|Nguyen, Ly Huong|
Submitted to: Pathogens and Disease
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/21/2015
Publication Date: 12/23/2015
Citation: Chen, C., Nguyen, L.T., Cottrell, B.J., Irwin, P.L., Uhlich, G.A. 2015. Multiple mechanisms responsible for strong Congo red-binding variants of Escherichia coli O157:H7 strains. Pathogens and Disease. 74:123.
Interpretive Summary: Foodborne illness causes severe health and economical impacts in the United States. Shiga toxin-producing Escherichia coli (STEC) are major foodborne pathogens associated with severe disease and large outbreaks; serotype O157:H7 in particular is the most recognized member. Pathogens utilize biofilms to attach to surfaces and host tissues for survival, persistence, and disease progression. The regulation of biofilm formation is complex and involves intricate pathways and environmental signals. Most strains of O157:H7 are deficient in biofilm formation due to a bacteriophage (bacterial virus) insertion in a key regulatory gene. We have obtained over 50 naturally occurring variants of E. coli O157:H7 that exhibited stronger biofilm-forming properties and sought to identify the root cause of these variants. Two major mechanisms were identified for the increased biofilm properties in approximately three-quarters of the variants, while the mechanisms of the remaining strains are yet to be determined. These findings revealed additional genes and regulations that may be exploited for reduction of biofilms and pathogen persistence.
Technical Abstract: High variability in the expression of csgD-dependent, biofilm-forming and adhesive properties is common among Shiga toxin-producing Escherichia coli (STEC). Although many strains of serotype O157:H7 form little biofilm, conversion to stronger biofilm phenotypes has been observed. In this study we screened different strains of serotype O157:H7 for the emergence of strong Cong-red (CR) affinity /biofilm-forming properties and investigated the underlying genetic mechanisms. Two major mechanisms which conferred stronger biofilm phenotypes were identified: mutations (insertion, deletion, single nucleotide change) in rcsB and stx-prophage excision from the mlrA site. Restoration of the native mlrA gene (due to prophage excision) resulted in strong biofilm properties to all variants. Whereas RcsB mutants showed weaker CR affinity and biofilm properties, it provided more possibilities for phenotypic presentations through heterogenic sequence mutations.