Editing Salmonella (section)

=== Switch to virulence ===
While travelling to their target tissue in the gastrointestinal tract, ''Salmonella'' is exposed to stomach acid, to the detergent-like activity of bile in the intestine, to decreasing oxygen supply, to the competing normal gut flora, and finally to antimicrobial peptides present on the surface of the cells lining the intestinal wall. All of these form stresses that ''Salmonella'' can sense and reacts against, and they form [[virulence factor]]s and as such regulate the switch from their normal growth in the intestine into [[virulence]].<ref>{{cite journal | vauthors = Rychlik I, Barrow PA | title = Salmonella stress management and its relevance to behaviour during intestinal colonisation and infection | journal = FEMS Microbiology Reviews | volume = 29 | issue = 5 | pages = 1021–1040 | date = November 2005 | pmid = 16023758 | doi = 10.1016/j.femsre.2005.03.005 | doi-access = free }}</ref>

The switch to virulence gives access to a replication [[niche differentiation|niche]] inside the host (such as humans), and can be summarised into several stages:{{citation needed|date=September 2022}}

# Approach, in which they travel towards a host cell via intestinal [[peristalsis]] and through active swimming via the [[Flagellum|flagella]], penetrate the mucus barrier, and locate themselves close to the [[epithelium]] lining the intestine,
# Adhesion, in which they adhere to a host cell using bacterial [[Bacterial adhesin|adhesins]] and a [[type III secretion system]],
# Invasion, in which ''Salmonella'' enter the host cell (see variant mechanisms below),
# Replication, in which the bacterium may reproduce inside the host cell,
# Spread, in which the bacterium can spread to other organs via cells in the blood (if it succeeded in avoiding the immune defence). Alternatively, bacteria can go back towards the intestine, re-seeding the intestinal population.
# Re-invasion (a ''secondary infection'', if now at a systemic site) and further replication.