Overview of pathogenic Escherichia coli, with a focus on Shiga toxin-producing serotypes, global outbreaks (1982-2024) and food safety criteria.

Abstract

Classification of pathogenic E. coli has been focused either in mammalian host or infection site, which offers limited resolution. This review presents a comprehensive framework for classifying all E. coli branches within a single, unifying figure. This approach integrates established methods based on virulence factors, serotypes and clinical syndromes, offering a more nuanced and informative perspective on E. coli pathogenicity. The presence of the LEE island in pathogenic E. coli is a key genetic marker differentiating EHEC from STEC strains. The coexistence of stx and eae genes within the bacterial genome is a primary characteristic used to distinguish STEC from other pathogenic E. coli strains. The presence of the inv plasmid, Afa/Dr adhesins, CFA-CS-LT-ST and EAST1 are key distinguishing features for identifying pathogenic E. coli strains belonging to EIEC, DAEC, ETEC and EAEC pathotypes respectively. Food microbiological criteria differentiate pathogenic E. coli in food matrices. 'Zero-tolerance' applies to most ready-to-eat (RTE) foods due to high illness risk. Non-RTE foods' roles may allow limited E. coli presence, which expose consumers to potential risk; particularly from the concerning Shiga toxin-producing E. coli (STEC) strains, which can lead to life-threatening complications in humans, including haemolytic uremic syndrome (HUS) and even death in susceptible individuals. These findings suggest that decision-makers should consider incorporating the separate detection of STEC serotypes into food microbiological criteria, in addition to existing enumeration methods. Contamination of STEC is mainly linked to food consumption, therefore, outbreaks of E. coli STEC has been reviewed here and showed a link also to water as a potential contamination route. Since their discovery in 1982, over 39,787 STEC cases associated with 1,343 outbreaks have been documented. The majority of these outbreaks occurred in the Americas, followed by Europe, Asia and Africa. The most common serotypes identified among the outbreaks were O157, the 'Big Six' (O26, O45, O103, O111, O121, and O145), and other serotypes such as O55, O80, O101, O104, O116, O165, O174 and O183. This review provides valuable insights into the most prevalent serotypes implicated in STEC outbreaks and identifies gaps in microbiological criteria, particularly for E. coli non-O157 and non-Big Six serotypes.