Listeria as an enteroinvasive gastrointestinal pathogen.

The bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Listeria spp. are isolated from a diversity of environmental sources, including soil, water, effluents, a large variety of foods, and the feces of humans and animals. Recent outbreaks demonstrated that L. monocytogenes can cause gastroenteritis in otherwise healthy individuals and more severe invasive disease in immunocompromised patients. Common symptoms include fever, watery diarrhea, nausea, headache, and pains in joints and muscles. The intestinal tract is the major portal of entry for L. monocytogenes, whereby strains penetrate the mucosal tissue either directly, via invasion of enterocytes, or indirectly, via active penetration of the Peyer's patches. Studies have revealed the strategy taken by the bacteria to overcome changes in oxygen tension, osmolarity, acidity, and the sterilizing effects of bile or antimicrobial peptides to adapt to conditions in the gut. In addition, L. monocytogenes has evolved species-specific strategies for intestinal entry by exploiting the interaction between the internalin protein and its receptor E-cadherin, or inducing diarrhea and an inflammatory response via the activity of its hemolytic toxin, listeriolysin. The ability of these bacteria to survive in bile-rich environments, and to induce depletion of sentinel cells such as Paneth cells that monitor the luminal burden of commensal bacteria, suggest strategies that have evolved to promote intestinal survival. Preexisting gastrointestinal disease may be a risk factor for infection of the gastrointestinal tract with L. monocytogenes. Currently, there is enough evidence to warrant consideration of L. monocytogenes as a possible etiology in outbreaks of febrile gastroenteritis, and for further studies to examine the genetic structure of Listeria strains that have a propensity to cause gastrointestinal versus systemic infections.