Abstract
Shiga toxins (Stx) of Shiga toxin-producing Escherichia coli (STEC) are generally encoded in the genome of lambdoid bacteriophages, which spend the most time of their life cycle integrated as prophages in specific sites of the bacterial chromosome. Upon spontaneous induction or induction by chemical or physical stimuli, the stx genes are co-transcribed together with the late phase genes of the prophages. After being assembled in the cytoplasm, and after host cell lysis, mature bacteriophage particles are released into the environment, together with Stx. As members of the group of lambdoid phages, Stx phages share many genetic features with the archetypical temperate phage Lambda, but are heterogeneous in their DNA sequences due to frequent recombination events. In addition to Stx phages, the genome of pathogenic STEC bacteria may contain numerous prophages, which are either cryptic or functional. These prophages may carry foreign genes, some of them related to virulence, besides those necessary for the phage life cycle. Since the production of one or more Stx is considered the major pathogenicity factor of STEC, we aim to highlight the new insights on the contribution of Stx phages and other STEC phages to pathogenicity.
Highlights
Soon after the first reported outbreak with pathogenic Shiga toxin-producing E. coli (STEC) O157:H7 (syn. enterohemorrhagic E. coli (EHEC)) in Oregon and Michigan, USA, in 1983, the ability of these pathogens to produce Shiga toxins (Stx)
A continuous transcription activity at phage late promoter pR’, which is Several chromosomal insertion sites have been described for Stx phages: yehV enterminated directly downstream at tR’, generates a short RNA byproduct under lysogenic coding a regulator for curli expression [51,52], wrbA encoding the Trp repressor-binding conditions [44]
The differential induction of Stx phages within the STEC population is considered an altruistic strategy shown by a fraction of the STEC cells, rendering the expression of Stx a positive force for the benefit of the whole population [94]. It has been seen in cells spontaneously inducing Stx phages [41] under natural conditions and in the presence of H2 O2, which is produced by neutrophiles during STEC infection in the human body [94]
Summary
Soon after the first reported outbreak with pathogenic Shiga toxin-producing E. coli (STEC) O157:H7 (syn. enterohemorrhagic E. coli (EHEC)) in Oregon and Michigan, USA, in 1983, the ability of these pathogens to produce Stx Stx phage H-19B contains four operator sites in the right operator region [40] It is not well understood how these differences in the early regulatory region affect repressor/operator interactions and, thereby, expression of Stx. it was demonstrated that spontaneous induction occurs more readily in Stx phages than in lambdoid prophages without stx genes [39,41]. A continuous transcription activity at phage late promoter pR’, which is Several chromosomal insertion sites have been described for Stx phages: yehV enterminated directly downstream at tR’, generates a short RNA byproduct under lysogenic coding a regulator for curli expression [51,52], wrbA encoding the Trp repressor-binding conditions [44]. It has been seen in cells spontaneously inducing Stx phages [41] under natural conditions and in the presence of H2 O2 , which is produced by neutrophiles during STEC infection in the human body [94]
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