Relationship between stress adaptation and virulence in foodborne pathogenic bacteria

Bacteria capable of causing foodborne infections must negotiate a long and tortuous passage from the environment to the site of infection in the susceptible host. Foodborne pathogens may encounter stressful environments during the production, preparation and storage of food. Following consumption they are exposed to the low pH of the stomach and survivors subsequently encounter volatile fatty acids, bile and low oxygen in the small intestine. Bacteria that survive to this point must compete with established gut flora for niches and nutrients and must overcome, among other insults, antimicrobial peptides produced by their competitors (Dunne et al., 1999). Those organisms capable of invasion subsequently penetrate the gut epithelium and are internalized within phagosomes, specialized organelles which prevent bacterial multiplication by means of acidic pH, and through the production of defensins (oxygen-independent mechanisms), hydrogen peroxide and superoxide radicals (oxygen-dependent mechanisms). To survive and grow in these inhospitable environments, foodborne pathogens possess mechanisms to overcome these stresses, and thus are capable of colonization resulting in either clinical or sub-clinical infection. In this chapter, the mechanisms employed by foodborne pathogens to adapt to the host environment and cause disease have been considered. Our primary focus is the pathogenesis of Listeria monocytogenes and Salmonella enterica serovar Typhimurium as examples of Gram-positive and Gram-negative foodborne pathogens capable of causing invasive disease in a mouse model of infection.