Potentiation of Antibiotics by a Novel Antimicrobial Peptide against Shiga Toxin Producing E. coli O157:H7.

Infection with Shiga toxin-producing Escherichia coli (STEC) results in hemorrhagic colitis and can lead to life-threatening sequelae including hemolytic uremic syndrome (HUS). Conventional treatment is intravenous fluid volume expansion. Antibiotic treatment is contraindicated, due in part to the elevated risk of HUS related to increased Shiga toxin (Stx) release associated with some antibiotics.

Differential modulation of flagella expression in enterohaemorrhagic Escherichia coli O157: H7 by intestinal short-chain fatty acid mixes.

During passage through the gastrointestinal tract, enterohaemorrhagic Escherichia coli (EHEC) encounters numerous stresses, each producing unique antimicrobial conditions. Beyond surviving these stresses, EHEC may also use them as cues about the local microenvironment to modulate its virulence. Of particular interest is how exposure to changing concentrations of short-chain fatty acids (SCFAs) associated with passage through the small and large intestines affects EHEC virulence, as well as flagella expression and motility specifically.

Acid and bile-salt stress of enteropathogenic Escherichia coli enhances adhesion to epithelial cells and alters glycolipid receptor binding specificity.

Background: Enteropathogenic Escherichia coli (EPEC), a diarrheagenic pathogen, is exposed to stress during ingestion, and yet little is known about the impact of stress on EPEC-host cell adhesion.

Methods: EPEC adhesion to human epithelial cells was assessed by plate-count assay before and after bacterial stress. Stress treatments included exposure to low pH (with or without acid adaptation) and exposure to physiological concentrations of 4 intestinal bile salts.