Open Access Open Badges Research article

SPC-P1: a pathogenicity-associated prophage of Salmonella paratyphi C

Qing-Hua Zou1, Qing-Hai Li26, Hong-Yun Zhu1, Ye Feng26, Yong-Guo Li3, Randal N Johnston4, Gui-Rong Liu26* and Shu-Lin Liu12356*

Author affiliations

1 Department of Microbiology, Peking University Health Science Center, Beijing, PR China

2 Genomics Research Center (one of The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), Harbin Medical University, Harbin, PR China

3 Genetic Detection Center of First Hospital, Harbin Medical University, Harbin, PR China

4 Department of Biochemistry and Molecular Biology, University of Calgary, Calgary, Canada

5 Department of Microbiology and Infectious Diseases, University of Calgary, Calgary, Canada

6 Systemomics Research Center, School of Pharmacy, Harbin Medical University, Harbin, PR China

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Citation and License

BMC Genomics 2010, 11:729  doi:10.1186/1471-2164-11-729

Published: 30 December 2010



Salmonella paratyphi C is one of the few human-adapted pathogens along with S. typhi, S. paratyphi A and S. paratyphi B that cause typhoid, but it is not clear whether these bacteria cause the disease by the same or different pathogenic mechanisms. Notably, these typhoid agents have distinct sets of large genomic insertions, which may encode different pathogenicity factors. Previously we identified a novel prophage, SPC-P1, in S. paratyphi C RKS4594 and wondered whether it might be involved in pathogenicity of the bacteria.


We analyzed the sequence of SPC-P1 and found that it is an inducible phage with an overall G+C content of 47.24%, similar to that of most Salmonella phages such as P22 and ST64T but significantly lower than the 52.16% average of the RKS4594 chromosome. Electron microscopy showed short-tailed phage particles very similar to the lambdoid phage CUS-3. To evaluate its roles in pathogenicity, we lysogenized S. paratyphi C strain CN13/87, which did not have this prophage, and infected mice with the lysogenized CN13/87. Compared to the phage-free wild type CN13/87, the lysogenized CN13/87 exhibited significantly increased virulence and caused multi-organ damages in mice at considerably lower infection doses.


SPC-P1 contributes pathogenicity to S. paratyphi C in animal infection models, so it is possible that this prophage is involved in typhoid pathogenesis in humans. Genetic and functional analyses of SPC-P1 may facilitate the study of pathogenic evolution of the extant typhoid agents, providing particular help in elucidating the pathogenic determinants of the typhoid agents.