FIGURE 1.

Model of intestinal colonization by Salmonella. Most Salmonella remain associated to specific anatomical segments of the intestines using cyclical multiplication steps in the lumen and enterocytes, using (1) near surface swimming, (2) adhesion (several adhesins), (3) invasion with formation of SCV, (4.1) intravacuolar replication, (5) escape in the cytoplasm, pyroptosis and return to the intestinal surface and lumen. After intravacuolar replication, (4.2) Salmonella can also escape toward the lamina propria, resulting in their potential uptake by dendritic cells and macrophages. (6) Some Salmonella can be further transported to the mesenteric lymph nodes which frequently contain further spreading. Typically for host-restricted (e.g., serovar Typhi in humans) or host-adapted strains (e.g., serovar Dublin in bovines), but also for Salmonella with broad host range encountering stressed hosts or weakened host immune responses, (7) Salmonella can cause bacteremia. When disseminating Salmonella (whether or not host-adapted or restricted) can be somewhat controlled by the host, they typically settle in the liver, gallbladder (for mammals with this organ*), on calculi and in the biliary tract, where they can replicate and be released in the bile to return to the intestines (Oboegbulem and Muogbo, 1981; Cavallini et al., 1991; Wood et al., 1991; Pellegrini-Masini et al., 2004; Akoachere et al., 2009; He et al., 2010).