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Infection and Immunity, April 2001, p. 1994-2000, Vol. 69, No. 4
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.4.1994-2000.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Streptococcus iniae Virulence Is Associated with a Distinct Genetic Profile

Jeffrey D. Fuller,1,2 Darrin J. Bast,1,2 Victor Nizet,3 Donald E. Low,1,2 and Joyce C. S. de Azavedo1,2,*

Department of Laboratory Medicine and Pathobiology, University of Toronto,1 and Mount Sinai Hospital and Toronto Medical Laboratories, University Health Network,2 Toronto, Ontario, Canada, and Division of Pediatric Infectious Diseases, University of California, San Diego School of Medicine, La Jolla, California3

Received 6 July 2000/Returned for modification 3 January 2001/Accepted 8 January 2001

Streptococcus iniae causes meningoencephalitis and death in commercial fish species and has recently been identified as an emerging human pathogen producing fulminant soft tissue infection. As identified by pulsed-field gel electrophoresis (PFGE), strains causing disease in either fish or humans belong to a single clone, whereas isolates from nondiseased fish are genetically diverse. In this study, we used in vivo and in vitro models to examine the pathogenicity of disease-associated isolates. Strains with the clonal (disease-associated) PFGE profile were found to cause significant weight loss and bacteremia in a mouse model of subcutaneous infection. As little as 102 CFU of a disease-associated strain was sufficient to establish bacteremia, with higher inocula (107) resulting in increased mortality. In contrast, non-disease-associated (commensal) strains failed to cause bacteremia and weight loss, even at inocula of 108 CFU. In addition, disease-associated strains were more resistant to phagocytic clearance in a human whole blood killing assay compared to commensal strains, which were almost entirely eradicated. Disease-associated strains were also cytotoxic to human endothelial cells as measured by lactate dehydrogenase release from host cells. However, both disease-associated and commensal strains adhered to and invaded cultured human epithelial and endothelial cells equally well. While cellular invasion may still contribute to the pathogenesis of invasive S. iniae disease, resistance to phagocytic clearance and direct cytotoxicity appear to be discriminating virulence attributes of the disease-associated clone.

* Corresponding author. Mailing address: Department of Microbiology Rm 1483, Mount Sinai Hospital, 600 University Ave., Toronto, Ontario, Canada M5G 1X5. Phone: (416) 586-8459. Fax: (416) 586-8746. E-mail: jdeazavedo{at}mtsinai.on.ca.

Infection and Immunity, April 2001, p. 1994-2000, Vol. 69, No. 4
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.4.1994-2000.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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