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Infection and Immunity, June 2003, p. 2993-2999, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.2993-2999.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Examination of Diverse Toxin-Coregulated Pilus-Positive Vibrio cholerae Strains Fails To Demonstrate Evidence for Vibrio Pathogenicity Island Phage

Shah M. Faruque,1 Jun Zhu,2 Asadulghani,1 M. Kamruzzaman,1 and John J. Mekalanos2*

Molecular Genetics Laboratory, International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka-1212, Bangladesh,1 Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 021152

Received 9 October 2002/ Returned for modification 23 December 2002/ Accepted 11 February 2003

The major virulence factors of toxigenic Vibrio cholerae are cholera toxin, which is encoded by a lysogenic filamentous bacteriophage (CTX{Phi}), and toxin-coregulated pilus (TCP), an essential colonization factor that is also the receptor for CTX{Phi}. The genes involved in the biosynthesis of TCP reside in a pathogenicity island, which has been reported to correspond to the genome of another filamentous phage (designated VPI{Phi}) and to encode functions necessary for the production of infectious VPI{Phi} particles. We examined 46 V. cholerae strains having diverse origins and carrying different genetic variants of the TCP island for the production of the VPI{Phi} and CTX{Phi} in different culture conditions, including induction of prophages with mitomycin C and UV irradiation. Although 9 of 10 V. cholerae O139 strains and 12 of 15 toxigenic El Tor strains tested produced extracellular CTX{Phi}, none of the 46 TCP-positive strains produced detectable VPI{Phi} in repeated assays, which detected as few as 10 particles of a control CTX phage per ml. These results contradict the previous report regarding VPI{Phi}-mediated horizontal transfer of the TCP genes and suggest that the TCP island is unable to support the production of phage particles. Further studies are necessary to understand the mechanism of horizontal transfer of the TCP island.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Genetics, Armenise I-421, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115. Phone: (617) 432-1935. Fax: (617) 738-7664. E-mail: jmekalanos{at}hms.harvard.edu.

Editor: V. J. DiRita

Infection and Immunity, June 2003, p. 2993-2999, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.2993-2999.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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