Shigella spp. are transmitted by the fecal-oral route and enter the human body via the ingestion of contaminated food or water. The bacteria are highly infectious, since as few as 10 to 100 microorganisms are sufficient to cause disease.
The organisms invade the cells lining the colonic mucosa and multiply there, killing the cell; this is the cause of the symptoms produced. However, it occasionally invades the bowel beyond the surface lining.
The pathogenesis of Shigella is based on the bacteria’s ability to invade and replicate within the colonic epithelium, which triggers an intense acute inflammatory response with infiltration by polymorphonuclear leukocytes.
An early symptom, diarrhea (possibly elicited by enterotoxins and/or cytotoxin), may occur as the organisms pass through the small intestine.
The pathogenesis of Shigella is a multi-step process which depends on the capacity of the bacteria to cross the colonic mucosa via M cells (microfold cells) associated with Gastrointestinal Associated Lymphoid Tissue (GALT). M cells are specialized epithelial cells (EC), which continuously sample particles from the gut lumen and deliver them to the underlying mucosal lymphoid tissue, where immune responses can be initiated.
The bacteria then invade epithelial cells and have the capacity to reprogram these cells to produce pro-inflammatory mediators, such as interleukin 8, which play a major role in the strong inflammatory response facilitating further bacterial invasion.
Colitis in the rectosigmoid mucosa, with concomitant malabsorption, results in the characteristic sign of bacillary dysentery: scanty, unformed stools tinged with blood and mucus.
The severity of Shigella infections is dependent upon many factors such as previous exposure and infecting dose. These infections are usually self-limiting, but dysentery can be a life-threatening illness in infants and in the elderly or malnourished.
Pathogenesis of Shigella
