Abstract

The emergence of novel pathogens poses a major public health threat causing widespread epidemics in susceptible populations. The Escherichia coli O104:H4 strain implicated in a 2011 outbreak in northern Germany caused the highest frequency of hemolytic uremic syndrome (HUS) and death ever recorded in a single E. coli outbreak. Therefore, it has been suggested that this strain is more virulent than other pathogenic E. coli (e.g., E. coli O157:H7). The E. coli O104:H4 outbreak strain possesses multiple virulence factors from both Shiga toxin (Stx)-producing E. coli (STEC) and enteroaggregative E. coli (EAEC), though the mechanism of pathogenesis is not known. Here, we demonstrate that E. coli O104:H4 produces a stable biofilm in vitro and that in vivo virulence gene expression is highest when E. coli O104:H4 overexpresses genes required for aggregation and exopolysaccharide production, a characteristic of bacterial cells residing within an established biofilm. Interrupting exopolysaccharide production and biofilm formation may therefore represent effective strategies for combating future E. coli O104:H4 infections.

Highlights

  • The 2011 E. coli O104:H4 outbreak strain caused the highest frequency of hemolytic uremic syndrome (HUS) and deaths ever recorded

  • The number of HUS cases and deaths was 2.4 and 1.4 times higher in the E. coli O104:H4 outbreak, respectively, than the number reported for 350 E. coli O157:H7 outbreaks between 1982 and 2001 in the U.S These 350 E. coli O157:H7 outbreaks resulted in 8,598 cases, 354 cases of HUS and 40 deaths in the U.S [1], while over 3,816 cases were reported in the 2011 E. coli O104:H4 outbreak, with 845 cases of HUS and 54 deaths [2]

  • The results described provide insight into the mechanism of E. coli O104:H4 pathogenesis

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Summary

Introduction

The 2011 E. coli O104:H4 outbreak strain caused the highest frequency of hemolytic uremic syndrome (HUS) and deaths ever recorded. The E. coli O104:H4 outbreak strain harbors multiple virulence genes from both Shiga toxin (Stx)-producing E. coli (STEC) and enteroaggregative E. coli (EAEC) It carries the phage-borne gene encoding Stx, the primary virulence factor of STEC and enterohemorrhagic E. coli [3]. ShET1 induced fluid accumulation in rabbit ileal loops [10], while Pic facilitated intestinal colonization by enabling the bacterium to utilize mucus as a growth substrate [11]. Because this combination of factors has not previously been observed in pathogenic E. coli, the role that they play in colonization and pathogenesis is not known

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