Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0017160 (gastroenteritis)
11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diarrhea in children is often caused by enteropathogen infections that might benefit from early empirical antibiotic therapy. However, when the definition of the pathogen requires sophisticated laboratory studies, the etiology of enteritis is not known early in illness. Empirical therapy may be dangerous if the child is infected with a Shiga toxin-producing Escherichia coli (STEC) strain because antimicrobials may increase Shiga toxin (Stx) release, resulting in increased risk of microangiopathic hemolytic anemia with acute renal failure (hemolytic-uremic syndrome [HUS]) and death. There is a need for antimicrobials that would be effective against multiple bacterial enteropathogens yet not induce Stx release or increase the risk of HUS. Rifaximin has been evaluated in adults for treatment of bacterial enteritis and has a good record for safety and efficacy, but it has not been evaluated extensively in children with gastroenteritis. We therefore evaluated rifaximin's potential for phage induction, drug-induced bacteriolysis, and toxin release in 57 STEC strains (26 O157 and 31 non-O157 strains). Growth in ciprofloxacin, a known Stx phage inducer, caused bacteriolysis and release of toxin in 25/26 (96%) O157 strains and 15/31 (48%) non-O157 strains. In contrast, rifaximin did not induce phage replication or lysis in any strain. Toxin release in the presence of rifaximin was not different from release in the absence of antibiotic. Rifaximin, unlike many antibiotics used to treat pediatric gastroenteritis, does not induce phage-mediated bacteriolysis and Stx release.
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PMID:Rifaximin does not induce toxin production or phage-mediated lysis of Shiga toxin-producing Escherichia coli. 1752 59

Defining etiology of acute diarrhea is critical to disease therapy and prevention. In this review we look at recent developments in etiologic agents of acute diarrhea and advances in therapy and prevention of the illness. Newly appreciated agents include enterotoxigenic Bacteroides fragilis, Klebsiella oxytoca and Laribacter hongkongensis. Atypical enteropathogenic E. coli (EPEC) strains lacking the gene for epithelial attachment appear to be more important as causes of diarrhea than traditional EPEC strains. Enterotoxigenic E. coli and enteroaggregative E. coli diarrhea known to be important abroad, have recently been shown to occur in the United States. Non-O157:H7 strains of Shiga toxin-producing E. coli are increasing and infrequently are being sought. There is currently a serious epidemic of nosocomial diarrhea due to a fluoroquinolone-resistant and more virulent and difficult to treat strain of C. difficile. Rotavirus vaccine development should lead to reduction of infant gastroenteritis mortality in infants living in developing regions. Noroviruses produce outbreaks of water- and food-borne disease but show broad genetic diversity. Reduced osmolarity oral rehydration treatment (ORT) and recombinant human lactoferrin/lysozyme plus rice-based ORT effectively treat acute diarrhea. Probiotics were shown to be effective in preventing antibiotic associated- and C. difficile-diarrhea. Rifaximin prevents and azithromycin effectively treats travelers' diarrhea.
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PMID:Advances in defining etiology and new therapeutic approaches in acute diarrhea. 1782 22

Shiga toxin-producing Escherichia coli (STEC) cause severe gastroenteritis and life-threatening hemolytic-uremic syndrome. For STEC of serogroup O157, association between disease incidence and cattle contact has been established in some countries. For other (non-O157) serogroups, however, accounting for approximately 80% of notified STEC gastroenteritis in Germany, the role of cattle in human infection is less clear. For example, an association of non-O157 STEC infection and cattle density has not been investigated. The aim of this study was thus to investigate a potential association between STEC incidence and cattle density in Germany, with special attention to the non-O157 serogroups. We modeled district-level incidence of notified human STEC cases in relation to cattle density, utilizing German notification data from 2001 through 2003. Cattle numbers came from the national "Proof of Origin and Information Database for Animals." A Bayesian Poisson regression model was used, incorporating independent, as well as spatially correlated, district-level random effects into the analysis. We analyzed 3216 German STEC cases. Cattle density was positively associated with overall STEC incidence. The risk for STEC infection increased by 68% per 100 additional cattle/km(2). The magnitude of the risk estimates differed by serogroup and was greatest for O111. A positive association was found for all major disease-causing serogroups (O26, O103, O111, O128, O145, O157) except O91. The association with serogroup O26 (lowest median age of patients) was only borderline significant. Residual variation indicates that additional factors not under study may also be of importance, and that they may be serogroup- and region-specific, too. In conclusion, this study suggests that living in a cattle-raising region appears to imply risk not only for STEC O157, but also for most non-O157 serogroups. Furthermore, the varying magnitude of this risk and the residual variation found for different serogroups indicate that risk profiles for human STEC infection may be serogroup-specific. This needs to be taken into account in risk factor studies for non-O157 STEC, ideally by reporting risks separately by serogroup.
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PMID:Cattle density and Shiga toxin-producing Escherichia coli infection in Germany: increased risk for most but not all serogroups. 1840 49

This report describes the clinical spectrum of disease among a series of pediatric and adult patients with symptoms of gastroenteritis that subsequently tested positive for Shiga toxin-producing Escherichia coli in their stool. All diarrheal stools (n = 1712) between July 2005 and November 2006 were tested with Premier EHEC (Meridian Bioscience, Cincinnati, OH). A total of 1.6% patients (27/1712) tested positive and 41% of patients had non-0157 E. coli, which can cause moderate disease requiring hospitalization. Cases of non-0157 E. coli would have been missed without testing for Shiga toxin. All bloody stools, and perhaps all stools, should be tested for Shiga toxin.
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PMID:Clinical spectrum of Shiga toxin-producing Escherichia coli (STEC) in adults and children. 1864 77

To estimate multipliers linking surveillance of salmonellosis, campylobacteriosis, and Shiga toxin-producing Escherichia coli (STEC) infections to community incidence, we used data from a gastroenteritis survey and other sources. Multipliers for severe (bloody stool/long duration) and milder cases were estimated from the component probabilities of doctor visit, stool test, sensitivity of laboratory test, and reporting to surveillance system. Pathogens were classified by the same severity criteria and appropriate multipliers applied. Precision of estimates was quantified by using simulation techniques to construct 95% credible intervals (CrIs). The multiplier for salmonellosis was estimated at 7 (95% CrI 4-16), for campylobacteriosis at 10 (95% CrI 7-22), and for STEC at 8 (95% CrI 3-75). Australian annual community incidence rates per 100,000 population were estimated as 262 (95% CrI 150-624), 1,184 (95% CrI 756-2,670), and 23 (95% CrI 13-54), respectively. Estimation of multipliers allows assessment of the true effects of these diseases and better understanding of public health surveillance.
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PMID:Estimating community incidence of Salmonella, Campylobacter, and Shiga toxin-producing Escherichia coli infections, Australia. 1882 25

Shiga toxin (Stx)-producing Escherichia coli (STEC) bacteria are a frequent cause of food-borne gastroenteritis, hemorrhagic colitis, and hemolytic uremic syndrome. Because antimicrobial agents are generally contraindicated in patients infected with STEC, a sensitive and specific diagnostic test with rapid turnaround is essential. Current culture methods may fail to detect non-O157 STEC. We evaluated a Stx gene real-time PCR assay using hybridization probes and the LightCycler instrument with 204 prospectively collected stool specimens, which were also tested for Stx by enzyme immunoassay (EIA) (ProSpecT STEC; Remel, Lenexa, KS) and by culturing on chromogenic agar (Chromagar O157; BD BBL, Sparks, MD). In addition, 85 archived stool specimens previously tested for Stx (by EIA) and/or E. coli O157:H7 (by culture) were tested by PCR. Sample preparation for PCR included mixing the stool in sterile water and extraction of nucleic acid using the MagNA Pure LC instrument (Roche Diagnostics). The PCR assay had 100% sensitivity and specificity compared to EIA and culture for specimens collected prospectively (4 of 204 specimens were positive) and compared to culture and/or EIA for archival specimens (42 of 85 specimens were positive). Both the EIA and PCR produced positive results from a specimen containing an O103 serotype STEC in the prospective specimens, and the PCR test detected three positive specimens that contained nonviable STEC in the archived specimens. The PCR assay demonstrated 100% sensitivity and specificity compared to EIA and/or culture and more rapid turnaround than either EIA or culture.
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PMID:Rapid and sensitive detection of Shiga toxin-producing Escherichia coli from nonenriched stool specimens by real-time PCR in comparison to enzyme immunoassay and culture. 1943 39

The isolation of Shiga toxin-producing Escherichia coli (STEC) other than serogroup O157 from clinical stool samples is problematic due to the lack of differential phenotypic characteristics from non-pathogenic E. coli. The development of molecular reagents capable of identifying both toxin and serogroup-specific genetic determinants holds promise for a more comprehensive characterization of stool samples and isolation of STEC strains. In this study, 876 stool samples from paediatric patients with gastroenteritis were screened for STEC using a cytotoxicity assay, commercial immunoassay and a conventional PCR targeting Shiga-toxin determinants. In addition, routine culture methods for isolating O157 STEC were also performed. The screening assays identified 45 stools presumptively containing STEC, and using non-differential culture techniques a total of 20 O157 and 22 non-O157 strains were isolated. These included STEC serotypes O157 : H7, O26 : H11, O121 : H19, O26 : NM, O103 : H2, O111 : NM, O115 : H18, O121 : NM, O145 : NM, O177 : NM and O5 : NM. Notably, multiple STEC serotypes were isolated from two clinical stool samples (yielding O157 : H7 and O26 : H11, or O157 : H7 and O103 : H2 isolates). These data were compared to molecular serogroup profiles determined directly from the stool enrichment cultures using a LUX real-time PCR assay targeting the O157 fimbrial gene lpfA, a microsphere suspension array targeting allelic variants of espZ and a gnd-based molecular O-antigen serogrouping method. The genetic profile of individual stool cultures indicated that the espZ microsphere array and lpfA real-time PCR assay could accurately predict the presence and provide preliminary typing for the STEC strains present in clinical samples. The gnd-based molecular serogrouping method provided additional corroborative evidence of serogroup identities. This toolbox of molecular methods provided robust detection capabilities for STEC in clinical stool samples, including co-infection of multiple serogroups.
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PMID:Isolation and detection of Shiga toxin-producing Escherichia coli in clinical stool samples using conventional and molecular methods. 1950 73

Shiga toxin-producing Escherichia coli (STEC) are major food-borne pathogens associated with gastroenteritis and sometimes fatal haemolytic uraemic syndrome complication. Farm animals are asymptomatic carriers of STEC and contaminated meat is an important vehicle for zoonotic transmission from animals to humans. This study investigated the presence, virulence traits and antimicrobial susceptibility of seven potentially human pathogenic STEC serogroups (O157, O26, O91, O103, O111, O128 and O145) in the faeces and meat of food-producing animals in Ibadan, Nigeria. One hundred and fifty-four (7.3%) of 2133 samples were positive for STEC serogroups. The pathogens were detected in the faeces of cattle (15.2%), sheep (10.7%), goats (7.5%) and pigs (5.6%) as well as in beef (3.8%), goat-meat (1.7%) and pork (4.0%). All seven investigated STEC serogroups were found in cattle, all except O145 were found in sheep, three serogroups (O157, O26 and O111) were found in goats and three (O157, O111 and O128) in pigs. The rate of detection of each of the serogroups in all 2133 samples was: O157 (5.0%), O26 (0.2%), O91 (0.3%), O103 (0.3%), O111 (1.0%), O128 (0.2%) and O145 (0.1%). Of all 154 isolates, 11.0% had shiga toxin type 1 gene (stx(1)), 25.3% had stx(2) and 41.6% had stx(1)/stx(2); intimin gene (eaeA) was detected in 56.5% and enterohaemolysin gene (hlyA) in 75.3%. Among the O157 isolates, 24.5% were negative for stx genes but positive for eaeA and/or hlyA while 7.6% were negative for all four virulence genes. Fourteen different combinations of virulence genes were encountered but stx(1)/stx(2)/eaeA/hlyA combination was the most predominant. The percentage resistance of the isolates to the tested antimicrobial agents was: ampicillin (82.5%), chloramphenicol (42.9%), ciprofloxacin (22.1%), enrofloxacin (25.3%), nalidixic acid (37.7%), neomycin (24.0%), norfloxacin (20.8%), streptomycin (50.7%) and tetracycline (75.3%). One hundred and forty-eight (96.1%) of all 154 isolates were resistant to at least one of the tested antimicrobial agents while 69.5% were categorised as multi-drug resistant. Potentially pathogenic multi-drug resistant STEC isolates were recovered from the meat production chain in Nigeria. Unhygienic practices that predominate during slaughter and processing were observed to have contributed to faecal contamination and presence of STEC in meat.
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PMID:Potentially zoonotic shiga toxin-producing Escherichia coli serogroups in the faeces and meat of food-producing animals in Ibadan, Nigeria. 2064 88

Shiga toxin-producing Escherichia coli (STEC) bacteria can cause outbreaks and sporadic cases of gastroenteritis in humans. Ruminants are seen as the main reservoir. The aim of this study was to evaluate the spatial association between reported human STEC O157 infections in The Netherlands and different livestock densities. Data were collected at the municipality level and a spatial regression analysis was performed. Between April 1999 and December 2008, 409 symptomatic sporadic cases were registered. Adding an interaction term between season, age, and livestock density showed an increased risk of STEC cases in summer for living in areas with cattle, in particular for young children. In conclusion, cattle, but not pigs or poultry, are indicated as an important source for human STEC O157 infections in rural areas. The association is probably due to direct or indirect contact with cattle, resulting in symptomatic infections, especially in young children.
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PMID:Geographical association between livestock density and human Shiga toxin-producing Escherichia coli O157 infections. 2082 76

Shiga-toxigenic Escherichia coli (STEC) is an important cause of diarrheal disease. The most notorious STEC serotype is O157:H7, which is associated with hemorrhagic colitis and hemolytic-uremic syndrome (HUS). As a result, this serotype is routinely screened for in clinical microbiology laboratories. With the bias toward the identification of the O157 serogroup in routine diagnostic processes, non-O157 STEC has been largely underrepresented in the epidemiology of STEC infections. This diagnostic bias is further complicated by the fact that many non-O157 STEC infections cause nonspecific gastroenteritis symptoms reminiscent of enteric viral infections. In this study, real-time PCR was used to amplify Shiga toxin genetic determinants (stx(1) and stx(2)) from enriched stool samples that were initially submitted for the testing of enteric viruses in patients with suspected viral gastroenteritis between May and September of 2006, 2007, and 2008 (n = 2,702). Samples were submitted from the province of Alberta, Yukon, the Northwest Territories, and Nunavut, Canada. A total of 38 samples (1.4%) tested positive for Shiga toxin genes, and 15 isolates were cultured for further characterization. Several of the serotypes identified (O157:H7, O26:HNM, O26:H11, O103:H25, O121:H19, and O145:HNM) have been previously associated with outbreaks and HUS. This study outlines the importance of combining molecular methods with classical culture techniques to enhance the detection of emerging non-O157 as well as O157 serotypes in diarrheal stool samples. Furthermore, atypical diarrhea disease caused by non-O157 STEC can be routinely missed due to screening only for viral agents.
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PMID:Shiga-toxigenic Escherichia coli detection in stool samples screened for viral gastroenteritis in Alberta, Canada. 2114 49


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