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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 #401751

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: Non-fimbrial adhesins effect Escherichia coli O157:H7 biofilm formation on post-harvest food products

item DOUKAKIS, SOFIA - Salve Regina University
item FARKOUH, MOUNA - Salve Regina University
item WINTERS, SAMANTHA - Salve Regina University
item HOLCOMB, SARAH - Salve Regina University
item Kudva, Indira
item MOREAU, MATHEW - Salve Regina University

Submitted to: American Society for Microbiology
Publication Type: Abstract Only
Publication Acceptance Date: 3/3/2023
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Shiga toxin producing Escherichia coli (STEC) serovar O157:H7 (O157) remains a major source of morbidity and mortality associated with bloody diarrhea and life-threatening hemolytic uremic syndrome in humans. Cattle, the primary reservoir of STEC, are asymptomatically colonized by STEC at the mucosal interface of the recto-anal junction (RAJ). From this site STEC can be shed at various rates from normal shedding of 100 CFU/g to ‘super shedding’ of greater than 10^4 CFU/g. Once in the environment, STEC can disseminate to cattle hide and even produce, such as spinach or lettuce. STEC can form biofilms that are highly resistant to decontamination measures on produce, generating possible sources of STEC infection. We recently characterized the importance of several non-fimbrial adhesins in the ability of STEC to form a unique aggregative adherent phenotype on cells from the bovine RAJ. This study demonstrates that some of these adhesins, including defined adhesins EivA and Iha and predicted adhesins SS17_2873, YfaL, and EaeH, could play a role in biofilm formation on cattle hide, spinach, and lettuce. The effects that each adhesin gene deletion had was strain and host dependent similar to our previous observations with these adhesins in relation to the RAJ-STEC and/or the HEp2-STEC interface. For instance, loss of YfaL in O157 strain EDL933 enhanced biofilm formation while reducing biofilm formation in O157 strain SS17. Overall, these results indicate potentially important roles (and possibly a sequence of expression) for these genes to be expressed throughout various stages of transmission, colonization, and biofilm formation. Taken together, these investigations continue to improve our understanding of the gene products and molecular mechanisms involved in colonization of the cattle, subsequent shedding phenotypes, and the final transmission and survival of STEC prior to human consumption and transmission.