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Helge Karch - One of the best experts on this subject based on the ideXlab platform.
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Shiga Toxin mediated hemolytic uremic syndrome time to change the diagnostic paradigm
PLOS ONE, 2007Co-Authors: Martina Bielaszewska, Robin Kock, Alexander W Friedrich, Christof Von Eiff, Lothar Bernd Zimmerhackl, Helge Karch, Alexander MellmannAbstract:BACKGROUND: Hemolytic uremic syndrome (HUS) is caused by enterohemorrhagic Escherichia coli (EHEC) which possess genes encoding Shiga Toxin (stx), the major virulence factor, and adhesin intimin (eae). However, the frequency of stx-negative/eae-positive E. coli in stools of HUS patients and the clinical significance of such strains are unknown. METHODOLOGY/PRINCIPAL FINDINGS: Between 1996 and 2006, we sought stx-negative/eae-positive E. coli in stools of HUS patients using colony blot hybridization with the eae probe and compared the isolates to EHEC causing HUS. stx-negative/eae-positive E. coli were isolated as the only pathogens from stools of 43 (5.5%) of 787 HUS patients; additional 440 (55.9%) patients excreted EHEC. The majority (90.7%) of the stx-negative/eae-positive isolates belonged to serotypes O26:H11/NM (nonmotile), O103:H2/NM, O145:H28/NM, and O157:H7/NM, which were also the most frequent serotypes identified among EHEC. The stx-negative isolates shared non-stx virulence and fitness genes with EHEC of the corresponding serotypes and clustered with them into the same clonal complexes in multilocus sequence typing, demonstrating their close relatedness to EHEC. CONCLUSIONS/SIGNIFICANCE: At the time of microbiological analysis, approximately 5% of HUS patients shed no longer the causative EHEC, but do excrete stx-negative derivatives of EHEC that lost stx during infection. In such patients, the EHEC etiology of HUS is missed using current methods detecting solely stx or Shiga Toxin; this can hamper epidemiological investigations and lead to inappropriate clinical management. While maintaining the paradigm that HUS is triggered by Shiga Toxin, our data demonstrate the necessity of considering genetic changes of the pathogen during infection to adapt appropriately diagnostic strategies.
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sorbitol fermenting Shiga Toxin producing escherichia coli o157 h strains epidemiology phenotypic and molecular characteristics and microbiological diagnosis
Journal of Clinical Microbiology, 2001Co-Authors: Helge Karch, Martina BielaszewskaAbstract:The significance of Shiga Toxin (Stx)-producing Escherichia coli (STEC) O157:H7 as the major cause of hemorrhagic colitis and the hemolytic-uremic syndrome (HUS) worldwide has been well established (for reviews, see references[21][1], [31][2], [41][3], and [60][4]). The recognition of this pathogen
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a new Shiga Toxin 2 variant stx2f from escherichia coli isolated from pigeons
Applied and Environmental Microbiology, 2000Co-Authors: Herbert Schmidt, Alfredo Caprioli, Stefano Morabito, J Scheef, Lothar H Wieler, Helge KarchAbstract:We have isolated Shiga Toxin (Stx)-producing Escherichia coli (STEC) strains from the feces of feral pigeons which contained a new Stx2 variant gene designated stx(2f). This gene is most similar to sltIIva of patient E. coli O128:B12 isolate H.I.8. Stx2f reacted only weakly with commercial immunoassays. The prevalence of STEC organisms carrying the stx(2f) gene in pigeon droppings was 12.5%. The occurrence of a new Stx2 variant in STEC from pigeons enlarges the pool of Stx2 variants and raises the question whether horizontal gene transfer to E. coli pathogenic to humans may occur.
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bovine colostrum ameliorates diarrhea in infection with diarrheagenic escherichia coli Shiga Toxin producing e coli and e coli expressing intimin and hemolysin
Journal of Pediatric Gastroenterology and Nutrition, 1999Co-Authors: Hansiko Huppertz, Stefan Rutkowski, Dirk H Busch, Reinhard Eisebit, Reinhard Lissner, Helge KarchAbstract:Background: Diarrheagenic Escherichia coli may cause serious extraintestinal complications, but there is no specific treatment. Methods: Patients with diarrhea caused by diarrheagenic E. coli, specifically Shiga Toxin-producing E. coli and E. coli-expressing intimin and enterohemorrhagic E. coli-hemolysin were treated by administration of pooled bovine colostrum, rich in antibodies to Shiga Toxin and enterohemorrhagic E. coli-hemolysin, in a placebo-controlled, double-blind study. Symptom resolution and fecal excretion of infecting strains were assessed. Results: No side effects were attributable to colostrum. Stool frequencies in the group treated with bovine colostrum were significantly reduced compared with those in the placebo group. No effect of therapy on the carriage of the pathogens or on complications of the infection could be demonstrated. Conclusions: Bovine colostrum is well tolerated and diminishes frequency of loose stools in children with E. coli-associated diarrhea. A prospective study should be conducted among a larger number of children with Shiga Toxin-producing E. coli identified early in illness, to determine the effectiveness of colostrum therapy.
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enteroaggregative Shiga Toxin producing escherichia coli o111 h2 associated with an outbreak of hemolytic uremic syndrome
Journal of Clinical Microbiology, 1998Co-Authors: Stefano Morabito, Helge Karch, Fabio Minelli, Herbert Schmidt, Patrizia Marianikurkdjian, E Bingen, Alfredo CaprioliAbstract:Shiga Toxin-producing Escherichia coli O111:H2 strains from an outbreak of hemolytic-uremic syndrome showed aggregative adhesion to HEp-2 cells and harbored large plasmids which hybridized with the enteroaggregative E. coli probe PCVD432. These strains present a novel combination of virulence factors and might be as pathogenic to humans as the classic enterohemorrhagic E. coli.
Alfredo Caprioli - One of the best experts on this subject based on the ideXlab platform.
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Shiga Toxin producing escherichia coli infections associated with hemolytic uremic syndrome italy 1988 2000
Emerging Infectious Diseases, 2003Co-Authors: Alberto Eugenio Tozzi, Alfredo Caprioli, Fabio Minelli, Alessandra Gianviti, Laura De Petris, Alberto Edefonti, Giovanni Montini, Alfonso Ferretti, Tommaso De Palo, Maurizio GaidoAbstract:The mean annual incidence of hemolytic uremic syndrome in persons <15 years of age in Italy from 1988 to 2000 was 0.28 per 100,000 population. Laboratory investigations showed that Shiga Toxin–producing Escherichia coli (STEC) infection occurred in 73.1% of patients. STEC O157 was the most common serotype, but a considerable number of cases were from infections by non-O157 STEC.
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a new Shiga Toxin 2 variant stx2f from escherichia coli isolated from pigeons
Applied and Environmental Microbiology, 2000Co-Authors: Herbert Schmidt, Alfredo Caprioli, Stefano Morabito, J Scheef, Lothar H Wieler, Helge KarchAbstract:We have isolated Shiga Toxin (Stx)-producing Escherichia coli (STEC) strains from the feces of feral pigeons which contained a new Stx2 variant gene designated stx(2f). This gene is most similar to sltIIva of patient E. coli O128:B12 isolate H.I.8. Stx2f reacted only weakly with commercial immunoassays. The prevalence of STEC organisms carrying the stx(2f) gene in pigeon droppings was 12.5%. The occurrence of a new Stx2 variant in STEC from pigeons enlarges the pool of Stx2 variants and raises the question whether horizontal gene transfer to E. coli pathogenic to humans may occur.
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enteroaggregative Shiga Toxin producing escherichia coli o111 h2 associated with an outbreak of hemolytic uremic syndrome
Journal of Clinical Microbiology, 1998Co-Authors: Stefano Morabito, Helge Karch, Fabio Minelli, Herbert Schmidt, Patrizia Marianikurkdjian, E Bingen, Alfredo CaprioliAbstract:Shiga Toxin-producing Escherichia coli O111:H2 strains from an outbreak of hemolytic-uremic syndrome showed aggregative adhesion to HEp-2 cells and harbored large plasmids which hybridized with the enteroaggregative E. coli probe PCVD432. These strains present a novel combination of virulence factors and might be as pathogenic to humans as the classic enterohemorrhagic E. coli.
Martina Bielaszewska - One of the best experts on this subject based on the ideXlab platform.
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Shiga Toxin mediated hemolytic uremic syndrome time to change the diagnostic paradigm
PLOS ONE, 2007Co-Authors: Martina Bielaszewska, Robin Kock, Alexander W Friedrich, Christof Von Eiff, Lothar Bernd Zimmerhackl, Helge Karch, Alexander MellmannAbstract:BACKGROUND: Hemolytic uremic syndrome (HUS) is caused by enterohemorrhagic Escherichia coli (EHEC) which possess genes encoding Shiga Toxin (stx), the major virulence factor, and adhesin intimin (eae). However, the frequency of stx-negative/eae-positive E. coli in stools of HUS patients and the clinical significance of such strains are unknown. METHODOLOGY/PRINCIPAL FINDINGS: Between 1996 and 2006, we sought stx-negative/eae-positive E. coli in stools of HUS patients using colony blot hybridization with the eae probe and compared the isolates to EHEC causing HUS. stx-negative/eae-positive E. coli were isolated as the only pathogens from stools of 43 (5.5%) of 787 HUS patients; additional 440 (55.9%) patients excreted EHEC. The majority (90.7%) of the stx-negative/eae-positive isolates belonged to serotypes O26:H11/NM (nonmotile), O103:H2/NM, O145:H28/NM, and O157:H7/NM, which were also the most frequent serotypes identified among EHEC. The stx-negative isolates shared non-stx virulence and fitness genes with EHEC of the corresponding serotypes and clustered with them into the same clonal complexes in multilocus sequence typing, demonstrating their close relatedness to EHEC. CONCLUSIONS/SIGNIFICANCE: At the time of microbiological analysis, approximately 5% of HUS patients shed no longer the causative EHEC, but do excrete stx-negative derivatives of EHEC that lost stx during infection. In such patients, the EHEC etiology of HUS is missed using current methods detecting solely stx or Shiga Toxin; this can hamper epidemiological investigations and lead to inappropriate clinical management. While maintaining the paradigm that HUS is triggered by Shiga Toxin, our data demonstrate the necessity of considering genetic changes of the pathogen during infection to adapt appropriately diagnostic strategies.
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sorbitol fermenting Shiga Toxin producing escherichia coli o157 h strains epidemiology phenotypic and molecular characteristics and microbiological diagnosis
Journal of Clinical Microbiology, 2001Co-Authors: Helge Karch, Martina BielaszewskaAbstract:The significance of Shiga Toxin (Stx)-producing Escherichia coli (STEC) O157:H7 as the major cause of hemorrhagic colitis and the hemolytic-uremic syndrome (HUS) worldwide has been well established (for reviews, see references[21][1], [31][2], [41][3], and [60][4]). The recognition of this pathogen
Debora Barnett E Foster - One of the best experts on this subject based on the ideXlab platform.
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potentiation of antibiotics by a novel antimicrobial peptide against Shiga Toxin producing e coli o157 h7
Scientific Reports, 2020Co-Authors: Juan Punosarmiento, Erin M Anderson, Amber J Park, Cezar M Khursigara, Debora Barnett E FosterAbstract:Infection with Shiga Toxin-producing Escherichia coli (STEC) results in hemorrhagic colitis and can lead to life-threatening sequelae including hemolytic uremic syndrome (HUS). Conventional treatment is intravenous fluid volume expansion. Antibiotic treatment is contraindicated, due in part to the elevated risk of HUS related to increased Shiga Toxin (Stx) release associated with some antibiotics. Given the lack of effective strategies and the increasing number of STEC outbreaks, new treatment approaches are critically needed. In this study, we used an antimicrobial peptide wrwycr, previously shown to enhance STEC killing without increasing Stx production, in combination with antibiotic treatments. Checkerboard and time-kill assays were used to assess peptide wrwycr-antibiotic combinations for synergistic STEC killing. Cytotoxicity and real-time PCR were used to evaluate Stx production and stx expression, respectively, associated with these combinations. The synergistic combinations that showed rapid killing, no growth recovery and minimal Stx production were peptide wrwycr-kanamycin/gentamicin. Transmission electron microscopy revealed striking differences in bacterial cell morphology associated with various treatments. This study provides proof of principle for the design of an antibiotic-peptide wrwycr combination effective in killing STEC without enhancing release of Shiga Toxins. It also offers a strategy for the repurposing of antibiotics for treatment of STEC infection.
Nancy A Strockbine - One of the best experts on this subject based on the ideXlab platform.
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outbreaks of non o157 Shiga Toxin producing escherichia coli infection usa
Epidemiology and Infection, 2014Co-Authors: Ruth E Lunagierke, Patricia M Griffin, L H Gould, Karen M Herman, Cheryl A Bopp, Nancy A Strockbine, Rajal K ModyAbstract:Non-O157 Shiga Toxin-producing Escherichia coli (STEC) infections are increasingly detected, but sources are not well established. We summarize outbreaks to 2010 in the USA. Single-aetiology outbreaks were defined as ⩾2 epidemiologically linked culture-confirmed non-O157 STEC infections; multiple-aetiology outbreaks also had laboratory evidence of ⩾2 infections caused by another enteric pathogen. Twenty-six states reported 46 outbreaks with 1727 illnesses and 144 hospitalizations. Of 38 single-aetiology outbreaks, 66% were caused by STEC O111 (n = 14) or O26 (n = 11), and 84% were transmitted through food (n = 17) or person-to-person spread (n = 15); food vehicles included dairy products, produce, and meats; childcare centres were the most common setting for person-to-person spread. Of single-aetiology outbreaks, a greater percentage of persons infected by Shiga Toxin 2-positive strains had haemolytic uraemic syndrome compared with persons infected by Shiga Toxin 1-only positive strains (7% vs. 0·8%). Compared with single-aetiology outbreaks, multiple-aetiology outbreaks were more frequently transmitted through water or animal contact.
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clinical isolates of Shiga Toxin 1a producing shigella flexneri with an epidemiological link to recent travel to hispaniola
Emerging Infectious Diseases, 2014Co-Authors: Miranda D Gray, Nancy A Strockbine, Keith A Lampel, Reinaldo E Fernandez, Angela R Meltoncelsa, Anthony T MaurelliAbstract:Shiga Toxins (Stx) are cytoToxins involved in severe human intestinal disease. These Toxins are commonly found in Shigella dysenteriae serotype 1 and Shiga-Toxin–producing Escherichia coli; however, the Toxin genes have been found in other Shigella species. We identified 26 Shigella flexneri serotype 2 strains isolated by public health laboratories in the United States during 2001–2013, which encode the Shiga Toxin 1a gene (stx1a). These strains produced and released Stx1a as measured by cytotoxicity and neutralization assays using anti-Stx/Stx1a antiserum. The release of Stx1a into culture supernatants increased ≈100-fold after treatment with mitomycin C, suggesting that stx1a is carried by a bacteriophage. Infectious phage were found in culture supernatants and increased ≈1,000-fold with mitomycin C. Whole-genome sequencing of several isolates and PCR analyses of all strains confirmed that stx1a was carried by a lambdoid bacteriophage. Furthermore, all patients who reported foreign travel had recently been to Hispaniola, suggesting that emergence of these novel strains is associated with that region.
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non o157 Shiga Toxin producing escherichia coli infections in the united states 1983 2002
The Journal of Infectious Diseases, 2005Co-Authors: John T Brooks, Patricia M Griffin, Evangeline G Sowers, Joy G Wells, Katherine D Greene, Robert M Hoekstra, Nancy A StrockbineAbstract:BACKGROUND Shiga Toxin-producing Escherichia coli (STEC) O157:H7 is a well-recognized cause of bloody diarrhea and hemolytic-uremic syndrome (HUS). Non-O157 STEC contribute to this burden of illness but have been underrecognized as a result of diagnostic limitations and inadequate surveillance. METHODS Between 1983 and 2002, 43 state public health laboratories submitted 940 human non-O157 STEC isolates from persons with sporadic illnesses to the Centers for Diseases Control and Prevention reference laboratory for confirmation and serotyping. RESULTS The most common serogroups were O26 (22%), O111 (16%), O103 (12%), O121 (8%), O45 (7%), and O145 (5%). Non-O157 STEC infections were most frequent during the summer and among young persons (median age, 12 years; interquartile range, 3-37 years). Virulence gene profiles were as follows: 61% stx(1) but not stx(2); 22% stx(2) but not stx(1); 17% both stx(1) and stx(2); 84% intimin (eae); and 86% enterohemolysin (E-hly). stx(2) was strongly associated with an increased risk of HUS, and eae was strongly associated with an increased risk of bloody diarrhea. STEC O111 accounted for most cases of HUS and was also the cause of 3 of 7 non-O157 STEC outbreaks reported in the United States. CONCLUSIONS Non-O157 STEC can cause severe illness that is comparable to the illness caused by STEC O157. Strains that produce Shiga Toxin 2 are much more likely to cause HUS than are those that produce Shiga Toxin 1 alone. Improving surveillance will more fully elucidate the incidence and pathological spectrum of these emerging agents. These efforts require increased clinical suspicion, improved clinical laboratory isolation, and continued serotyping of isolates in public health laboratories.