Shigatoxigenic Escherichia coli ( STEC ) and verotoxigenic E. coli ( VTEC ) are strains of the bacterium Escherichia coli that produce Shiga toxin (or verotoxin). Only a minority of the strains cause illness in humans. The ones that do are collectively known as enterohemorrhagic E. coli ( EHEC ) and are major causes of foodborne illness . When infecting the large intestine of humans, they often cause gastroenteritis , enterocolitis , and bloody diarrhea (hence the name "enterohemorrhagic") and sometimes cause a severe complication called hemolytic-uremic syndrome (HUS). Cattle are an important natural reservoir for EHEC because the colonised adult ruminants are asymptomatic . This is because they lack vascular expression of the target receptor for Shiga toxins. The group and its subgroups are known by various names . They are distinguished from other strains of intestinal pathogenic E. coli including enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enteroinvasive E. coli (EIEC), enteroaggregative E. coli (EAEC), and diffusely adherent E. coli (DAEC).
22-451: (Redirected from STEC ) Stec or STEC may refer to: Shigatoxigenic Escherichia coli , bacterial strains sTec, Inc. , solid-state data storage company based in Santa Ana, California Daewoo S-TEC engine Stec (surname) Topics referred to by the same term [REDACTED] This disambiguation page lists articles associated with
44-483: A hemorrhagic colitis with severe abdominal pain. Serotype O157:H7 may trigger an infectious dose with 100 bacterial cells or fewer; other strain such as 104:H4 has also caused an outbreak in Germany 2011. 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. Initially a non-bloody diarrhea develops in patients after
66-527: Is a fibrous , non-globular protein involved in the clotting of blood . It is formed by the action of the protease thrombin on fibrinogen , which causes it to polymerize . The polymerized fibrin, together with platelets , forms a hemostatic plug or clot over a wound site. When the lining of a blood vessel is broken, platelets are attracted, forming a platelet plug . These platelets have thrombin receptors on their surfaces that bind serum thrombin molecules, which in turn convert soluble fibrinogen in
88-412: Is carried on chromosome 4) are both quantitative and qualitative in nature and include afibrinogenaemia , hypofibrinogenaemia , dysfibrinogenaemia, and hypodysfibrinogenemia . Reduced, absent, or dysfunctional fibrin is likely to render patients as hemophiliacs . Fibrin from various different animal sources is generally glycosylated with complex type biantennary asparagine-linked glycans . Variety
110-599: Is closer to the Shiga toxin. Practically, the choice of words and categories is not as important as the understanding of clinical relevance. The infectivity or the virulence of an EHEC strain depends on several factors, including the presence of fucose in the medium, the sensing of this sugar and the activation of EHEC pathogenicity island . Shiga toxins are a major virulence factor of EHEC. The toxins interact with intestinal epithelium and can cause systematic complications in humans like HUS and cerebral dysfunction if they enter
132-636: Is found in the degree of core fucosylation and in the type of sialic acid and galactose linkage. Fibrin is formed after thrombin cleavage of fibrinopeptide A (FPA) from fibrinogen Aalpha-chains, thus initiating fibrin polymerization. Double-stranded fibrils form through end-to-middle domain (D:E) associations, and concomitant lateral fibril associations and branching create a clot network. Fibrin assembly facilitates intermolecular antiparallel C-terminal alignment of gamma-chain pairs, which are then covalently 'cross-linked' by factor XIII ('plasma protransglutaminase') or XIIIa to form 'gamma-dimers'. The image at
154-540: The coagulation cascade leads to thrombosis , the blockage of a vessel by an agglutination of red blood cells, platelets, polymerized fibrin and other components. Ineffective generation or premature lysis of fibrin increases the likelihood of a hemorrhage . Dysfunction or disease of the liver can lead to a decrease in the production of fibrin's inactive precursor, fibrinogen , or to the production of abnormal fibrinogen molecules with reduced activity ( dysfibrinogenaemia ). Hereditary abnormalities of fibrinogen (the gene
176-501: The LEE) and QseF. QseE phosphorylates QseF. The products QseBC and QseEF repress the expression of FusK and FusR. FusK and FusR are the two components of a system to repress the transcription of the LEE genes. FusK is a sensor kinase which is able to sense many sugars among which fucose. When fucose is present in the medium FusK phosphorylates FusR which represses LEE expression. Thus when EHEC enters
198-505: The Shiga toxins cannot pass through the intestinal epithelium into circulation. EHEC becomes pathogenic through the expression of the locus of enterocyte effacement (LEE) encoded on its pathogenicity island. However, when EHEC is not in a host this expression is a waste of energy and resources, so it is only activated if some molecules are sensed in the environment. When QseC or QseE bind with one of their interacting signalling molecule, they autophosphorylate and transfer its phosphate to
220-521: The Stx-bearing bacteriophage and cause increased production of toxins. Attempts to block toxin production with antibacterials which target the ribosomal protein synthesis are conceptually more attractive. Plasma exchange offers a controversial but possibly helpful treatment. 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
242-1098: The bacterium attaches to the epithelium of the terminal ileum , cecum , and colon . The subsequent production of toxins mediates the bloody diarrhea. 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). EHECs that induce bloody diarrhea lead to HUS in 10% of cases. The clinical manifestations of postdiarrheal HUS include acute renal failure , microangiopathic hemolytic anemia , and thrombocytopenia . 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. Antibiotics are of questionable value and have not shown to be of clear clinical benefit. Antibiotics that interfere with DNA synthesis, such as fluoroquinolones , have been shown to induce
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#1733085747311264-422: The circulation. In EHEC, Shiga toxins are encoded by lysogenic bacteriophages. 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 . The reason EHEC are symptomless in cattle is because the cattle do not have vascular expression of Gb3 unlike humans. Thus,
286-510: The difference is negligible. Following this view, all "VTEC" (blue) should be called "STEC" (red). 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". The line can also be drawn to use "STEC" for Stx1 -producing strains and "VTEC" for Stx2 -producing strains, since Stx1
308-555: The epithelium, then the expression of LEE genes will not be repressed by FusR, and KpdE will strongly activate them. In summary, the combined effect of the QseC/QseF and FusKR provide a fine-tuning system of LEE expression which saves energy and allow the mechanisms of virulence to be expressed only when the chances of success are higher. There are rare STEC without LEE, see PMID 19239748 . Fibrin Fibrin (also called Factor Ia )
330-461: The gastrointestinal tract of cattle and sheep, and can infect humans. They are globally-occurring bacteria. The best known of these strains is O157:H7 , but non-O157 strains cause an estimated 36,000 illnesses, 1,000 hospitalizations and 30 deaths in the United States yearly. Food safety specialists recognize "Big Six" strains: O26; O45; O103; O111; O121 ; and O145. A 2011 outbreak in Germany
352-418: The gut there is a competition between the signals coming from QseC and QseF, and the signal coming from FusK. The first two would like to activate virulence, but Fusk stops it because the mucous layer, which is a source of fucose, isolates enterocytes from bacteria making the synthesis of the virulence factors useless. However, when fucose concentration decreases because bacterial cells find an unprotected area of
374-413: The red and blue have often been treated as synonyms of the purple. At least one reference holds "EHEC" to be mutually exclusive of "VTEC" and "STEC", but this does not match common usage, as many more publications lump all of the latter in with the former. The current microbiology-based view on "Shiga-like toxin" (SLT) or "verotoxin" is that they should all be referred to as (versions of) Shiga toxin , as
396-444: The response regulator. QseC senses adrenaline , noradrenaline , and an Endonuclease I-SceIII, encoded by a mobile group I intron within the mitochondrial COX1 gene (AI3); whereas QseE senses adrenaline, noradrenaline, SO4 and PO4. These signals are a clear indication to the bacteria that they are no longer free in the environment, but in the gut. As a result, QseC phosphorylates QseB (which activates flagella), KpdE (which activates
418-410: The risk of HUS with EHEC infections. Names of the group and its subgroups include the following. There is some polysemy involved. Invariable synonymity is indicated by having the same color. Beyond that there is also some wider but variable synonymity. The first two (purple) in their narrowest sense are generally treated as hypernyms of the others (red and blue), although in less precise usage
440-407: The serum into fibrin at the wound site. Fibrin forms long strands of tough insoluble protein that are bound to the platelets. Factor XIII completes the cross-linking of fibrin so that it hardens and contracts. The cross-linked fibrin forms a mesh atop the platelet plug that completes the clot. Fibrin was discovered by Marcello Malpighi in 1666. Excessive generation of fibrin due to activation of
462-570: The title Stec . If an internal link led you here, you may wish to change the link to point directly to the intended article. Retrieved from " https://en.wikipedia.org/w/index.php?title=Stec&oldid=1238305767 " Category : Disambiguation pages Hidden categories: Short description is different from Wikidata All article disambiguation pages All disambiguation pages Shigatoxigenic and verotoxigenic Escherichia coli Shiga toxin–producing Escherichia coli are zoonotic pathogens, in that they can be found in
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#1733085747311484-472: Was caused by another STEC, O104:H4 . This strain has both enteroaggregative and enterohemorrhagic properties. Both the O145 and O104 strains can cause hemolytic-uremic syndrome (HUS); the former strain shown to account for 2% to 51% of known HUS cases; an estimated 56% of such cases are caused by O145 and 14% by other EHEC strains. The clinical presentation in humans ranges from a mild and uncomplicated diarrhea to
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