Escherichia coli typically colonises the gastrointestinal tract of human infants wtihin a few hours after birth. Usually, E. coli and its human host coexist in good health and with mutual benefit for decades. However, there are several highly adapted E. coli clones that have acquired specific virulence attributes, which confirm an increased ability to adapt to new niches and allow them to cause a broad spectrum of disease. Three general clinical syndromes can result from E. coli infection: enteric/diarrhoeal disease, urinary tract infections (UTIs) and sepsis/meningitis.

Bacterial adhesion to and subsequent colonization of surfaces are the first steps towards forming biofilms, which are a major concern for implanted medical devices and in many diseases. Biofilms are resistant to innate host defences, mechanical removal and antibiotic treatments. It is therefore important to understand the physiological environment and mechanisms that lead to the spread of bacteria.

Type 1 fimbriae are the most common type of adhesive organelles in E. coli and mediate mannose-specific adhesion via the fimbrial tip-associated lectin-like subunit FimH. FimH mediates ‘catch-bonds’ with mannose that are strengthened by tensile mechanical force. The environmental shear stress is of great importance in gaining an insight into the mechanism by which bacteria thrive, becoming resistant to therapies.