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Shiga toxins are a family of related toxins with two major groups, Stx1 and Stx2, expressed by genes considered to be part of the genome of lambdoid prophages. [1] The toxins are named after Kiyoshi Shiga, who first described the bacterial origin of dysentery caused by Shigella dysenteriae. [2]
Shiga-toxin directly activates the alternative complement pathway and also interferes with complement regulation by binding to complement factor H, an inhibitor of the complement cascade. Shiga-toxin causes complement-mediated platelet, leukocyte, and endothelial cell activation, resulting in systemic hemolysis, inflammation and thrombosis.
The European Commission (EC) integrated approach to food safety [8] defines a case of Shiga-like toxin-producing E. coli (STEC) diarrhea caused by O104:H4 by an acute onset of diarrhea or bloody diarrhea together with the detection of the Shiga toxin 2 (Stx2) or the Shiga gene stx2. [9]
The verocytotoxin (shiga-like toxin) can directly damage renal and endothelial cells. Thrombocytopenia occurs as platelets are consumed by clotting. Hemolytic anemia results from intravascular fibrin deposition, increased fragility of red blood cells, and fragmentation.
Escherichia coli O157:H7 is a serotype of the bacterial species Escherichia coli and is one of the Shiga-like toxin–producing types of E. coli.It is a cause of disease, typically foodborne illness, through consumption of contaminated and raw food, including raw milk and undercooked ground beef.
The strain has a number of virulence genes typical of enteroaggregative E. coli, including attA, aggR, aap, aggA, and aggC, in addition to the Shiga toxin variant 2. [26] All bacteria isolated from patients in this outbreak were resistant to beta-lactam antibiotics, third-generation cephalosporins , and partially resistant to nalidixic acid ...
Tests for toxin production can use mammalian cells in tissue culture, which are rapidly killed by shiga toxin. Although sensitive and very specific, this method is slow and expensive. [49] Typically, diagnosis has been done by culturing on sorbitol-MacConkey medium and then using typing antiserum.
Some exotoxins act directly at the ribosome to inhibit protein synthesis. An example is Shiga toxin. Other toxins act at elongation factor-2. In the case of the diphtheria toxin, EF2 is ADP-ribosylated and becomes unable to participate in protein elongation, and, so, the cell dies. Pseudomonas exotoxin has a similar action.