8

In general, differences in pathogenic potential among bacterial species and among strains within a species are due to the presence and expression of virulence genes (i.e., genes that encode virulence factors) in pathogenic strains and to their absence in related nonpathogenic strains. Many virulence factor-encoding genes of facultative pathogens (e.g., Escherichia coli, Listeria monocytogenes, Pseudomonas aeruginosa, Streptococcus spp., Staphylococcus aureus, and Vibrio cholerae) are present in various mobile genetic elements, such as transposons, plasmids, bacteriophages, and pathogenicity islands. In that regard, it has become increasingly evident that one group of mobile genetic elements, the bacteriophages, plays an important role in the evolution and emergence of pathogenic bacteria. In a process called phage conversion, bacteriophage-encoded virulence genes can convert their bacterial host from a nonpathogenic strain to a virulent strain, or to a strain with increased virulence, by providing mechanisms for the invasion of host tissues and the avoidance of host immune defenses (Table 8.1). Indeed, the loss of those bacteriophages may render the bacteria nonpathogenic. However, the majority of bacteriophages possessing virulence genes are temperate bacteriophages that form stable lysogens. Therefore, lysogenic conversion does not result in bacterial lysis but, instead, allows both vertical and horizontal gene transfer-which may confer a selective advantage to the host and result in clonal expansion. This hypothesis is supported by the recent epidemic spread of cholera from Asia to South America after nearly a century of absence. The ctxAB genes, which encode cholera toxin (CT), reside in the genome of a filamentous bacteriophage CTXf (Waldor and Mekalanos, 1996). Therefore, V. cholerae’s lysogenic conversion by the CTXf enables it to produce CT, the main cause of the secretory diarrhea so characteristic of cholera, thus facilitating the spread of V. cholerae to new hosts and enhancing its pandemic spread.