A complex network of regulatory systems ensures a coordinated and effective response to different types of stress that can act on a bacterium. Bacterial stress response generates changes that influence efflux system and virulence factor expression. Thus, partial or total loss of pathogenicity islands in uropathogenic Escherichia coli can be induced by SOS-dependent or SOS-independent pathways related to selection of quinolone-resistant mutants. Likewise, hyperosmolarity and some chemicals, including fluoroquinolones, salicylate, nonantimicrobial medicaments like diazepam and anti-inflammatory drugs are all able to induce an increased active efflux, cyclohexane tolerance, loss of porins, and decreased susceptibility to multiple antimicrobials in enterobacterial strains, suggesting that bacterial response to the stress caused by an increase in osmolarity might be linked to the development of the multidrug-resistant phenotypes. Finally, a sudden downshift of the growth temperature (cold-shock) triggers a drastic reprogramming of bacterial gene expression to allow cell survival under the new unfavorable conditions. The strategy developed by E. coli to reach this goal consists in the induction of a set of (cold-shock) genes whose expression is regulated at both transcriptional and posttranscriptional levels.