SEN1001, encoding a hypothetical protein containing a lysin motif (LysM) domain associated with peptidoglycan binding. Proliferation defects for mutants in these individual genes and in exemplar genes for each of these clusters were confirmed in competitive infections with wild-type S. Enteritidis. A ⌬SEN1001 mutant was defective for survival within RAW264.7 murine macrophages in vitro. Complementation assays directly linked the SEN1001 gene to phenotypes observed in vivo and in vitro. The genes identified here may perform novel virulence functions not characterized in previous Salmonella models.

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“…A Salmonella Enteritidis hilAssrAfliG deletion mutant has been shown to colonise spleen and caecum to a lesser extent and was cleared rapidly from poultry, but also offered relatively less protection against Salmonella Enteritidis infection [15]. These and earlier observations suggest thus that there will be a trade-off between persistence and protection, as a highly colonising and thus protective strain will probably not be eliminated by slaughter age [26]. In contrast, a strain that is poorly colonising will be eliminated by slaughter age, but will probably not offer a long lasting protection.…”

Section: Discussionmentioning

confidence: 82%