For many years the Gram-positive facultatively intracellular food-borne pathogen Listeria monocytogenes has been used as a model organism for the study of intracellular parasitism. Whilst the basic mechanisms of cellular pathogenesis have been elucidated by a series of elegant studies, recent research has begun to focus upon the gastrointestinal (GI) phase of L. monocytogenes infection. Epidemiological studies of outbreaks of human disease now demonstrate that the pathogen can cause gastroenteritis in the absence of invasive disease and associated mortality. Furthermore, the pathogen has the ability to colonize the gallbladder in infected mice and this may function as a significant focus of infection during pathogenesis. The ability of the pathogen to survive within the various microenvironments of the GI tract is essential for the causation of food- borne infection. Survival of the pathogen within gastric acid requires the glutamate decarboxylase ( GAD) system. In addition, the carnitine uptake system, OpuC is essential for adaptation within the murine GI tract and subsequent invasive disease. Survival of bile salts both in vitro and in vivo requires a number of mechanisms including bile salt hydrolase (Bsh) and the recently described bile exclusion system, BilE ( previously OpuB). Finally a number of these systems (including Bsh, OpuC and BilE) are regulated by both the alternative stress sigma factor, Sigma B and by the regulator of virulence gene expression, PrfA.