The basal body of the type-III secretion system of Yersinia enterocolitica within bacterial membranes shows elasticity and is longer than related isolated systems.

The major evolutionary routes to drug resistance in Salmonella Typhi are associated with fitness benefits, not fitness costs, implying that prudent antimicrobial use will have no effect as a public health intervention in controlling typhoid fever.

Metabolite analysis of plasma from enteric fever patients define signals of organism specific host–pathogen interactions and provides opportunities for new diagnostics.

Serum amyloid A proteins bind retinol with nanomolar affinity, and do so by forming oligomers that create a hydrophobic pocket that shields retinol from the aqueous environment.

The regulatory RNA RydC binds to Hfq to make an effector complex for the recognition of targeted mRNA in the regulation of genetic information.

Receptor recognition of antimicrobial peptides is important for Salmonellae to survive inside macrophages and cause disease.

Yersinia pseudotuberculosis and enteropathogenic Escherichia coli promote pathogenicity by deamidating the ubiquitin-like protein NEDD8 to block ubiquitin-dependent trafficking of Perforin-2, which is an effector of innate immunity.

A response regulator acquired via lateral gene transfer has rewired an ancestral genetic circuitry and regulates alternative pathogenic lifestyles.

Live intracellular bacterial pathogens can transfer from infected cells to uninfected macrophages upon cell-to-cell contact.