Quick Facts Shigella flexneri, Scientific classification ...

Shigella flexneri
Shigella flexneri
Scientific classification
Domain:	Bacteria
Phylum:	Pseudomonadota
Class:	Gammaproteobacteria
Order:	Enterobacterales
Family:	Enterobacteriaceae
Genus:	Shigella
Species:	S. flexneri
Binomial name
Shigella flexneri Castellani & Chalmers 1919

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Shigella flexneri is a species of Gram-negative bacteria in the genus Shigella that can cause diarrhea in humans. Several different serogroups of Shigella are described; S. flexneri belongs to group B. S. flexneri infections can usually be treated with antibiotics, although some strains have become resistant. Less severe cases are not usually treated because they become more resistant in the future.^[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.^[2]

The species was named after the American physician Simon Flexner; the genus Shigella is named after Japanese physician Kiyoshi Shiga, who researched the cause of dysentery. 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. In 1897, Shiga focused his efforts on what the Japanese referred to as a "Sekiri" (dysentery) outbreak. These epidemics were detrimental to the Japanese people and occurred often in the late 19th century. The 1897 sekiri epidemic affected >91,000, with a mortality rate of >20%.^[3] Shiga studied 32 dysentery patients and used Koch's Postulates to successfully isolate and identify the bacterium causing the disease. He continued to study and characterize the bacterium, identifying its methods of toxin production i.e. Shiga Toxin, and worked tirelessly to create a vaccine for the disease.

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Shigella flexneri contains a virulence plasmid that codes for three virulence factors: a type-3 secretion system (T3SS), invasion plasmid antigen proteins (IPA proteins), and IcsA (used for cell-to-cell spread).^[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. These ipa proteins induce "membrane ruffling" by the host cell. Membrane ruffling creates membrane pockets which capture and engulf the bacteria. Once inside, S. flexneri uses host cell actin for propulsion to move directly from cell to cell using a cellular mechanism known as paracytophagy,^[18][19] similarly to the bacterial pathogen Listeria monocytogenes.

Shigella flexneri is able to inhibit the acute inflammatory response in the initial stage of infection^[20] by using an effector protein, OspI, which is encoded by ORF169b on the Shigella large plasmid and secreted by the type III secretion system. It dampens the inflammatory response during bacterial invasion by suppressing the TNF-α-receptor-associated factor 6 (TRAF6)-mediated signalling pathway.^[20] OspI has glutamine deamidase activity, and is able to selectively deaminate glutamine at position 100 in UBC13 to glutamate, and this results in a failure of the E2 ubiquitin-conjugating activity which is required for TRAF6 activation.^[20]