|ELDER, J. - Washington State University|
|CHIOK, K. - Washington State University|
|PAUL, NARAYAN - Washington State University|
|HALDORSON, GARY - Washington State University|
|SHAH, D. - Washington State University|
Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/31/2016
Publication Date: 5/2/2016
Citation: Elder, J.R., Chiok, K.L., Paul, N., Haldorson, G.J., Guard, J.Y., Shah, D.H. 2016. The Salmonella Pathogenicity Island 13 contributes to pathogenesis in streptomycin pre-treated mice but not in day-old chickens. Veterinary Microbiology. Available:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852409/.
Interpretive Summary: People and poultry differ in the way that they respond to exposure to Salmonella. Whereas people often experience gastrointestinal illness following infection, chickens show few signs of illness. Part of the reason chickens remain a source of Salmonella for people is that farmers cannot tell from looking at a flock if they are carriers of pathogenic serotypes. The research here was done to see how a certain region of the Salmonella genome, called SPI-13, impacted disease in two different models. The first one was a chicken model and it was based on infecting one-day old chicks with strains of Salmonella enterica serovar Enteritidis that varied in the presence and absence of certain genes in SPI-13. The second model was to use mice pretreated with streptomycin one time as a substitute for people. Results strongly suggest that SPI-13 has genes that vary in impact within the two models. Whereas mice became ill from exposure, one-day old chicks did not. These results may impact how vaccines are designed to decrease the incidence of dangerous strains of Salmonella in chickens.
Technical Abstract: Salmonella 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 to Salmonella pathogenesis. The objective of the current study was to determine the contribution of SPI-13 to S. Enteritidis pathogenesis. We deleted the entire SPI-13 ('SPI-13) from the S. 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 (WT) 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. The deletion of the SPI-13 resulted in significantly impaired infection kinetics of S. Enteritidis in streptomycin pre-treated mice with significantly lower viable counts in the ceca, liver and spleen. In addition, of 'SPI-13 mutant was significantly impaired in its ability to induce intestinal inflammation in mice and survive 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 or its survival within chicken macrophages. The results of this study show that SPI-13 contributes to the pathogenesis of S. Enteritidis in streptomycin pre-treated mice but not in day-old chickens, raising the possibility that SPI-13 may play a role in the host adaptation/restriction of Salmonella serovars.