[1] Shigella are closely related to Escherichia coli, but can be differentiated from E.coli based on pathogenicity, physiology (failure to ferment lactose or decarboxylate lysine) and serology.

Shiga entered the Tokyo Imperial University School of Medicine in 1892, during which he attended a lecture by Dr. Shibasaburo Kitasato.

Shiga was impressed by Dr. Kitasato's intellect and confidence, so after graduating, he went to work for him as a research assistant at Institute for Infectious Diseases.

[3] Shiga studied 32 dysentery patients and used Koch's Postulates to successfully isolate and identify the bacterium causing the disease.

It produces the protein actin in a swift and continuous fashion to propel itself forward within and between the host's cells.

[6] Shigella flexneri is an intracellular bacterium that infects the epithelial lining of the mammalian intestinal tract.

[7] Once inside of the colon, S. flexneri can penetrate the epithelium in three ways: 1) The bacterium can alter the tight junctions between the epithelial cells, allowing it to cross into the sub-mucosa.

The influx of PMN cells across the epithelial layer in response to Shigella disrupts the integrity of the epithelium allowing lumenal bacteria to cross into the sub-mucosa in an M-cell independent mechanism.

[8] S. flexneri can pass to neighboring epithelial cells by using its own outer membrane protein, IcsA, to activate the host's actin assembly machinery.

Arp 2/3 Complex is the protein responsible for rapidly initiating actin polymerization and propelling the bacteria forward.

All of the genes needed for S. flexneri to invade the epithelial lining of the colon are found on a virulence plasmid called pINV.

It utilizes the Embden-Meyerhof-Parnas (EMP), Entner-Doudoroff (ED), or pentose phosphate pathway (PPP) to metabolize sugars.

[15] Ssr1 sRNA, which could play role in resistance to acidic stress and regulation of virulence was shown to exist only in Shigella.

[17] Upon infection, S. flexneri injects the host cell cytoplasm with ipa proteins using the T3SS—a needle-and-syringe-like apparatus common to many Gram-negative pathogens.