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Shiga-like toxin (SLT) is a historical term for similar or identical toxins produced by Escherichia coli. [3] The most common sources for Shiga toxin are the bacteria S. dysenteriae and some serotypes of Escherichia coli (shigatoxigenic or STEC), which include serotypes O157:H7 , and O104:H4 .
Genome assembly and copy-number analysis both confirmed that two copies of the Shiga toxin stx2 prophage gene cluster are a distinctive characteristic of the genome of the O104:H4 outbreak strain. [5] [6] The O104:H4 strain is characterized by these genetic markers: [6] [7] Shiga toxin stx2 positive; tellurite resistance gene cluster positive
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.
HUS is caused by ingestion of bacteria that produce Shiga toxins, with Shiga-toxin producing E. coli (STEC) being the most common type. [34] E. coli can produce shigatoxin-1, shigatoxin-2, or both; with shigatoxin-2 producing organisms being more virulent and being much more likely to cause HUS. [34]
The term shiga-like toxins was previously used to further distinguish the shiga toxins produced by E. coli, but nowadays, they are collectively referred to as shiga toxins. [8] Within the STEC strains, a subgroup classified as enterohemorrhagic E. coli (EHEC) represent a class of pathogens with more severe virulence factors in addition to the ...
With correct treatment, most cases of amoebic and bacterial dysentery subside within 10 days, and most individuals achieve a full recovery within two to four weeks after beginning proper treatment. If the disease is left untreated, the prognosis varies with the immune status of the individual patient and the severity of disease.
Intracellular toxins must be able to gain access to the cytoplasm of the target cell to exert their effects. Some bacteria deliver toxins directly from their cytoplasm to the cytoplasm of the target cell through a needle-like structure. The effector proteins injected by the type III secretion apparatus of Yersinia into target cells are one example.