The Prophage and Us - Shiga Toxin Phages revisited

Abstract

The authors first met in 1998 at the University of Würzburg, Germany, at the Institute of Hygiene and Microbiology, in Helge Karch's lab, where Herbert Schmidt worked as a PostDoc and Maite Muniesa visited the lab for a postdoctoral research stay to work on phages encoding Shiga toxin 2e (Stx2e) [1]. Since that time, we have been more or less, as much as our university duties allow, connected by Stx-phage research. Initially described in the early 1980s, Shiga toxin-converting bacteriophages (Stx-phages) have been the subject of numerous publications [ 2,3 ]. The ability to produce Stx, the major pathogenicity factor of enterohemorrhagic E. coli (EHEC), seems to be essentially connected to the location of the Shiga toxin genes (stx) in the genome of lysogenic phages, found always in a similar location within the late transcribed region, and upstream of the lysis and capsid genes [4 - 11]. Stx-phages are double-stranded DNA tailed phages showing a lambdoid or a non-lambdoid genome structure. To the best of our knowledge, stx genes have never been found in other mobile genetic elements other than phages, such as plasmids or pathogenicity islands [12 - 16 ]. Although the genetics and function of Stx-phages have been described in many publications, some basic questions remain still open, for example, (1) why are Stx-phages so successful in terms of evolution and spread among E. coli strains? (2) why do Stx-phages occur mainly in enteropathogenic E. coli strains but not, or only accidentally, in others such as extraintestinal pathogenic E. coli (EXPEC), (3) which advantage do EHEC strains have from the lysogenic state carrying single or multiple Stx-phages?