The formation of biofilms and subsequent encasement of bacterial cells in a complex matrix can enhance resistance to antimicrobials and sterilizing agents making these organisms difficult to eradicate and control. The aim of this study was to evaluate and compare the capacity of 40 E. coli O26 isolates of enterohemorrhagic E. coli (EHEC, n = 27), potential EHEC (pEHEC, n = 3), atypical enteropathogenic E. coli (aEPEC, n = 8) and non-toxigenic E. coli (NTEC, n = 2) from human and cattle sources to form biofilms on different surfaces, and determine whether extracellular matrix (ECM) components (cellulose, curli), motility, prophage insertion in mlrA and cell surface hydrophobicity could influence biofilm formation. Finally, the influence of biofilm formation on the sensitivity of isolates to quaternary ammonium compounds (QACs; Profoam, Kwiksan 22) and peracetic acid-based sanitizer (Topactive Des.) for 2 min on polystyrene plate were also evaluated. Biofilm production on one surface may not indicate biofilm formation on a different surface. Biofilm was formed by different pathotypes on polystyrene (70%), stainless steel (87.5%) and glass slides (95%), however only 50% demonstrated pellicle formation. EHEC isolates were significantly more likely to form a pellicle at the air-liquid interface and biofilms on polystyrene surface at 48 h than aEPEC. Strains that don’t produce ECM (curli or cellulose), harbor a prophage insertion in mlrA, and are non-motile have lower biofilm forming capacities than those isolates possessing combinations of these attributes. Hydrophobicity had no impact on biofilm formation. After 2 min exposure, none of the disinfectants tested were able to completely inactivate all cells within a biofilm regardless of pathotypes and the amount of biofilm formed. Pathotypes of E. coli O26 showed varying capacities to form biofilms, however, most EHEC strains had the capacity to form biofilm on all surfaces and at the air-liquid interface under the conditions used in this study. Biofilms provided a protective effect to E. coli O26 strains against the three sanitizers, previously shown to successfully control the growth of their planktonic counterparts. Whether the characteristics of biofilm forming and non-biofilm forming strains observed in this study reflect their attributes within the food and meat-processing environments is unknown. Further studies that represent the food and meat-processing environments are required.

After E. coli O157, E. coli O26 is the second most prevalent enterohaemorrhagic E. coli (EHEC) serotype identified in cases of foodborne illness in Australia and throughout the world. E. coli O26 associated foodborne outbreaks have drawn attention to the survival capabilities of this organism in a range of environments. The aim of the present study was to assess the ability of E. coli O26 to survive the effects of disinfectants, acids and antimicrobials and investigate the possible influence of virulence genes in survival and persistence of E. coli O26 from human and cattle sources from Australia. Initial characterization indicated that E. coli O26 are a genetically diverse group that were shown to belong to a number of pathotypes. Overall, 86.4% of isolates were susceptible to all antimicrobials tested with no significant differences in resistance observed between pathotypes. A representative subset of isolates (n = 40) were selected to determine their ability to survive disinfectants at proposed industry working concentrations and acid stress. Profoam, Kwiksan 22, and Topactive DES. were able to inhibit the growth of 100% of isolates. The remaining three disinfectants (Dairy Chlor 12.5%, Envirosan and Maxifoam) were not effective against the subset of 40 E. coli O26. Finally, elevated MICs (1,024 to 4,096 μg/ml) of acetic, propionic, lactic, and citric acids were determined for the majority of the isolates (85%). Australian E. coli O26 isolates belong to a range of pathotypes that harbor differing virulence markers. Despite this, their response to antimicrobials, disinfectants and acids is similar confirming that stress response appears unrelated to the presence of EHEC virulence markers. Notwithstanding, the tolerance to disinfectants and the elevated acid MICs for EHEC and the other E. coli O26 pathotypes examined in this study may contribute to bacterial colonization on food contact surfaces and subsequent foodborne illness caused by this pathogen.

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