Impacts of grape seed extract on shiga toxin production, motility and biofilm formation in Shiga toxin producing Escherichia coli.

摘要

Shiga toxin producing Escherichia coli (STEC) include many serotypes that are capable of causing human illness including gastric upset, hemolytic colitis, hemorrhagic uremic syndrome (HUS) and possibly death. E. coli O157:H7 is the most common serotype in the United States capable of causing foodborne illness. To ensure food safety, both live E. coli O157:H7 and its toxin production in food products need to be controlled. Centers for Disease Control and Prevention (CDC) has designated six strains of non-O157 Shiga toxin producing E. coli (STEC) to be of growing concern in the food industry and causing illness. These six serotypes are referred to as the "top-six" and include: O26, O45, O103, O111, O121 and O145. Even though these six strains are usually not regarded to be dangerous as E. coli O157:H7 they still are capable of producing Shiga toxin (Stx), which can cause bloody diarrhea and even death. Natural ingredients with inhibitory effects on STEC growth and toxin production are preferred choices of antimicrobials for the food industry. The objectives of this study were to quantify the effect of grape seed extract (GSE) on the growth, Shiga toxin production, motility and biofilm formation of E. coli O157:H7 strain EDL933 and the "top-six" non-O157 STEC. The MIC indicated that STEC serotypes O157:H7, O45:NM, O103:H2, and O121:H19 were equally sensitive to GSE. Serotypes O145:NT was the most sensitive to GSE followed by serotypes O111:H2 and O26:H11. In E. coli O157:H7, western blotting indicated that GSE at a level 0.125-2 mg/ml all had lower Stx production (P < 0.05) as compared to the no GSE control. There was a dose dependent decrease in Stx production until 2 mg/ml, then a subsequent increase with 4 mg/ml Stx production reaching levels comparable to 0 mg/ml control. In all STEC tested, GSE inhibited motility while causing an increase in biofilm formation. At 5×105 CFU/ml inoculation level, low concentrations, 0.125-0.5 mg/ml, of GSE have the propensity to increase growth in O26:H11, O103:H2, O111:H2 and O157:H7. In conclusion, GSE at 4 mg/ml effectively inhibited the growth of E. coli O157:H7 as well as non-O157 STEC, decreased motility of the pathogens, but enhanced biofilm formation. GSE concentrations between 0.25 and 2 mg/ml showed inhibitory effects on Stx production of E. coli O157:H7.