Shigella is a genus of bacteria that is Gram negative, facultatively anaerobic, Endospore, nonmotile, rod shaped, and is genetically nested within Escherichia. The genus is named after Kiyoshi Shiga, who discovered it in 1897.
Shigella causes disease in , but not in other mammals; it is the causative agent of human shigellosis.
Shigella is a leading cause of bacterial diarrhea worldwide, with 80–165 million annual cases (estimated) and 74,000 to 600,000 deaths.
It is one of the top four pathogens that cause moderate-to-severe diarrhea in African and South Asian children.
Groups A– C are physiologically similar; S. sonnei (group D) can be differentiated based on biochemical metabolism assays.
Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants. The Shigella share most of their genes with those of E. coli K12 strain MG1655, a well-studied model strain.
Phylogenetics studies indicate Shigella is more appropriately treated as a subgroup of Escherichia (see Escherichia coli#Diversity for details).
Because they do not interact with the apical surface of epithelial cells — preferring the basolateral side — Shigella species invade the host through the M-cells interspersed in the epithelia of the small intestine. Shigella uses a type-III secretion system that acts as a biological syringe to translocate toxic effector proteins to the target human cell. The effector proteins can alter the metabolism of the target cell — leading, for example, to the lysis of Vacuole membranes or reorganization of actin polymerization to facilitate intracellular motility of Shigella bacteria inside the host cell. For instance, the IcsA effector protein (an autotransporter, not a type-III secretion-system effector) triggers actin reorganization by N-WASP recruitment of Arp2/3 complexes, promoting cell-to-cell spread. The Type III Secretion System (T3SS) plays a crucial role when Shigella secretes its OspC1 and OspC3 proteins to suppress the interferon (IFN) signaling pathway and inhibit the host defense against Shigella. These proteins have been found to target the JAK/STAT signaling pathway, reducing and preventing interferon-stimulated gene (ISG) expression.
OspC1 and OspC3 inhibit IFN signaling by binding to calmodulin (CaM), which is required for the phosphorylation of STAT. These Shigella proteins interact with CaM through their N-terminal α-helix, which mimics the interaction with CaMKII. As a result, CaM mistakenly recognizes the bacterial proteins as CaMKII, preventing the normal function of the signaling pathway and blocking ISG expression.
After infection, Shigella cells multiply intracellularly and spread to neighboring epithelial cells, resulting in tissue destruction and the characteristic pathology of shigellosis. The most common symptoms are diarrhea, fever, nausea, vomiting, , and flatulence. Infection is also commonly known to cause large and painful bowel movements. The stool may contain blood, mucus, or pus. Hence, Shigella cells may cause dysentery. In rare cases, young children may have seizures. Symptoms can take as long as a week to appear, but most often begin two to four days after ingestion. Symptoms usually last for several days, but can last for weeks. Shigella is implicated as one of the pathogenic causes of reactive arthritis worldwide.
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