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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #398644

Research Project: Intestinal Microbial Ecology and Non-Antibiotic Strategies to Limit Shiga Toxin-Producing Escherichia coli (STEC) and Antimicrobial Resistance Transmission in Food Animals

Location: Food Safety and Enteric Pathogens Research

Title: Phenotypic and genomic comparison of three human outbreak and one cattle-associated Shiga toxin-producing Escherichia coli O157:H7

Author
item PEROUTKA-BIGUS, NATHAN - Oak Ridge Institute For Science And Education (ORISE)
item NIELSEN, DANIEL - Oak Ridge Institute For Science And Education (ORISE)
item Trachsel, Julian
item MOU, KATHY - Oak Ridge Institute For Science And Education (ORISE)
item Sharma, Vijay
item Kudva, Indira
item Loving, Crystal

Submitted to: Microbiology Spectrum
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/2/2024
Publication Date: 9/10/2024
Citation: Peroutka-Bigus, N., Nielsen, D.W., Trachsel, J.M., Mou, K.T., Sharma, V.K., Kudva, I.T., Loving, C.L. 2024. Phenotypic and genomic comparison of three human outbreak and one cattle-associated Shiga toxin-producing Escherichia coli O157:H7. Microbiology Spectrum. https://doi.org/10.1128/spectrum.04140-23.
DOI: https://doi.org/10.1128/spectrum.04140-23

Interpretive Summary: Foodborne illness has major impacts on global health and imposes financial hardships on food industries. Escherichia coli serotype O157:H7 (O157) is associated with foodborne illness. Cattle feces are a source of O157, and routine surveillance has led to an abundance of O157 genomic data, as shown in the National Center for Biotechnology Information’s Pathogen Detection database. The relationship between O157 genome and phenotype is not clearly discerned and improved understanding could lead to additional strategies to limit O157 in the food chain. The goal of the research was to evaluate genomic and phenotypic attributes of O157 associated with cattle colonization and shedding, environmental persistence, and human illness. Our results indicate variations in biofilm formation and in vitro cellular adherence was not associated with differences in cattle colonization or shedding. Overall, processes involved in cattle colonization and various phenotypes in relation to genotype are complex and not well understood.

Technical Abstract: Escherichia coli O157:H7 (O157)-adulterated food products, including beef and produce, are associated with disease outbreaks in humans. Although cattle feces are a source for O157 contamination, it is unclear if human-associated outbreak isolates differentially colonize and shed in the feces of cattle at quantities varying from that of non-outbreak O157 isolates. It is also unclear if other phenotypes, such as biofilm formation, cell attachment, or toxin production, differentiate environmental O157 isolates from those associated with human illness. Genomic profiling of O157 isolates acquired through routine surveillance can inform if the isolates encode virulence genes associated with human disease, but many genotype-phenotype relationships remain unclear for O157. Therefore, the objective of this study was to compare a diverse set of O157 isolates, with the intent of identifying potential genotypic differences that could inform phenotypes such as cattle colonization and fecal shedding, in vitro cell attachment, biofilm production, and Shiga toxin production. No significant differences in cattle colonization and fecal shedding were detected for the tested isolates, despite broad genomic differences and in vitro phenotypes. Tested isolates differed in attachment phenotypes on human Caco-2 cells and bovine derived recto-anal junction squamous epithelial cells, with curli expression having a larger impact on attachment to the human derived cell line. Overall, the relationship between O157 genotype and phenotype is complex, and further investigation is warranted to improve our understanding of surveillance data.