Shigella Infection

Shigella infection is caused by Gram-negative, facultative anaerobic rods of the Enterobacteriaceae family, primarily transmitted via the fecal-oral route through contaminated food or water, resulting in a spectrum of disease from mild diarrhea to severe bacillary dysentery. Unlike Campylobacter jejuni, Shigella employs distinct molecular mechanisms for pathogenesis, characterized by actin-dependent invasion of intestinal mucosa through M cells via macropinocytosis, followed by rapid vacuolar membrane disruption and intracellular replication. The bacterium produces the IcsA protein, which nucleates actin tails that propel it through host cells, facilitating cell-to-cell spread. Internalization into submucosal monocytes triggers apoptosis and release of proinflammatory IL-1β, while infected epithelial cells secrete IL-8, recruiting lymphocytes from the lamina propria. The resulting tissue destruction and intense local inflammation underlie the clinical manifestations of dysentery.