Persistent cross-species transmission systems dominate Shiga toxin-producingEscherichia coliO157:H7 epidemiology in a high incidence region: a genomic epidemiology study

Background: Several areas of the world suffer notably high incidence of Shiga toxin-producingEscherichia coli, among them Alberta, Canada. We assessed the role of persistent cross-species transmission systems in Alberta'sE. coliO157:H7 epidemiology. Methods: We sequenced and assembled 229E. coliO157:H7 isolates originating from collocated cattle (n=108) and human (n=121) populations from 2007-2015 in Alberta. We constructed a timed phylogeny using BEAST2 using a structured coalescent model. We then extended the tree with human isolates through 2019 (n=432) to assess the long-term disease impact of local persistent lineages. Shiga toxin gene (stx) profile was determined for all isolates. Results: During 2007 to 2015, we estimated 107 (95% HPD 101, 111) human lineages arose from cattle lineages, and 31 (95% HPD 22, 43) from other human lineages; i.e., 77.5% of human lineages arose from cattle lineages. We identified 11 persistent lineages local to Alberta, which were associated with 36.4% (95% CI 27.8%, 45.6%) of human isolates. Of 115 isolates in local persistent lineages, 6.1% carried onlystx2aand the reststx1a/stx2a. During the later period, six local persistent lineages continued to be associated with human illness, including 74.7% (95% CI 68.3%, 80.3%) of reported cases in 2018 and 2019. Thestxprofile of isolates in local persistent lineages shifted from the earlier period, with 51.2% encoding onlystx2a. Conclusions: Our study identified multiple locally evolving lineages transmitted between cattle and humans persistently associated withE. coliO157:H7 illnesses for up to 13 years. Of concern, there was a dramatic shift in the local persistent lineages toward strains with the more virulentstx2a-only profile. We hypothesize that the large proportion of disease associated with local transmission systems is a principal cause of Alberta's highE. coliO157:H7 incidence.