Shigatoxigenic and verotoxigenic Escherichia coli
[6] Shiga toxin–producing Escherichia coli are zoonotic pathogens, in that they can be found in the gastrointestinal tract of cattle and sheep, and can infect humans.
[citation needed] The clinical presentation in humans ranges from a mild and uncomplicated diarrhea to a hemorrhagic colitis with severe abdominal pain.
Infections are most common in warmer months and in children under five years of age and are usually acquired from uncooked beef and unpasteurized milk and juice.
In children, a complication can be hemolytic uremic syndrome which then uses cytotoxins to attack the cells in the gut, so that bacteria can leak out into the blood and cause endothelial injury in locations such as the kidney by binding to globotriaosylceramide (Gb3).
The clinical manifestations of postdiarrheal HUS include acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia.
Hemolytic anemia results from intravascular fibrin deposition, increased fragility of red blood cells, and fragmentation.
Antibiotics that interfere with DNA synthesis, such as fluoroquinolones, have been shown to induce the Stx-bearing bacteriophage and cause increased production of toxins.
The use of antimotility agents (medications that suppress diarrhea by slowing bowel transit) in children under 10 years of age or in elderly patients should be avoided, as they increase the risk of HUS with EHEC infections.
At least one reference holds "EHEC" to be mutually exclusive of "VTEC" and "STEC",[3] but this does not match common usage, as many more publications lump all of the latter in with the former.
[1][11]: 2–3 Historically, a different name was sometimes used because the toxins are not exactly the same as the one found in Shigella dysenteriae, down to every last amino acid residue, although by this logic every "STEC" would be a "VTEC".
[citation needed] To successfully colonize the gut of its host, EHEC relies on attaching itself to epithelial cells in the large intestine.
The toxins interact with intestinal epithelium and can cause systematic complications in humans like HUS and cerebral dysfunction if they enter the circulation.
[citation needed] When QseC or QseE bind with one of their interacting signalling molecule, they autophosphorylate and transfer its phosphate to the response regulator.
However, when fucose concentration decreases because bacterial cells find an unprotected area of the epithelium, then the expression of LEE genes will not be repressed by FusR, and KpdE will strongly activate them.
