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Journal of Clinical Microbiology, April 2008, p. 1330-1336, Vol. 46, No. 4
0095-1137/08/$08.00+0     doi:10.1128/JCM.01255-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Salmonella enterica Serovar Senftenberg Human Clinical Isolates Lacking SPI-1

Qinghua Hu,^1,* Bryan Coburn,^2,3, Wanyin Deng,² Yuling Li,² Xiaolu Shi,¹ Quanxue Lan,¹ Bing Wang,¹ Brian K. Coombes,^2, and B. Brett Finlay^2,3

Shenzhen Centre for Disease Control and Prevention, Shenzhen, Guangdong Province, China,¹ Michael Smith Laboratories, University of British Columbia,² Department of Microbiology and Immunology, University of British Columbia, Vancouver, Canada³

Received 22 June 2007/ Returned for modification 6 July 2007/ Accepted 6 February 2008

Nontyphoidal Salmonella species cause gastrointestinal disease worldwide. The prevailing theory of Salmonella enteropathogenesis is that bacterial invasion of the intestinal epithelium is essential for virulence and that this requires the virulence-associated genomic region Salmonella pathogenicity island 1 (SPI-1). Recent studies of Salmonella enterica infection models have demonstrated that enterocolitis and diarrhea in mice and cows can occur independently of SPI-1. In this study, we sought to confirm whether two S. enterica serovar Senftenberg clinical isolates lacked genes essential for SPI-1 function. Two clinical strains were isolated and identified as being S. enterica serovar Senftenberg from four stool samples from a food-borne disease outbreak affecting seven individuals in Shenzhen, Guangdong Province, China, using conventional methods, pulsed-field gel electrophoresis and multilocus sequence typing. The possibility of coinfection with other potential bacteria or usual viruses was excluded. Two isolates were analyzed for the presence of invA, sipA, ssaR, sifA, and sopE2 by PCR and Southern blotting and were then assayed for the presence of SPI-1 by PCR and long-range PCR for fhlA-hilA, hilA-spaP, and spaP-invH and Southern blot analysis. A long-range PCR fragment from fhlA to mutS covering the 5' and 3' flanks of SPI-1 was also amplified from the two clinical isolates and sequenced. In addition, the two clinical isolates were assayed for enteroinvasiveness in vitro. Murine infection models were also examined. Biochemical tests and serotyping confirmed that the two clinical isolates are S. enterica serovar Senftenberg. However, they lacked genes critical for SPI-1 function but contained SPI-2 genes and were attenuated for the invasion of cultured intestinal epithelial cells. In conclusion, clinical S. enterica serovar Senftenberg strains isolated from a food-borne disease outbreak lack the invasion-associated locus SPI-1, indicating that SPI-1 is not essential for human gastroenteritis.

Published ahead of print on 13 February 2008.

Q.H. and B.C. contributed equally to this work.

Present address: Department of Biochemistry and Biomedical Sciences, Public Health Agency of Canada and McMaster University, Ontario, Canada.