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Coli is poorly understood. Enteroaggregative E. Coli with proven pathogenicity typically contain a large set of virulence-associated genes regulated by the AggR transcription factor. These include plasmid genes encoding the aggregative adherence fimbriae (AAF), which anchor the bacterium to the intestinal mucosa and induce inflammation, as well as a protein-coat secretion system (Aat), its secreted dispersin protein, and a putative type VI secretion system termed Aai. Enteroaggregative E. Coli strains often elaborate toxins and a variable number of serine protease autotransporters of Enterobacteriaceae (SPATEs) implicated in mucosal damage and colonization. Before the current outbreak of enteroaggregative E.
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The insertion site of the Shiga-toxin–encoding lambdalike prophage in the outbreak strain is similar to that of the Shiga-toxin–encoding lambdalike prophage in E. Coli strain EDL933. Moreover, the similarity between 933W (the Shiga-toxin–producing phage carried by EDL933) and the prophage of the outbreak strain — particularly in the regions that flank the Shiga toxin genes, which control Shiga toxin production and toxin release (Fig. 8 and 9 in the ) — suggests that production of Shiga toxin 2 by the outbreak strain may be increased by certain antibiotics. Consistent with this possibility is our finding that growth of C227-11 in medium containing ciprofloxacin (25 ng per milliliter) increased expression of the stxAB2 genes by a factor of about 80 (Fig. 10 in the ), which is similar to the elevation of Shiga toxin 2 expression reported for the enterohemorrhagic E. Coli strain EDL933 after exposure to ciprofloxacin.

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