Abstract
BackgroundShiga toxin (stx) genes have been transferred to numerous bacteria, one of which is E. coli O157:H7. It is a common belief that stx gene is transferred by bacteriophages, because stx genes are located on lambdoid prophages in the E. coli O157:H7 genome. Both E. coli O157:H7 and non-pathogenic E. coli are highly enriched in cattle feedlots. We hypothesized that strong UV radiation in combination with high temperature accelerates stx gene transfer into non-pathogenic E. coli in feedlots.Methodology/Principal Findings E. coli O157:H7 EDL933 strain were subjected to different UV irradiation (0 or 0.5 kJ/m2) combination with different temperature (22, 28, 30, 32, and 37°C) treatments, and the activation of lambdoid prophages was analyzed by plaque forming unit while induction of Stx2 prophages was quantified by quantitative real-time PCR. Data showed that lambdoid prophages in E. coli O157:H7, including phages carrying stx2, were activated under UV radiation, a process enhanced by elevated temperature. Consistently, western blotting analysis indicated that the production of Shiga toxin 2 was also dramatically increased by UV irradiation and high temperature. In situ colony hybridization screening indicated that these activated Stx2 prophages were capable of converting laboratory strain of E. coli K12 into new Shiga toxigenic E. coli, which were further confirmed by PCR and ELISA analysis.Conclusions/SignificanceThese data implicate that high environmental temperature in combination with UV irradiation accelerates the spread of stx genes through enhancing Stx prophage induction and Stx phage mediated gene transfer. Cattle feedlot sludge are teemed with E. coli O157:H7 and non-pathogenic E. coli, and is frequently exposed to UV radiation via sunlight, which may contribute to the rapid spread of stx gene to non-pathogenic E. coli and diversity of shiga toxin producing E. coli.
Highlights
Escherichia coli (E. coli) O157:H7 and non-O157 Shiga toxin producing E. coli (STEC) serotypes, most commonly O26, O111, and O103, are responsible for many food-borne diseases [1] and cause deadly diseases or even death in humans
It is widely regarded that E. coli O157:H7 and other STEC obtained the Shiga toxin genes through horizontal gene transfer mediated by lambda phages, because stx genes are located in lambdoid prophages within E. coli O157:H7 genome [6,7]
Rates of lambdoid prophage activation differed among E. coli O157:H7 strains
Summary
Escherichia coli (E. coli) O157:H7 and non-O157 Shiga toxin producing E. coli (STEC) serotypes, most commonly O26, O111, and O103, are responsible for many food-borne diseases [1] and cause deadly diseases or even death in humans. It is widely regarded that E. coli O157:H7 and other STEC obtained the Shiga toxin (stx) genes through horizontal gene transfer mediated by lambda phages, because stx genes are located in lambdoid prophages within E. coli O157:H7 genome [6,7]. Whether lambdoid prophages in STEC is sensitized by temperature as lambda prophages, and whether there is a synergistic effect of UV light and elevated temperature on its activation has not been tested This is an important question, because global warming increases environmental average temperature, which may accelerate phage activation and the spread of stx genes. It is a common belief that stx gene is transferred by bacteriophages, because stx genes are located on lambdoid prophages in the E. coli O157:H7 genome Both E. coli O157:H7 and non-pathogenic E. coli are highly enriched in cattle feedlots. We hypothesized that strong UV radiation in combination with high temperature accelerates stx gene transfer into nonpathogenic E. coli in feedlots
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