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  Pathogenesis of Shigella

Pathogenesis of Shigella:

Bacillary dysentery might follow ingestion of as few as ten viable bacteria. The location of infection is the M cells in the Peyer’s patches of the large intestine. The shigellae multiply in the epithelial cells and spread laterally into adjacent cells, and ulcers are produced. The infected epithelial cells are killed and another cell builds up an inflammatory reaction with capillary thrombosis. As an outcome, polymorphonuclear leucocytes, red blood cells and damaged epithelial cells are poured in the lumen of intestine. They are excreted in the stool all along with other materials.

Shigellae rarely attack other tissues. Rare bacteraemia can take place, however septicemia is very rare.

Sh. dysenteriae I generates a potent protein toxin (i.e., Shigatoxin). Shiga toxin stays active within endosomes. It prevents protein synthesis and cause cell death. Hemolytic uraemic syndrome is considered to be caused by the action of shiga toxin on kidney tissues. It has too been revealed to have neurotoxic properties.

 

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