Shigella: Virulence Factors and Pathogenicity

Abstract

Each year, Shigella species are responsible for an estimated 100–150 million infections worldwide, with nearly 500,000 of these infections occurring in the United States, where approximately 30% of cases can be attributed to the ingestion of contaminated foods. Clinical symptoms associated with shigellosis (otherwise known as bacillary dysentery) include diarrhea, sometimes bloody; fever; stomach cramps; and tenesmus. Possible sequellae of Shigella infection can include hemolytic uremic syndrome (HUS) or rheumatoid arthritis. This pathogen possesses a repertoire of virulence factors that modulate the host innate/adaptive immune systems and enable the bacteria to invade colonic epithelial cells, escape from phagocytic vesicles, and finally destroy mucosal cells lining the intestinal tract. One of the hallmarks of Shigella pathogenesis is utilization of the type three secretion system (T3SS) to insert bacterial effector proteins into host cells. Most of the genetic factors necessary for pathogenicity reside on a large virulence plasmid (pINV), while a few of these genes are in chromosomal pathogenicity islands.