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ARS Home » Plains Area » Clay Center, Nebraska » U.S. Meat Animal Research Center » Meat Safety and Quality » Research » Publications at this Location » Publication #412519

Research Project: Holistic Tactics to Advance the Microbiological Safety and Quality of the Red Meat Continuum

Location: Meat Safety and Quality

Title: Pathogenomes of Shiga toxin positive and negative Escherichia coli O157:H7 strains TT12A and TT12B: Comprehensive phylogenomic analysis using closed genomes

item KALALAH, ANWAR - University Of Texas At San Antonio
item KOENIG, SARA - University Of Texas At San Antonio
item FENG, PETER - Food And Drug Administration(FDA)
item Bosilevac, Joseph - Mick
item Bono, James - Jim
item EPPINGER, MARK - University Of Texas

Submitted to: Microorganisms
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/26/2024
Publication Date: 3/29/2024
Citation: Kalalah, A.A., Koenig, S.S., Feng, P.C., Bosilevac, J.M., Bono, J.L., Eppinger, M. 2024. Pathogenomes of Shiga toxin positive and negative Escherichia coli O157:H7 strains TT12A and TT12B: Comprehensive phylogenomic analysis using closed genomes. Microorganisms. 12(4). Article 699.

Interpretive Summary: Escherichia coli O157:H7 can cause very severe disease because it expresses Shiga toxins. Two different E. coli O157:H7 were isolated from an infected person. One strain was the expected disease-causing E. coli O157:H7 that had Shiga toxins, while the other lacked Shiga toxins. This work used high resolution DNA sequencing to produce and compare full closed genomes of the strains. It was found that the two strains were identical except for the loss of the DNA elements that provide Shiga toxin. The results help to understand how E. coli O157:H7 has evolved and will continue to evolve.

Technical Abstract: Shiga toxin-producing Escherichia coli are zoonotic pathogens that cause food-borne human disease. Among these, the O157:H7 serotype has evolved from an enteropathogenic O55:H7 ancestor through the displacement of the somatic gene cluster and recurrent toxigenic conversion by Shiga toxin-converting bacteriophages. However, atypical strains that lack the Shiga toxin, the characteristic virulence hallmark, are circulating in this lineage. For this study, we analyzed the pathogenome and virulence inventories of the stx+ strain, TT12A, isolated from a patient with hemorrhagic colitis, and its respective co-isolated stx- strain, TT12B. Sequencing the genomes to closure proved critical to the cataloguing of subtle strain differentiating sequence and structural polymorphisms at a high-level of phylogenetic accuracy and resolution. Phylogenomic profiling revealed SNP and MLST profiles similar to the near clonal outbreak isolates. Their prophage inventories, however, were notably different. The attenuated atypical non-shigatoxigenic status of TT12B is explained by the absence of both the FStx1a- and FStx2a-prophages carried by TT12A, and we also recorded further alterations in the non-Stx prophage complement. Phenotypic characterization indicated that culture growth was directly impacted by the strains’ distinct lytic phage complement. Altogether, our phylogenomic and phenotypic analyses show that these intimately related isogenic strains are on divergent Stx(+/stx-) evolutionary paths.