Shiga toxin-producing Escherichia coli (STEC): a diagnostic conundrum

Shiga toxin-producing Escherichia coli (STEC) represents one of the most critical foodborne pathogens worldwide. Responsible for a clinical spectrum ranging from self-limited diarrhoea to life-threatening systemic complications such as haemolytic uraemic syndrome (HUS). STEC infections arise from a complex interaction between bacterial virulence, host susceptibility, and environmental factors. Notably, STEC has an extremely low infectious dose, with less than 100 bacteria capable of eliciting severe disease.¹ In an era of globalisation that interconnects food supply chains, coupled with climate change which reshapes pathogen ecology; our understanding and mitigation of STEC risks must be both multifaceted and dynamic. Here, we review the historical evolution and scientific advances in STEC research, including transmission dynamics, molecular pathogenicity, diagnostic challenges, and the broader socio-economic and public health implications of STEC outbreaks.

Historical overview of STEC 

In 1885, Theodor Escherich isolated E. coli from neonatal intestinal tracts, establishing its status as a commensal inhabitant of the gastrointestinal system.² Over time, scientists identified that while most E. coli strains are commensals, a subset could cause disease. An example is the identification of enteropathogenic E. coli (EPEC) in the 1940s, which identified that certain strains were able to cause diarrhoea and dysentery,³ indicating the underlying pathogenic potential of some E. coli pathotypes.