A small inoculum of Shigella (10 to 200 organisms) is sufficient to cause<unk> . Shigella is commonly spread by the fecal-oral route in regions of poor sanitation (foodborne or waterborne transmission). Shigella first invades the epithelial cells of the large intestine by using M cells as entry ports for transcytosis. Shigella then invades macrophages and induces cellular apoptosis, which results in inflammation, generation of proinflammatory cytokines, and recruitment of polymorphonuclear neutrophils (PMNs). Following transcytosis and macrophage apoptosis, Shigella avoids extracellular exposure and spreads intercellularly using actin polymerization processes (rocket propulsion). As PMN invade the site of active inflammation, the integrity of the intestinal epithelial barrier is lost, and adsorption of fluids and nutrients is impaired, resulting in clinical manifestations of<unk>  (e.g. diarrhea). On gross pathology, hyperemia with development of ulcers and edema are typical findings. On microscopic pathology, infiltration of PMN and inflammatory pseudomembranes are characteristic features.
Shigellosis pathophysiology
Brucellosis pathophysiology
Salmonellosis pathophysiology
Campylobacteriosis pathophysiology
Legionellosis pathophysiology
Babesiosis pathophysiology
Escherichia coli enteritis pathophysiology
Schistosomiasis pathophysiology