A highly contagious intestinal disease caused by rod-shaped bacteria of the genus Shigella. Bacillary dysentery is a significant infection of children in the developing world, where it is transmitted by the fecal-oral route. The global disease burden is estimated as 165 million episodes and 1.3 million deaths annually. Common-source outbreaks occasionally occur in developed countries, usually as a result of contaminated food. The most common species isolated in developed countries is S. sonnei, while S. flexneri serotypes predominate in endemic areas. Epidemics of S. dysenteriae 1 occur in equatorial regions, and these outbreaks can involve adults as well as children.
When ingested even in very small numbers, shigellae multiply in the intestine and invade the epithelial lining of the colon. Infection of this tissue elicits an acute inflammatory response (colitis) that is manifested as diarrhea or bloody, mucoid stools (dysentery). The virulence of all Shigella species, and Shigella-like enteroinvasive Escherichia coli, depends on an extrachromosomal genetic element (virulence plasmid) that encodes four invasion plasmid antigen (Ipa) proteins and a secretory system (Type III) for these proteins. Secreted Ipa proteins help shigellae to initiate colonic invasion through specialized endocytic intestinal cells (M cells). After shigellae pass through these M cells, they are phagocytized by tissue macrophages in the underlying lymphoid tissue. Ipa proteins then induce apoptosis (programmed cell death) in infected macrophages, releasing cytokines (primarily IL-1) that initiate an acute, localized inflammatory infiltrate. This infiltrate of polymorphonuclear leukocytes destabilizes tight junctions between absorptive epithelial cells (enterocytes), making the tissue more susceptible to additional Shigella invasion. Secreted Ipa proteins induce uptake of shigellae by the colonic enterocytes. The virulence plasmid also encodes an intercellular spread protein (IcsA) that recruits mammalian cytoskeletal elements (primarily actin) to the bacterial surface. This actin is organized into a cytoplasmic motor that facilitates spread of shigellae to adjacent enterocytes. See Escherichia
In otherwise healthy individuals, bacillary dysentery is typically a short-term disease lasting less than a week. The symptoms can be truncated by appropriate antibiotic therapy (such as oral ampicillin or cyprofloxacin) that rapidly eliminates shigellae from the intestinal lumen and tissues. When S. dysenteriae 1 is the etiologic agent, however, hemolytic uremic syndrome can be manifested as a serious consequence of disease. This species produces a cytotoxin (Shiga toxin or Stx) that is functionally identical to the toxin of enterohemorrhagic E. coli (for example, O157:H7). Stx inhibits protein synthesis, damaging endothelial cells of the intestinal capillary bed; the toxin may also damage renal tubules, causing acute renal failure with chronic sequela in up to one-third of hemolytic uremic syndrome patients. See Medical bacteriology