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Infection and Immunity, February 2003, p. 1020-1025, Vol. 71, No. 2
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.2.1020-1025.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Molecular Genetics Laboratory, International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka-1000, Bangladesh,1 Department of International Health, Johns Hopkins University,2 Center of Marine Biotechnology, University of Maryland Biotechnology Institute, Baltimore, Maryland3
Received 15 August 2002/ Returned for modification 23 October 2002/ Accepted 8 November 2002
The major virulence factors of toxigenic Vibrio cholerae are cholera toxin (CT), which is encoded by a lysogenic bacteriophage (CTX
), and toxin-coregulated pilus (TCP), an essential colonization factor which is also the receptor for CTX
. The genes for the biosynthesis of TCP are part of a larger genetic element known as the TCP pathogenicity island. To assess their pathogenic potential, we analyzed environmental strains of V. cholerae carrying genetic variants of the TCP pathogenicity island for colonization of infant mice, susceptibility to CTX
, and diarrheagenicity in adult rabbits. Analysis of 14 environmental strains, including 3 strains carrying a new allele of the tcpA gene, 9 strains carrying a new allele of the toxT gene, and 2 strains carrying conventional tcpA and toxT genes, showed that all strains colonized infant mice with various efficiencies in competition with a control El Tor biotype strain of V. cholerae O1. Five of the 14 strains were susceptible to CTX
, and these transductants produced CT and caused diarrhea in adult rabbits. These results suggested that the new alleles of the tcpA and toxT genes found in environmental strains of V. cholerae encode biologically active gene products. Detection of functional homologs of the TCP island genes in environmental strains may have implications for understanding the origin and evolution of virulence genes of V. cholerae.
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