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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 .
The toxins bind to cell-surface glycolipid receptor Gb3, which causes the cell to take the toxin in via endocytosis. The Shiga toxins target ribosomal RNA, which inhibits protein synthesis and causes apoptosis. [14] The reason EHEC are symptomless in cattle is because the cattle do not have vascular expression of Gb3 unlike humans.
P k antigen is a receptor for Shiga toxins produced by Shigella dysenteriae and some strains of Escherichia coli, which may cause hemolytic uremic syndrome (HUS). [2] [6] [7] [8] It is also a receptor for Streptococcus suis (zoonotic bacterium which can cause bacterial meningitis). [6]
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.
This process involves inactivating the toxin, creating a toxoid that does not induce toxin-related illness and is well tolerated. [8] A widely used toxoid vaccine is the DPT vaccine , which is usually administered in multiple doses throughout childhood with adjuvants and boosters for long-term immunity. [ 8 ]
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 ...
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]
Kiyoshi Shiga attended the Medical School of Tokyo Imperial University in 1896, after his high school studies. [1] It was at the university when he was introduced to Kitasato ShibasaburÅ, one of Robert Koch's successors, who was a world-famous Japanese scientist studying the bacteriology and immunology of deadly disease at the time. [1]