Caused by Shigella species (S. sonnei, S. flexneri, S. boydii, S. dysenteriae), which are Gram-negative, non-lactose fermenting, non-motile rods.
Transmission: Fecal-oral route, often via contaminated food or water, or person-to-person contact. It is common in young children, particularly those in daycare.
Mechanism: Highly virulent with a very low infectious dose (as few as 10-100 organisms) because it is acid-stable. It invades the gastrointestinal mucosa, primarily in the large intestine, through M cells of Peyer’s patches. It then escapes the phagosome and spreads laterally from cell to cell using the host’s actin filaments (no hematogenous spread), causing mucosal ulceration and inflammation.
Toxin: Some strains, particularly S. dysenteriae, produce Shiga toxin, which inactivates the 60S ribosomal subunit, inhibiting protein synthesis. However, the primary cause of pathology is direct mucosal invasion.
Cholera
Pathogen: Vibrio cholerae
Infectivity
Acid-labile (grows well in an alkaline medium)
High infective dose required (over 108 pathogens)
Gastric acid provides a natural barrier against V. cholerae infection
Patients on long PPI are more easily to get infected
