Abstract
Bacteria belonging to the genus Shigella cause bacillary dysentery, an invasive disease of the human colon. This disease is prevalent in tropical regions, particularly in some overcrowded areas of the developing world. The essential characteristics of the pathogenic potential of Shigella reside in its capacity to invade cells of the colonic epithelium (LaBrec et al., 1964; Takeuchi et al., 1968). This communication will review recent data on the molecular and cellular basis of this invasive process. “Invasion” is a general term that summarizes several stages of interaction of the bacterium with its host cell such as entry into epithelial cells, intracellular multiplication, intracellular movement and cell to cell spread, and eventually death of the host-cell (Maurelli et al., 1988). This sequence of events leads to an amplification of the bacterial inoculum within the intestinal epithelium which allows subsequent passage of numerous bacteria into the lamina propria (the connective tissue of the intestinal villus) and causes a strong inflammatory reaction which accounts for multiple abscesses ulcerated within the intestinal lumen, thus for the dysenteric symptoms characteristic of the disease: fever, abdominal cramps and tenesmus, bloody and mucopurulent stools.
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