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

Toxigenic Escherichia coli of human and animal origin have been classified into three categories: enterotoxigenic E. coli (ETEC), verotoxigenic E. coli (VTEC), and necrotoxigenic E. coli (NTEC), ETEC are a major cause of infant diarrhoea in less-developed countries and frequently cause colibacillosis in domestic animals. Human ETEC strains may synthesize LT-I and/or STa enterotoxins and they may possess the colonization factors CFA/I to CFA/IV; porcine strains synthesize LT-I, STa and/or STb, and possess the colonization antigens K88, P987, K99 or F41; and bovine strains are usually STa producers harbouring on the bacterial surface K99 or F41 colonization factors. There is a high host-specificity, because of that ETEC from animals are not pathogen for humans. VTEC strains may produce three mainly types of verotoxins (VT1, VT2, VT2vp1) that are functionally and structurally related to the shiga toxin. The VTEC of human and bovine origins produce VT1, VT2 or both, whereas VT2vp1 is elaborated by E. coli that cause edema disease in swine. The VTEC strains belonging mainly to serotypes O157:H7 or H-, O26:H11 and O111:H-, are now considered to be the major cause of two human syndromes of hitherto unknown cause: hemorrhagic colitis and hemolytic uremic syndrome. Most outbreaks of VTEC infection occurred in USA, Canada and United Kingdom during the last ten years and have been linked to consumption of undercooked ground beef, and, to a lesser extent, to the drinking of unpasteurized milk. Thus, the principal reservoir of VTEC is the intestinal tract of cattle. By contrast, it is presumed that human beings are the major reservoir of ETEC, and that contaminated water is a principal vehicle for transmission of ETEC infections. NTEC strains are able to elaborate two types of cytotoxic necrotizing factors (CNF1 and CNF2). Strains of human origin usually produce CNF1, whereas bovine NTEC generally synthesize CNF2. NTEC strains are not responsible for food-associated outbreaks of gastroenteritis, but CNF1 and CNF2 are very good markers of the source of food contamination.
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PMID:[Enterotoxigenic, verotoxigenic, and necrotoxigenic Escherichia coli in food and clinical samples. Role of animals as reservoirs of strains pathogenic for humans]. 754 50

Enhanced nitric oxide (NO) generation by stimulated NO synthase (NOS) activity may, through its oxidative metabolism contribute to tissue injury in experimental colitis. In this study the possible amelioration of experimental colitis by NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS activity, was evaluated. Colitis was induced in rats by intracolonic administration of 30 mg trinitrobenzene sulphonic acid (TNB) dissolved in 0.25 ml 50% ethanol or by flushing the colon of capsaicin pretreated rats with 2 ml of 5% acetic acid. In several experiments, L-NAME 0.1 mg/ml was added to the drinking water at the time of colitis induction with TNB or seven days before acetic acid treatment. Rats were killed at various time intervals after induction of colitis. A 10 cm distal colonic segment was isolated, weighed, lesion area measured, and explants organ cultured for 24 hours for determination of NO generation by the Greiss reaction. The rest of the mucosa was scraped for determination of myeloperoxidase and NOS activities and leukotriene generation. In TNB treated rats mean arterial pressure was also determined up to 72 hours after damage induction, with or without cotreatment with nitroprusside. L-NAME significantly decreased the extent of tissue injury in TNB treated rats. Seven days after TNB treatment lesion area was reduced by 55%, colonic weight by 37%, and myeloperoxidase and NOS activity by 59% and 42%, respectively. Acetic acid induced colitis in capsaicin pretreated rats was also significantly decreased by L-NAME. Twenty four hours after acetic acid treatment lesion area was reduced by 61%, colonic weight by 21% and NOS activity by 39%. Mean (SEM) arterial blood pressure in TNB+L-NAME treated rats was 37.6 (8.1) mm Hg higher than in TNB treated rats, an effect that was only partially abolished by nitroprusside. These results show that inhibition of NO synthesis by an L-arginine analogue significantly ameliorates the extent of tissue injury in two models of experimental colitis, an effect that is not due only to its vasoconstrictor properties. Modulation of NO generation may be a novel therapeutic approach in inflammatory bowel disease.
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PMID:Experimental colitis is ameliorated by inhibition of nitric oxide synthase activity. 867 8

The efficacy of lactulose as an antiendotoxin was studied and the effect of lactulose or colistin on faecal flora was investigated in a hapten-induced rat model of colitis. Enteral administration of lactulose to rats with colitis was associated with a significant reduction in the systemic concentration of endotoxin (median (range) 5.4 (0-19.9) versus 23.7 (0-145.0) pg/ml in colitic rats treated with water; 4.6 (0-10.8) pg/ml in healthy animals). Enteral administration of colistin significantly reduced the faecal count of aerobic Gram-negative bacilli (median (range) 2.84 (1.40-8.43) versus 8.26 (4.50-10.40) log10 colony-forming units per g faeces after treatment with water) but not the faecal load of endotoxin. Patients with inflammatory bowel disease may benefit from enteral treatment with lactulose to prevent systemic endotoxaemia and/or with colistin to modify enteric bacteria.
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PMID:Lactulose as an antiendotoxin in experimental colitis. 761 87

Mast cell alterations have been implicated in the pathogenesis of chronic ulcerative colitis (UC). We studied the effect of mast cell deficiency of the severity of inflammation in a murine model of colitis. Colitis was induced in mice using dextran sodium sulfate (DSS). Mast-cell-deficient mice (WBB6F1/J-W/WV; N = 17) and normal littermates (WBB6F1/J-+/+; N = 17) were administered DSS 4% w/v for seven days, then water alone for one week, followed by 5% DSS for six days. Animals were sacrificed at the end of the protocol. Segments of proximal, mid-, and distal colon of each animal were processed for histopathological examination. Mortality and morbidity (diarrhea and weight loss) for each group were assessed. There was no significant difference between the two groups in either their clinical parameters (mortality and morbidity) or the severity of colitis as graded histopathologically. Our findings suggest that mast cells are not crucial for the development of DSS-induced colitis.
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PMID:Lack of crucial role of mast cells in pathogenesis of experimental colitis in mice. 764 76

Although potentially noxious compounds are used routinely to disinfect endoscopes, reports of their inadvertent introduction to the gastrointestinal tract, usually attributed to the retention of disinfectant within endoscope channels, are rare. This case report describes the clinical features of glutaraldehyde-induced colitis and the pathology of the mucosal injury in four patients, in at least one of whom the disinfectant was not retained in the endoscope itself. Within 3 months, three patients experienced severe acute proctocolitis < 6 hours after a sigmoidoscopy showing no abnormalities, performed in a small endoscopy unit. Investigation of the unit's protocols suggested that the most likely cause was retention of 2% glutaraldehyde disinfectant in the endoscope channels, and changes were made to prevent this. When a fourth case occurred 5 months later, the source of the glutaraldehyde was found to be the tubing connecting water bottles to the endoscopes, which was disinfected rigorously but flushed inconsistently between cases. Glutaraldehyde-induced colitis seems similar to ischemic colitis in biopsy specimens and cannot be diagnosed by histological analysis alone. Acute colitis occurring within 24 hours of a colonoscopy showing no abnormalities should be considered iatrogenic and should lead to an investigation of procedures in use for cleaning and disinfecting endoscopic equipment.
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PMID:Glutaraldehyde colitis following endoscopy: clinical and pathological features and investigation of an outbreak. 769 92

E. coli O157:H7 is one of many E. coli organisms that contain genes encoding one or more toxins similar in structure and function to Shiga toxin. E. coli O157:H7 is the most frequently isolated diarrheagenic type of E. coli isolated in North America today; this pathogen can cause serious, even fatal disease. Syndromes caused by E. coli O157:H7 include diarrhea, hemorrhagic colitis, and HUS. Poorly cooked ground beef has been the most frequently implicated vehicle of transmission, but additional vehicles are being identified. Treatment consists of rehydration during hemorrhagic colitis and support of the patient during the multiple systemic complications of HUS. A policy of routine screening for E. coli O157:H7 in clinical microbiology laboratories, without reliance on the physician to request that this organism be sought or the technician to notice blood in the stool, is the most effective way to find cases. Timely and accurate diagnosis can prevent secondary transmission, avert unnecessary and possibly dangerous procedures and/or therapies, and detect continuing outbreaks. SLTEC strains other than E. coli O157:H7 may cause diseases similar to or less severe than those caused by E. coli O157:H7. At present, however, screening for such pathogens in clinical laboratories is too labor-intensive to be practical. Education and legislation should promote safe food-preparation and food-handling practices. Research should be directed at reducing the carriage of E. coli O157:H7 at its bovine source, minimizing the microbial content of food and water, and averting systemic microangiopathic hemolytic anemia after infection with this pathogen.
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PMID:Escherichia coli O157:H7: clinical, diagnostic, and epidemiological aspects of human infection. 1107 78

Olsalazine (OLZ), a relatively new form of 5-aminosalicylic acid (5-ASA), is being used for the treatment of colitis. A major side effect of olsalazine is diarrhea, reported in 12-25% of patients. One suggested mechanism for this side effect is enhanced ileal water and electrolyte secretion. We propose that OLZ may also inhibit ileal bile acid (BA) transport, resulting in choleretic diarrhea. This would result in excess BAs reaching the colon, with consequent BA-induced secretory diarrhea. Therefore, we studied the effect of OLZ on rat ileal absorption of taurocholate. BA uptake was determined in rat ileal segments, everted sacs, brush border membrane vesicles (BBMV), and Xenopus laevis oocytes. Segments and everted sacs were treated with 5 mM OLZ for 30 min prior to and throughout 10-min taurocholate (Tc) uptake. Terminal ileal BBMV were used to study the effect of OLZ on sodium-dependent bile acid uptake independent of cellular metabolism. Direct effects on the bile acid carrier were examined using Xenopus laevis oocytes expressing the cloned apical rat ileal BA transporter. In ileal segments 5 mM OLZ inhibited 10-min Tc uptake by 69.4 +/- 8.8% (P < 0.01) (N = 10 animals). Increasing concentrations of OLZ resulted in a dose-dependent inhibition of Tc uptake. Ten-minute Tc uptake with 0.5, 1.0, 2.0, 2.5, and 5 mM OLZ was inhibited by 13.5, 39.6, 49.7, and 70.5%, respectively. In BBMV, OLZ inhibited 45-sec Tc uptake in a dose-dependent manner but did not effect Na-dependent L-alanine uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of olsalazine on sodium-dependent bile acid transport in rat ileum. 772 83

This study was aimed at assessing the diagnostic value of hydrocolonic sonography (HS), a new technique of US examination of the colon during water enema, in colonic diseases. HS was performed on 120 clinically selected patients and was followed by double contrast barium enema (DCBE) in all patients, by endoscopy in 85, by pathology in 50 and by surgery in 36 patients. We obtained good quality images in 86% of cases, middle quality findings in 10% and poor results in 4% of cases. HS allowed the 5 layers of the colonic wall to be visualized. Forty of 50 polyps bigger than 1 cm, 9/10 cases of granulomatous colitis and diverticulitis were recognized and distinguished from cancer and 31/32 carcinomas were found--3 of them were locally invasive tumors, even though endoscopic biopsy had diagnosed them as adenomas. Compared with DCBE, HS exhibited lower sensitivity in recognizing small polyps (80% vs. 92%) but higher specificity (100% vs. 92.8%); in the diagnosis of carcinoma, HS exhibited higher sensitivity (96.8% vs. 90.6%) and the same specificity (about 100%); the depiction of parietal layers allowed also tumor staging. At present, HS cannot be proposed as the examination of choice to study polyps because of its limitations in recognizing them; nevertheless, HS appears to exhibit some advantages over DCBE in tumor detection and staging. HS is a simple, fast and safe technique which is well tolerated and easily repeatable, which calls for further investigation of its potentials, also because improved operator's experience is sure to increase HS reliability.
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PMID:[Hydrocolonic sonography in the study of colonic diseases. Comparison with double-contrast enema]. 775 18

Emerging infectious diseases such as prolonged diarrheal illness due to water-borne Cryptosporidium, hemorrhagic colitis and renal failure from food-borne E. coli O157:H7, and rodent-borne hantavirus pulmonary syndrome as well as reemerging infections such as tuberculosis, pertussis, and cholera vividly illustrate that we remain highly vulnerable to the microorganisms with which we share our environment. Prompt detection of new and resurgent infectious disease threats depends on careful monitoring by modern surveillance systems. This article focuses on five important elements of improved surveillance for emerging infections: 1) strengthening the national notifiable disease system, 2) establishing sentinel surveillance networks, 3) establishing population-based emerging infections programs, 4) developing a system for enhanced global surveillance, and 5) applying new tools and novel approaches to surveillance.
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PMID:Emerging infectious diseases in the United States, Improved surveillance, a requisite for prevention. 784 Apr 68

Marine lipids contain eicosapentaenoic acid (EPA) which has anti-inflammatory effects. The aim of this research was to study, using the dextran sulfate induced acute colitis (AC) model, the effect of an EPA-rich shark fin supplemented diet on the mucosal lipid composition. The histology score increased in AC (p < 0.05), but only slightly in the EPA group. Similarly, colonic permeability to a intraluminally instilled water-soluble contrast medium significantly increased in the AC group, but not in EPA group. As compared with controls, the AC group showed lower levels of phosphatidylethanolamine, phosphatidylinositol, free fatty acid C20:5, and PL-FA C18:1 and C18:2 and higher levels of sphingomyelin, lysophosphatidylcholine, and C18:1 and free fatty acid C20:4 (p < 0.01) after 2 and 7 days. In the EPA group sphinogmyelin and lysophosphatidylcholine slightly increased and free fatty acid C20:4 decreased (p < 0.05) after 7 days, and no PL-FA change occurred. This study confirms the protective properties of EPA-rich marine food. EPA-enriched diet is protecting the colonic mucosa from the early derangements of lipid components occurring in this experimental AC model. This effect is likely to contribute to maintain an effective mucosal lining barrier.
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PMID:Shark fin enriched diet prevents mucosal lipid abnormalities in experimental acute colitis. 789 32


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