The Salmonella pathogenicity island 13 contributes to pathogenesis in streptomycin pre-treated mice but not in day-old chickens. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Elder, Jacob; Chiok, Kim; Paul, Narayan; Haldorson, Gary; Guard, Jean; Shah, Devendra
• Is Part Of: Gut pathogens. Volume 8:Issue 1(2016)
• Page Start: 1
• Page End: 12
• Publication Date: 2016-12
• Subjects: Salmonella -- Salmonella pathogenicity island -- Salmonella Enteritidis -- Pathogenesis -- SPI-13 -- Host-specificity -- Chicken -- Streptomycin pre-treated mice; Gastrointestinal system -- Microbiology -- Periodicals; 616.3
• DOI: 10.1186/s13099-016-0098-0
• Languages: English
• ISSNs: 1757-4749

Abstract

Abstract Background Salmonella enterica serovar Enteritidis (S. Enteritidis) is a human and animal pathogen that causes gastroenteritis characterized by inflammatory diarrhea and occasionally an invasive systemic infection.Salmonella pathogenicity islands (SPIs) are horizontally acquired genomic segments known to contribute toSalmonella pathogenesis. The objective of the current study was to determine the contribution of SPI-13 toS. Enteritidis pathogenesis. Methods We deleted the entire SPI-13 (∆SPI-13) from the genome ofS . Enteritidis CDC_2010K_0968 strain isolated from a human patient during the 2010 egg-associated outbreak in the US. The kinetics of infection of the wild-type parent and the ∆SPI-13 were compared in orally challenged day-old chickens and streptomycin pre-treated mice. The degree of intestinal inflammation and the survival of mutant strain within the avian (HD11) and murine (RAW264.7) macrophages were also determined. Results The deletion of the SPI-13 resulted in impaired infection kinetics ofS. Enteritidis in streptomycin pre-treated mice which was characterized by significantly lower (P < 0.05) viable counts in the ceca, liver and spleen, impaired ability to induce intestinal inflammation and reduced survival within murine macrophages. Conversely, there were no significant differences in the infection kinetics of ∆SPI-13 in day-old chickens in any of the organs tested and the survival of ∆SPI-13 within chicken macrophages remained unaltered. Conclusions The results of this study show that SPI-13 contributes to the pathogenesis ofS. Enteritidis in streptomycin pre-treated mice but not in day-old chickens and raises the possibility that SPI-13 may play a role in pathogenesis and the host adaptation/restriction ofSalmonella serovars.