Bacteriophage biology and bacterial virulence

Abstract

Temperate bacteriophages often encode properties that alter the host bacterium following the establishment of lysogeny. This process, referred to as `lysogenic conversion', has played a critical role in the evolution of many Gram-positive and Gram-negative pathogens. The structural genes encoding exotoxins, such as diphtheria toxin, botulinum toxin types C1 and D, streptococcal erythrogenic toxin, staphylococcal enterotoxin A, Shiga toxins 1 and 2 (Stx1 and Stx2), Pseudomonas cytotoxin, and cholera toxin (CT), are located in the genomes of temperate bacteriophages that confer toxinogenicity upon their respective hosts (reviewed in Ref. [1]). Besides toxins, other potential virulence factors encoded by bacteriophages include extracellular enzymes (such as streptococcal hyaluronidase[2]and staphylokinase[3]), outer membrane proteins [such as Lom and Bor of phage λ (Ref. [4])], a G-protein-like open reading frame in Vibrio cholerae phage K139 (Ref. [5]), and enzymes that alter the antigenic properties of lipopolysaccharide (LPS) in Salmonella and Shigella[6]. The diverse bacteriophages that encode these virulence factors have been thought of primarily as means for the horizontal transmission of virulence genes within bacterial populations[7]. Recent studies of the lambdoid phage H-19B, which encodes Stx1 (Ref. [8]), and the filamentous phage CTXφ, which encodes CT (Ref. [9]), raise the possibility that, in addition to serving as vectors for the dissemination of the genes encoding these toxins, the life cycles of these phages may play a role in the regulation of the production and export of these potent toxins.