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Infection and Immunity, October 2001, p. 6186-6192, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.6186-6192.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Proteins PblA and PblB of Streptococcus mitis, Which Promote Binding to Human Platelets, Are Encoded within a Lysogenic Bacteriophage

Barbara A. Bensing, Ian R. Siboo, and Paul M. Sullam*

Veterans Affairs Medical Center and the University of California, San Francisco, California

Received 24 April 2001/Returned for modification 5 June 2001/Accepted 18 June 2001

The binding of platelets by bacteria is a proposed central mechanism in the pathogenesis of infective endocarditis. Platelet binding by Streptococcus mitis strain SF100 (an endocarditis isolate) was recently shown to be mediated in part by the surface proteins PblA and PblB. The genes encoding PblA and PblB are clustered with genes nearly identical to those of streptococcal phages r1t, 01205, and Dp-1, suggesting that pblA and pblB might reside within a prophage. To address this possibility, cultures of SF100 were exposed to either mitomycin C or UV light, both of which are known to induce the lytic cycle of many temperate phages. Both treatments caused a significant increase in the transcription of pblA. Treatment with mitomycin C or UV light also caused a substantial increase in the expression of PblA and PblB, as detected by Western blot analysis of proteins in the SF100 cell wall. By electron microscopy, phage particles were readily visible in the supernatants from induced cultures of SF100. The phage, designated SM1, had a double-stranded DNA genome of approximately 35 kb. Southern blot analysis of phage DNA indicated that pblA and pblB were contained within the SM1 genome. Furthermore, Western blot analysis of phage proteins revealed that both PblA and PblB were present in the phage particles. These findings indicate that PblA and PblB are encoded by a lysogenic bacteriophage, which could facilitate the dissemination of these potential virulence determinants to other bacterial pathogens.

* Corresponding author. Mailing address: Division of Infectious Diseases, VA Medical Center (111W), 4150 Clement St., San Francisco, CA 94121. Phone: (415) 221-4810, ext. 2550. Fax: (415) 750-0502. E-mail: sullam{at}itsa.ucsf.edu.

Infection and Immunity, October 2001, p. 6186-6192, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.6186-6192.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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