Shiga toxin

[1] The toxins are named after Kiyoshi Shiga, who first described the bacterial origin of dysentery caused by Shigella dysenteriae.

[4][5] Microbiologists use many terms to describe Shiga toxin and differentiate more than one unique form.

[2] In 1977, researchers in Ottawa, Ontario discovered the Shiga toxin normally produced by Shigella dysenteriae in a line of E.

It has been suggested by some researchers that the gene coding for Shiga-like toxin comes from a toxin-converting lambdoid bacteriophage, such as H-19B or 933W, inserted into the bacteria's chromosome via transduction.

[14]: 2–3 The toxin requires highly specific receptors on the cells' surface in order to attach and enter the cell; species such as cattle, swine, and deer which do not carry these receptors may harbor toxigenic bacteria without any ill effect, shedding them in their feces, from where they may be spread to humans.

[15] Symptoms of Shiga toxin ingestion include abdominal pain as well as watery diarrhea.

Destroying these structures leads to kidney failure and the development of the often deadly and frequently debilitating hemolytic uremic syndrome.

Food poisoning with Shiga toxin often also has effects on the lungs and the nervous system.

The B subunits of the toxin bind to a component of the cell membrane known as glycolipid globotriaosylceramide (Gb3).

Some toxin-receptor complexes reportedly bypass these steps and are transported to the nucleus rather than the cytosol, with unknown effects.