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Query: UMLS:C0009319 (colitis)
 19,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Shiga toxin-producing Escherichia coli (STEC) O157:H7 is an attaching and effacing pathogen that causes hemorrhagic colitis and the hemolytic-uremic syndrome. Although this organism causes adhesion pedestals, the cellular signals responsible for the formation of these lesions have not been clearly defined. We have shown previously that STEC O157:H7 does not induce detectable tyrosine phosphorylation of host cell proteins upon binding to eukaryotic cells and is not internalized into nonphagocytic epithelial cells. In the present study, tyrosine-phosphorylated proteins were detected under adherent STEC O157:H7 when coincubated with the non-intimately adhering, intimin-deficient, enteropathogenic E. coli (EPEC) strain CVD206. The ability to be internalized into epithelial cells was also conferred on STEC O157:H7 when coincubated with CVD206 ([158 +/- 21] % of control). Neither the ability to rearrange phosphotyrosine proteins nor that to be internalized into epithelial cells was evident following coincubation with another STEC O157:H7 strain or with the nonsignaling espB mutant of EPEC. E. coli JM101(pMH34/pSSS1C), which overproduces surface-localized O157 intimin, also rearranged tyrosine-phosphorylated and cytoskeletal proteins when coincubated with CVD206. In contrast, JM101 (pMH34/pSSS1C) demonstrated rearrangement of cytoskeletal proteins, but not tyrosine-phosphorylated proteins, when coincubated with intimin-deficient STEC (strains CL8KO1 and CL15). These findings indicate that STEC O157:H7 forms adhesion pedestals by mechanisms that are distinct from those in attaching and effacing EPEC. Taken together, these findings point to diverging signal transduction responses to infection with attaching and effacing bacterial enteropathogens.
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PMID:Divergent signal transduction responses to infection with attaching and effacing Escherichia coli. 952 99

Escherichia coli O157 was first identified as a human pathogen in 1982. One of several Shiga toxin-producing serotypes known to cause human illness, the organism probably evolved through horizontal acquisition of genes for Shiga toxins and other virulence factors. E. coli O157 is found regularly in the faeces of healthy cattle, and is transmitted to humans through contaminated food, water, and direct contact with infected people or animals. Human infection is associated with a wide range of clinical illness, including asymptomatic shedding, non-bloody diarrhoea, haemorrhagic colitis, haemolytic uraemic syndrome, and death. Since laboratory practices vary, physicians need to know whether laboratories in their area routinely test for E. coli O157 in stool specimens. Treatment with antimicrobial agents remains controversial: some studies suggest that treatment may precipitate haemolytic uraemic syndrome, and other studies suggest no effect or even a protective effect. Physicians can help to prevent E. coli O157 infections by counselling patients about the hazards of consuming undercooked ground meat or unpasteurised milk products and juices, and about the importance of handwashing to prevent the spread of diarrhoeal illness, and by informing public-health authorities when they see unusual numbers of cases of bloody diarrhoea or haemolytic uraemic syndrome.
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PMID:Escherichia coli O157:H7. 977 54

We report the case of an Escherichia coli O157:H7 infection in a patient with hemorrhagic colitis. Initial diagnosis was ischemic colitis because of the age of the patient and clinical presentation. After one week, a hemolytic-uremic syndrome occurred and serologic antibodies to the lipopolysaccharide O157 of Escherichia coli O157:H7 were positive, leading to the diagnosis of hemorrhagic colitis caused by this bacteria. Escherichia coli O157:H7 colonic infection is not well known, specially in France where only two cases has been reported in adults. This bacteria and the toxin produced (Shiga-like toxin) should be searched in cultures of stools and colonic biopsies in case of bloody diarrhea, in particular when a hemolytic-uremic syndrome is associated. As clinical, pathological and endoscopic findings in Escherichia coli O157:H7-associated colitis may be similar to the ischemic colitis pattern, differential diagnosis may be difficult.
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PMID:[Hemorrhagic colitis and hemolytic uremic syndrome caused by Escherichia coli O157:H7]. 979 63

The presence of virulence genes, encoding enterohemorrhagic Escherichia coli (EHEC)-hemolysin (EHEC-hlyA), intimin (eae), and Shiga toxins 1 (stx1) and 2 (stx2), in 178 isolates of pathogenic E. coli, was determined using the polymerase chain reaction with primers specific for each virulence gene. The tested organisms were 120 isolates of E. coli O157:H7 from human patients, cattle, sheep and foods, 16 non-O157:H7 EHEC isolates from patients suffering from hemorrhagic colitis or hemolytic uremic syndrome, 15 non-O157:H7 Shiga toxin-producing E. coli (STEC) isolates from cattle and foods, 26 isolates of enteropathogenic E. coli (EPEC), enteroinvasive E. coli (EIEC) and enterotoxigenic E. coli (ETEC), and an E. coli K12 strain. Results revealed that all isolates of O157:H7 carried EHEC-hlyA, eae, and one or both stx genes; 15 of the 16 non-O157:H7 EHEC isolates had EHEC-hlyA, but all possessed eae and one or both stx genes; only seven of the 15 non-O157 STEC isolated from cattle and foods contained both EHEC-hlyA and eae genes. The EPEC, EIEC, ETEC, and the E. coli K12 strain did not carry these virulence genes, except eight EPEC isolates were positive for eae. Results suggest that a combination of EHEC-hlyA and eae genes could serve as markers to differentiate EHEC from less pathogenic STEC, and other pathogenic or non-pathogenic E. coli.
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PMID:Virulence genes of Shiga toxin-producing Escherichia coli isolated from food, animals and humans. 992 1

Associations between known or putative virulence factors of Shiga toxin-producing Escherichia coli and disease in humans were investigated. Univariate analysis and multivariate logistic regression analysis of a set of 237 isolates from 118 serotypes showed significant associations between the presence of genes for intimin (eae) and Shiga toxin 2 (stx2) and isolates from serotypes reported in humans. Similar associations were found with isolates from serotypes reported in hemorrhagic colitis and hemolytic-uremic syndrome. The enterohemorrhagic E. coli (EHEC) hemolysin gene was significantly associated with isolates from serotypes found in severe diseases in univariate analysis but not in multivariate logistic regression models. A strong association between the intimin and EHEC-hemolysin genes may explain the lack of statistical significance of EHEC hemolysin in these multivariate models, but a true lack of biological significance of the hemolysin in humans or in disease cannot be excluded. This result warrants further investigations of this topic. Multivariate analysis revealed an interaction between the eae and stx2 genes, thus supporting the hypothesis of the synergism between the adhesin intimin and Shiga toxin 2. A strong statistical association was observed between the stx2 gene and severity of disease for a set of 112 human isolates from eight major serotypes. A comparison of 77 isolates of bovine origin and 91 human isolates belonging to six major serotypes showed significant associations of the genes for Shiga toxin 1 and EspP protease with bovine isolates and an increased adherence on HEp-2 cell cultures for human isolates, particularly from diarrheic patients and healthy persons.
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PMID:Associations between virulence factors of Shiga toxin-producing Escherichia coli and disease in humans. 998 2

Endothelial damage is characteristic of infection with Shiga toxin (Stx)-producing Escherichia coli (STEC). Because Stx-mediated endothelial cell damage at the site of infection may lead to the characteristic hemorrhagic colitis of STEC infection, we compared the effects of Stx1 and Stx2 on primary and transformed human intestinal microvascular endothelial cells (HIMEC) to those on macrovascular endothelial cells from human saphenous vein (HSVEC). Adhesion molecule, interleukin-8 (IL-8), and Stx receptor expression, the effects of cytokine activation and Stx toxins on these responses, and Stx1 and Stx2 binding kinetics and bioactivity were measured. Adhesion molecule and IL-8 expression increased in activated HIMEC, but these responses were blunted in the presence of toxin, especially in the presence of Stx1. In contrast to HSVEC, unstimulated HIMEC constitutively expressed Stx receptor at high levels, bound large amounts of toxin, were highly sensitive to toxin, and were not further sensitized by cytokines. Although the binding capacities of HIMEC for Stx1 and Stx2 were comparable, the binding affinity of Stx1 to HIMEC was 50-fold greater than that of Stx2. Nonetheless, Stx2 was more toxic to HIMEC than an equivalent amount of Stx1. The decreased binding affinity and increased toxicity for HIMEC of Stx2 compared to those of Stx1 may be relevant to the preponderance of Stx2-producing STEC involved in the pathogenesis of hemorrhagic colitis and its systemic complications. The differences between primary and transformed HIMEC in these responses were negligible. We conclude that transformed HIMEC lines could represent a simple physiologically relevant model to study the role of Stx in the pathogenesis of hemorrhagic colitis.
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PMID:Responses of human intestinal microvascular endothelial cells to Shiga toxins 1 and 2 and pathogenesis of hemorrhagic colitis. 1002 92

Lysogenic bacteriophages are major vehicles for the transfer of genetic information between bacteria, including pathogenicity and/or virulence determinants. In the enteric pathogen Escherichia coli O157:H7, which causes hemorrhagic colitis and hemolytic-uremic syndrome, Shiga toxins 1 and 2 (Stx1 and Stx2) are phage encoded. The sequence and analysis of the Stx2 phage 933W is presented here. We find evidence that the toxin genes are part of a late-phage transcript, suggesting that toxin production may be coupled with, if not dependent upon, phage release during lytic growth. Another phage gene, stk, encodes a product resembling eukaryotic serine/threonine protein kinases. Based on its position in the sequence, Stk may be produced by the prophage in the lysogenic state, and, like the YpkA protein of Yersinia species, it may interfere with the signal transduction pathway of the mammalian host. Three novel tRNA genes present in the phage genome may serve to increase the availability of rare tRNA species associated with efficient expression of pathogenicity determinants: both the Shiga toxin and serine/threonine kinase genes contain rare isoleucine and arginine codons. 933W also has homology to lom, encoding a member of a family of outer membrane proteins associated with virulence by conferring the ability to survive in macrophages, and bor, implicated in serum resistance.
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PMID:Sequence of Shiga toxin 2 phage 933W from Escherichia coli O157:H7: Shiga toxin as a phage late-gene product. 1007 68

During the Sakai outbreak of Escherichia coli O157:H7 infection, which was linked to contaminated cafeteria school lunches, there were several treatment modalities with regard to antimicrobial drugs. Patient outcomes among three hospitals with different modalities were compared retrospectively. Hemolytic uremic syndrome did not develop in any of the 15 patients treated with oral fluoroquinolone therapy; however, HUS did develop in three of 15 patients treated with intravenous (i.v.) fosfomycin and in two of 12 patients treated with i.v. cefotaxime and oral fosfomycin. The results indicate that oral fluoroquinolone therapy administered within 3 days of illness is effective in preventing the development of HUS; however, prospective randomized double-blind studies on early antimicrobial therapy of O157 hemorrhagic colitis are necessary. Several antibiotics, including fluoroquinolones, were reported to induce the production or release of Shiga-like toxins (STX) from E. coli O157:H7 in vitro. Although patients were examined for fecal STX, no STX were detected in the stools of patients treated with oral fluoroquinolones. In fact, treatment with fluoroquinolones for 5 days eradicated E. coli O157 in all patients.
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PMID:Effect of early oral fluoroquinolones in hemorrhagic colitis due to Escherichia coli O157:H7. 1022 Oct 35

A synthetic analog of Shiga toxin (Stx) receptor (Synsorb Pk) was quantitatively assessed to determine whether it can protect human renal adenocarcinoma cells (ACHN cells) from the cytotoxicity of Stx1 and Stx2 by coincubation experiments. Coincubation of 100 and 20 ng of Stxl and Stx2 with 50 mg of Synsorb Pk for 1 hr at 37 C in 1 ml of Eagle's Minimum Essential Medium supplemented with 1% (v/v) non-essential amino acid and 10% (v/v) fetal calf serum protected 50% of the cells from the cytotoxic effect. Chromosorb P, an inert matrix control, did not absorb the Stxs at all. Heat-treatment (boiled for 10 min) to Synsorb Pk caused a 50% decrease in Stx2-binding activity, but did not effect the Stx1 binding. Further, Stxs bound to Synsorb Pk could be demonstrated. When 20 mg of Synsorb Pk was coincubated for 30 min at 37 C in 1 ml of phosphate-buffered saline with 1 and 10 ng or more of Stx1 or Stx2, respectively, the toxins could be detected on the surface when the bound toxins on Synsorb Pk were used as the solid phase in enzyme immunoassay. The amount of 100 ng/ml of both Stxl and Stx2 appeared to saturate 20 mg/ml of Synsorb Pk after coincubating for 30 min at 37 C. While assessing the Stxs' binding activity to Synsorb Pk, it was demonstrated that Stxl had a higher affinity to Pk trisaccharide than Stx2. These observations provide useful information on the effectiveness of Synsorb Pk to trap and eliminate free Stxs produced in the gut of patients infected by Stx-producing Escherichia coli, and to prevent the progression of hemorrhagic colitis to hemolytic uremic syndrome.
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PMID:In vitro assessment of a chemically synthesized Shiga toxin receptor analog attached to chromosorb P (Synsorb Pk) as a specific absorbing agent of Shiga toxin 1 and 2. 1038 99

Bacterial virulence usually requires the interaction of multiple factors in order to cause disease. The enterotoxins produced by certain strains of bacteria are proteins which vary in their mode of action, but do fall into two general groups; the cytotoxic and the cytotonic enterotoxins. While cytotoxic enterotoxins typically kill eucaryotic cells (eg. by inhibiting protein synthesis), cytotonic enterotoxins derange cell metabolism in specific ways (eg. by elevating cyclic nucleotide levels). Some strains of Escherichia coli produce protein toxins that are biologically, structurally and antigenically related to a cytotoxin (Shiga toxin) (ShT) produced by Shigella dysenteriae type 1. Although this group of related, but not necessarily identical toxins have been referred to as Vero cell toxins or Verocytotoxins (VTs), the term Shiga-like toxins (SLTs) has been widely accepted. ShT and SLTs have been implicated as a cause of diarrhoea as well as haemorrhagic colitis (HC) and haemolytic uremic syndrome (HUS) in humans, whilst SLTs have been implicated as causal agents of oedema disease and HC in weaner pigs and calves, respectively. While S. dysenteriae is an invasive organism, the SLT-producing strains of E. coli have not been reported to be invasive, but cause diarrhoea that may contain blood and mucus. Thus, SLTs can be considered an important "new" type of enterotoxins whose role in the pathogenesis of diarrhoea, HC and HUS is beginning to emerge, not only in certain geographical settings, but worldwide. This mini review focuses on this family of SLTs, because of recent advances which have been made towards their detection, nomenclature, pathogenesis and possible management of their clinical presentations.
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PMID:Verocytotoxins (Shiga-like toxins) produced by Escherichia coli: a minireview of their classification, clinical presentations and management of a heterogeneous family of cytotoxins. 1046 26


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