Shigatoxigenic E. coli (STEC) cause several foodborne disease outbreaks and isolated cases per year resulting in potentially life-threatening cases of HUS and TTP. Shiga toxin (Stx) genes are horizontally transferred to susceptible hosts by temperate phages, which increase their host's pathogenic profile upon infection. During foodborne infection, phages released from STEC cells can infect other members of the gut microbiota, which increases the amount of Stx produced and the severity of the resulting disease.

An unexpectedly common infection strategy used by a large proportion (70%) of Stx-phages involves adsorption to the host cell via BamA, an essential outer-membrane protein. BamA is highly conserved across members of the Enterobacteriaceae, and this infection strategy is likely to have driven the rapid dissemination of Stx and the emergence of high-profile STEC outbreaks since 1982, e.g. O104:H4 and O157:H7.

Identification and characterisation of the phage BamA interaction is complicated by the essential nature of BamA. By fusing the membrane associated domain from the BamA orthologue of Pectobacterium atrosepticum, which cannot support Stx phage adsorption, a chimaera was generated that maintained BamA function whilst eliminating susceptibility to Stx-phage infection. The substitution of extracellular BamA sequences from E. coli with those of P. atrosepticum created a library from which adsorption studies were undertaken. It's hoped the information from these assays will help us understand how Stx-phages recognise their host. This knowledge might also improve our ability to limit Stx-phage infections in the gut environment for improved clinical outcomes.