Outbreak Of Hemolytic Uremic Syndrome Research Articles

O-Antigen Diversification Masks Identification of Highly Pathogenic Shiga Toxin-Producing Escherichia coli O104:H4-Like Strains.

Shiga toxin-producing Escherichia coli (STEC) can give rise to a range of clinical outcomes from diarrhea to the life-threatening systemic condition hemolytic-uremic syndrome (HUS). Although STEC O157:H7 is the serotype most frequently associated with HUS, a major outbreak of HUS occurred in 2011 in Germany and was caused by a rare serotype, STEC O104:H4. Prior to 2011 and since the outbreak, STEC O104:H4 strains have only rarely been associated with human infections. From 2012 to 2020, intensified STEC surveillance was performed in Germany where the subtyping of ~8,000 clinical isolates by molecular methods, including whole-genome sequencing, was carried out. A rare STEC serotype, O181:H4, associated with HUS was identified, and like the STEC O104:H4 outbreak strain, this strain belongs to sequence type 678 (ST678). Genomic and virulence comparisons revealed that the two strains are phylogenetically related and differ principally in the gene cluster encoding their respective lipopolysaccharide O-antigens but exhibit similar virulence phenotypes. In addition, five other serotypes belonging to ST678 from human clinical infection, such as OX13:H4, O127:H4, OgN-RKI9:H4, O131:H4, and O69:H4, were identified from diverse locations worldwide. IMPORTANCE Our data suggest that the high-virulence ensemble of the STEC O104:H4 outbreak strain remains a global threat because genomically similar strains cause disease worldwide but that the horizontal acquisition of O-antigen gene clusters has diversified the O-antigens of strains belonging to ST678. Thus, the identification of these highly pathogenic strains is masked by diverse and rare O-antigens, thereby confounding the interpretation of their potential risk.

Outbreak of hemolytic uremic syndrome with unusually severe clinical presentation caused by Shiga toxin-producing Escherichia coli O26:H11 in France

BackgroundIn spring 2019, an outbreak of Shiga toxin-producing Escherichia coli-associated hemolytic uremic syndrome (STEC HUS) occurred in France. Epidemiological investigations made by Santé publique France in connection with microbiological investigations at the national reference center for STEC promptly identified a common exposure to consumption of raw cow's milk cheese, and confirmed a cluster affiliation of the E. coli O26:H11 outbreak strain. Here, we report the clinical characteristics of the patients, the treatment used, as well as the outcome at 1 month. MethodPatients with STEC HUS linked to the E. coli O26:H11 outbreak strain were identified from the national surveillance network of pediatric STEC HUS cases coordinated by Santé publique France.Clinical data were analyzed from the patients’ hospital records obtained from the treating physicians. ResultsOverall, 20 pediatric cases of STEC HUS linked to the outbreak strain were identified.Their median age of the patients was 16 months (range: 5–60). Most of them presented with diarrhea but none had received prior antibiotherapy. A total of 13 patients required dialysis; 10 patients and four patients had central nervous system (CNS) and cardiac involvement, respectively. No deaths occurred.At the 1-month follow-up, only two patients had a decreased glomerular filtration rate, below 80 mL /min/1.73m2 and four had hypertension. One patient had neurological sequelae. ConclusionThe E. coli O26:H11 strain identified as the cause of an STEC HUS outbreak in France in spring 2019 is notable for the initial severe clinical presentation of the patients, with a particularly high frequency of CNS and cardiac involvement similar to the German E. coli O104:H4 outbreak described in 2011. However, despite the initial severity, the 1-month outcome was favorable in most cases. The patients’ young age in this outbreak highlights the need to improve information and caregiver awareness regarding consumption of at-risk foods by young children as key preventive measures against STEC infections.

Epidemiological investigation of recurrent outbreaks of haemolytic uraemic syndrome caused by Shiga toxin-producing Escherichia coli serotype O55:H7 in England, 2014-2018.

Recurrent outbreaks of haemolytic uraemic syndrome (HUS) caused by Shiga toxin-producing Escherichia coli (STEC) serotype O55:H7 occurred in England between 2014 and 2018. We reviewed the epidemiological evidence to identify potential source(s) and transmission routes of the pathogen, and to assess the on-going risk to public health. Over the 5-year period, there were 43 confirmed and three probable cases of STEC O55:H7. The median age of cases was 4 years old (range 6 months to 69 years old) and over half of all cases were female (28/46, 61%). There were 36/46 (78.3%) symptomatic cases, and over half of all cases developed HUS (25/46, 54%), including two fatal cases. No common food or environmental exposures were identified, although the majority of cases lived in rural or semi-rural environments and reported contact with both wild and domestic animals. This investigation informed policy on the clinical and public health management of HUS caused by STEC other than serotype O157:H7 (non-O157 STEC) in England, including comprehensive testing of all household contacts and household pets and more widespread use of polymerase chain reaction assays for the rapid diagnosis of STEC-HUS.

Top-Down Proteomic Identification of Shiga Toxin 1 and 2 from Pathogenic Escherichia coli Using MALDI-TOF-TOF Tandem Mass Spectrometry.

Shiga-toxin-producing Escherichia coli (STEC) are a burden on agriculture and a threat to public health. Rapid methods are needed to identify STEC strains and characterize the Shiga toxin (Stx) they produce. We analyzed three STEC strains for Stx expression, using antibiotic induction, matrix-assisted laser desorption/ionization time-of-flight-time-of-flight (MALDI-TOF-TOF) mass spectrometry, and top-down proteomic analysis. E. coli O157:H- strain 493/89 is a clinical isolate linked to an outbreak of hemolytic uremic syndrome (HUS) in Germany in the late 1980s. E. coli O145:H28 strains RM12367-C1 and RM14496-C1 were isolated from an agricultural region in California. The stx operon of the two environmental strains were determined by whole genome sequencing (WGS). STEC strain 493/89 expressed Shiga toxin 2a (Stx2a) as identified by tandem mass spectrometry (MS/MS) of its B-subunit that allowed identification of the type and subtype of the toxin. RM12367-C1 also expressed Stx2a as identified by its B-subunit. RM14496-C1 expressed Shiga toxin 1a (Stx1a) as identified from its B-subunit. The B-subunits of Stx1 and Stx2 both have an intramolecular disulfide bond. MS/MS was obtained on both the disulfide-bond-intact and disulfide-bond-reduced B-subunit, with the latter being used for top-down proteomic identification. Top-down proteomic analysis was consistent with WGS.

Shiga toxin producing Escherichia coli-associated diarrhea and hemolytic uremic syndrome in young children in Romania

BackgroundDiarrheagenic Escherichia coli (E. coli) is an important cause of diarrheal diseases in both developing countries and industrialized countries. An outbreak of hemolytic uremic syndrome (HUS) in young children from southern Romania was reported in early 2016 and was attributed to Shiga toxin producing E. coli (STEC) O26 infection. The aim of this study was to determine the prevalence, demographic and clinical characteristics of STEC infections in children hospitalized with diarrhea in Brașov in the central region of Romania. We also described the occurrence of HUS among hospitalized children, close in time to the 2016 HUS outbreak in southern Romania.MethodsA prospective study was conducted between March and December 2016 among 722 children aged 1–30 months hospitalized with acute diarrhea. Stool samples obtained from patients with diarrhea were tested for the presence of Shiga toxin type 1 (STX1) and type 2 (STX2) by an immunochromatographic assay, and other enteropathogens. Demographic and clinical information on cases of HUS diagnosed in the same hospital was obtained from medical records.ResultsOverall 46/722 (6.4%) children (mean age 10.3 months, 32.6% females) hospitalized with diarrhea tested positive for STX1 or STX2; of these 79% were positive for both STX1 and STX2, 16% for STX2 only, and 5% for STX1 only. Bloody diarrhea, vomiting and fever were documented in 32.6%, 52.1% and 50.0%, respectively of patients with STEC infection. Eleven confirmed HUS cases (mean age 20 months, five females) were identified between 2014 and 2016 with prodromal diarrhea reported in 10 of them. Three of the 11 HUS patients required hemodialysis.ConclusionsSTEC prevalence among young children with diarrhea in Romania was high and the risk of HUS is emerging. The establishment of a systematic laboratory-based surveillance program including identification of the circulating STEC strains coupled with epidemiological investigation of HUS patients is warranted to determine the source and mode of transmission of STEC and prevent of STEC-associated diarrhea and HUS.

SMRT sequencing reveals differential patterns of methylation in two O111:H- STEC isolates from a hemolytic uremic syndrome outbreak in Australia

In 1995 a severe haemolytic-uremic syndrome (HUS) outbreak in Adelaide occurred. A recent genomic analysis of Shiga toxigenic Escherichia coli (STEC) O111:H- strains 95JB1 and 95NR1 from this outbreak found that the more virulent isolate, 95NR1, harboured two additional copies of the Shiga toxin 2 (Stx2) genes encoded within prophage regions. The structure of the Stx2-converting prophages could not be fully resolved using short-read sequence data alone and it was not clear if there were other genomic differences between 95JB1 and 95NR1. In this study we have used Pacific Biosciences (PacBio) single molecule real-time (SMRT) sequencing to characterise the genome and methylome of 95JB1 and 95NR1. We completely resolved the structure of all prophages including two, tandemly inserted, Stx2-converting prophages in 95NR1 that were absent from 95JB1. Furthermore we defined all insertion sequences and found an additional IS1203 element in the chromosome of 95JB1. Our analysis of the methylome of 95NR1 and 95JB1 identified hemi-methylation of a novel motif (5′-CTGCm6AG-3′) in more than 4000 sites in the 95NR1 genome. These sites were entirely unmethylated in the 95JB1 genome, and included at least 177 potential promoter regions that could contribute to regulatory differences between the strains. IS1203 mediated deactivation of a novel type IIG methyltransferase in 95JB1 is the likely cause of the observed differential patterns of methylation between 95NR1 and 95JB1. This study demonstrates the capability of PacBio SMRT sequencing to resolve complex prophage regions and reveal the genetic and epigenetic heterogeneity within a clonal population of bacteria.

Shiga Toxin-Producing Escherichia coli Infections during Pregnancy.

Gastrointestinal infection with Shiga toxin-producing Escherichia coli (STEC) causes diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS), characterized by hemolytic anemia, thrombocytopenia and acute renal failure. The main virulence factor of STEC is Shiga toxin (Stx), which is responsible for HUS development. STEC can produce Stx type 1 and/or 2 (Stx1, Stx2) and their variants, Stx2 being more frequently associated with severe cases of HUS. This pathology occurs in 5–15% of cases with STEC infection when Stx gain access to the bloodstream and causes damage in the target organs such as the kidney and brain. STEC infections affect mainly young children, although the large HUS outbreak with a new Stx2-producing STEC O104:H4 in Europe in 2011 involved more adults than children, and women were over-represented. Maternal infections during pregnancy are associated with adverse pregnancy outcomes. Studies in rats showed that Stx2 binds to the utero-placental unit and causes adverse pregnancy outcomes. In this article, we provide a brief overview of Stx2 action on placental tissues and discuss whether they might cause pregnancy loss or preterm birth.

Outbreak of Shiga toxin-producing Escherichia-coli-associated hemolytic uremic syndrome in Istanbul in 2015: outcome and experience with eculizumab

This study aims to identify epidemiological and clinical characteristics of patients and report our experience with eculizumab treatment during an outbreak of hemolytic uremic syndrome (HUS) caused by Shiga toxin-producing Escherichia coli (STEC) in Istanbul in 2015. Thirty-two children (21 females, median age 3.25years) were included in this study. Demographic, clinical and laboratory data, and treatment details were retrospectively collected. Renal outcomes were assessed at last follow-up visit. To assess the effect of eculizumab on prognosis of STEC-HUS, subgroup analysis was performed on patients who required dialysis. A high number of cases occurred within a certain region of Istanbul. Stool samples were cultured from 21 patients (65%), and enteroaggregative E. coli (EAEC; n = 7) and enterohemorrhagic E. coli (EHEC; n = 3) strains were detected. Rates of dialysis treatment, neurological manifestations, and death were 59%, 25%, and 3%, respectively. Mean follow-up duration was 8.6 ± 2.6months (range 3-12months). None of the patients (n = 25) was on dialysis at the final visit. The complete renal recovery rate was 54%. Nine patients were treated with eculizumab. At final follow-up visit, no differences in estimated glomerular filtration rate, proteinuria level, or hypertension incidence were observed between patients treated with eculizumab and those not treated with eculizumab. An outbreak of EAEC occurred in a specific region of Istanbul. Livestock markets were suspected as the source. Evidence for beneficial effects of eculizumab on renal outcome was not clear in this cohort.

Escherichia coli O26 and O113:H21 on Carcasses and Beef from a Slaughterhouse Located in Mato Grosso, Brazil.

Shiga toxin-producing Escherichia coli (STEC) is a group of emerging pathogens that can cause human diseases, including hemolytic uremic syndrome (HUS) and hemorrhagic colitis (HC). Monitoring slaughtering stages and checking contamination points are crucial for the production of safe food. In this context, the aim of this study was to verify contamination by STEC strains, to determine the contamination points and evaluate the resistance profile to 12 antimicrobials used in both veterinary and human medicine. A total of 80 samples were obtained from eight collection points (pen floor, rectum, hide, carcass swabs and esophagus, diaphragm, masseter, and retail beef tissue samples). The isolates were collected by dilution plating on MacConkey agar with sorbitol, cefixime, and tellurite and analyzed by multiplex polymerase chain reaction for virulence genes. Serotyping of non-O157 was performed, and testing for 12 antibiotics by disk diffusion was carried out. A total of 18 STEC strains were isolated, presenting different virulence profiles. Contamination by STEC was observed in the rectum (5/18), carcass surface (5/18), hide (3/18), diaphragm (2/18), retail beef (2/18), and masseter muscle (1/18). Pen floor swabs and esophagus tissues showed no STEC contamination. Moreover, three strains were identified as O26 and three as O113:H21 strains, which have been linked to HUS and HC outbreak cases in Brazil. All STEC isolates were susceptible to all evaluated antimicrobials, except streptomycin. The presence of STEC strains is a direct risk to the consumer, especially when isolated from retail beef, and contamination can occur during different slaughter stages. However, antimicrobial resistance profiles did not identify multidrug-resistant strains, limiting potential antimicrobial resistance transmission to other pathogens.

Pro-inflammatory capacity of Escherichia coli O104:H4 outbreak strain during colonization of intestinal epithelial cells from human and cattle

In 2011, Germany was struck by the largest outbreak of hemolytic uremic syndrome. The highly virulent E. coli O104:H4 outbreak strain LB226692 possesses a blended virulence profile combining genetic patterns of human adapted enteroaggregative E. coli (EAEC), rarely detected in animal hosts before, and enterohemorrhagic E. coli (EHEC), a subpopulation of Shiga toxin (Stx)-producing E. coli (STEC) basically adapted to the ruminant host. This study aimed at appraising the relative level of adaptation of the EAEC/EHEC hybrid strain LB226692 to humans and cattle. Adherence and invasion of the hybrid strain to intestinal (jejunal and colonic) epithelial cells (IEC) of human and bovine origin was compared to that of E. coli strains representative of different pathovars and commensal E. coli by means of light and electron microscopy and culture. Strain-specific host gene transcription profiles of selected cytokines and chemokines as well as host-induced transcription of bacterial virulence genes were assessed. The release of Stx upon host cell contact was quantified. The outbreak strain’s immunomodulation was assessed by cultivating primary bovine macrophages with conditioned supernatants from IEC infection studies with E. coli, serving as model for the innate immunity of the bovine gut. The outbreak strain adhered to IEC of both, human and bovine origin. Electron microscopy of infected cells revealed the strain’s particular affinity to human small IEC, in contrast to few interactions with bovine small IEC. The outbreak strain possessed a high-level of adhesive power, similar to human-associated E. coli strains and in contrast to bovine-associated STEC strains. The outbreak strain displayed a non-invasive phenotype, in contrast to some bovine-associated E. coli strains, which were invasive. The outbreak strain provoked some pro-inflammatory activity in human cells, but to a lower extent as compared to other pathotypes. In contrasts to bovine-associated E. coli strains, the outbreak strain induced marked pro-inflammatory activity when interacting with bovine host cells directly (IEC) and indirectly (macrophages). Among stx2-positive strains, the human-pathogenic strains (LB226692 and EHEC strain 86-24) released higher amounts of Stx compared to bovine-associated STEC. The findings imply that the outbreak strain is rather adapted to humans than to cattle. However, the outbreak strain’s potential to colonize IEC of both host species and the rather mixed reaction patterns observed for all strains under study indicate, that even STEC strains with an unusual genotype as the EHEC O104:H4 outbreak strain, i.e. with an EAEC genetic background, may be able to conquer other reservoir hosts.

An outbreak of hemolytic uremic syndrome in southern Romania during 2015–2016: Epidemiologic, clinical, laboratory, microbiologic, therapeutic and outcome characteristics

To describe the epidemiologic, clinical, microbiological, therapeutic and outcome characteristics of a HUS outbreak occurring in southern Romania from 2015 to 2016. We retrospectively collected data from the medical records of all HUS cases hospitalized at the pediatric nephrology department of Marie Curie Children's Hospital of Bucharest, Romania. There were 32 HUS cases (19 girls/13 boys, 87.6% <2 years), all associated with diarrhea (bloody in 13, 40.6%). Thirteen (40.6%) and 4 (12.5%) patients had oliguria and anuria at admission. Extreme pallor, generalized edema, vomiting, dehydration, fever and seizures were found in 100%, 56.3%, 31.3%, 31.3%, 25% and 9.4% of patients, respectively. E. coli and STEC were identified in the stools of 6 and 8 patients, respectively; E. coli O26 and O157 infection were documented serologically in 10 and 3 children, respectively. There were 15/32 (46.9%) patients with confirmed HUS. Eighteen (56.3%) patients were hypertensive; other complications included infections, left ventricular hypertrophy, cardiopulmonary arrest, seizures and encephalopathy in 62.5%, 37.5%, 28.3%, 18.8% and 12.5%, respectively. Peritoneal dialysis and hemodialysis were performed in 23 (72%) and 2 patients, respectively. Three patients (9.4%) died early during hospitalization. A 6-12-month follow-up of 26 patients revealed that 65.4% had post-HUS sequelae (persistent hypertension and chronic renal failure in 34.6% and 30.8%, respectively). The principal STEC serotype involved was O26:H11 and the number of confirmed HUS cases reached half of the patients. Compared with the medical literature, this outbreak had a higher rate of complications and renal sequelae and was associated with a high fatality rate.

XTAG Luminex multiplex assay for rapid screening of verocytotoxin-producing Escherichia coli strains

Abstract The O26 verocytotoxin-producing Escherichia coli (VTEC)-associated outbreak of hemolytic uremic syndrome (HUS) cases in Romania during 2016 showed the need to improve the current methodology of non-O157 VTEC detection and surveillance. An in-house assay based on xTAG Luminex technology was optimized to identify seven of the most relevant diarrheagenic E.coli serogroups (O-specific wzx genes), two convenient VTEC virulence markers (eaeA and ehxA genes), and a species-specific control gene (uidA). Twenty-nine strains previously characterized in terms of serogroup and virulence genes were tested with the optimized protocol and the results were as expected. The ratio of sample signal to background varied from 66.7 (ehxA) to 7.6 (uidA) for positive samples, with a cut-off of 3. Sensitivity varied depending on the target to be amplified from approximately 102 genomic copies to approximately 104 genomic copies per reaction, respectively. The current approach seems an affordable alternative to commercially available assays that can be further exploited to improve existing autochthonous strategies to prevent future VTEC outbreaks.

Survival and interaction of Escherichia coli O104:H4 on Arabidopsis thaliana and lettuce (Lactuca sativa) in comparison to E. coli O157:H7: Influence of plant defense response and bacterial capsular polysaccharide

Shiga toxin-producing Escherichia coli (STEC) has been associated with illnesses and outbreaks linked to fresh vegetables, prompting a growing public health concern. Most studies regarding interactions of STEC on fresh produce focused on E. coli O157:H7. Limited information is available about survival or fitness of E. coli O104:H4, non-O157 pathogen that was linked to one of the largest outbreaks of hemolytic uremic syndrome in 2011. In this study, survival of E. coli O104:H4 was evaluated on Arabidopsis thaliana plant and lettuce for 5 days compared with E. coli O157:H7, and expression of pathogenesis-realted gene (PR1; induction of plant defense response) was examined by reverse transcription quantitative PCR, and potential influence of capsular polysaccharide (CPS) on the bacterial fitness on plant was investigated. Populations of E. coli O104:H4 strains (RG1, C3493, and LpfA) on Arabidopsis and lettuce were significantly (P < 0.05) greater than those of E. coli O157:H7 strains (7386 and sakai) at day 5 post-inoculation, indicating E. coli O104:H4 may have better survival ability on the plants. In addition, the E. coli O104:H4 strains produced significantly (P < 0.05) higher amounts of CPS compared with the E. coli O157:H7 strains. RG1 strain (1.5-fold) initiated significantly (P < 0.05) lower expression of PR1 gene indicating induction of plant defense response compared with E. coli O157:H7 strains 7386 (2.9-fold) and sakai (2.7-fold). Collectively, the results in this study suggests that different level of CPS production and plant defense response initiated by each STEC strain might influence the bacterial survival or persistence on plants. The present study provides better understanding of survival behavior of STEC, particularly E. coli O104:H4, using a model plant and vegetable under pre-harvest conditions with plant defense response.

Ongoing haemolytic uraemic syndrome (HUS) outbreak caused by sorbitol-fermenting (SF) Shiga toxin-producing Escherichia coli (STEC) O157, Germany, December 2016 to May 2017.

We report an ongoing, protracted and geographically dispersed outbreak of haemolytic uraemic syndrome (HUS) and gastroenteritis in Germany, involving 30 cases since December 2016. The outbreak was caused by the sorbitol-fermenting immotile variant of Shiga toxin-producing (STEC) Escherichia coli O157. Molecular typing revealed close relatedness between isolates from 14 cases. One HUS patient died. Results of a case–control study suggest packaged minced meat as the most likely food vehicle. Food safety investigations are ongoing.

Community-wide outbreak of haemolytic uraemic syndrome associated with Shiga toxin 2-producing Escherichia coli O26:H11 in southern Italy, summer 2013.

In summer 2013, an excess of paediatric cases of haemolytic uraemic syndrome (HUS) in a southern region of Italy prompted the investigation of a community-wide outbreak of Shiga toxin 2-producing Escherichia coli (STEC) O26:H11 infections. Case finding was based on testing patients with HUS or bloody diarrhoea for STEC infection by microbiological and serological methods. A case–control study was conducted to identify the source of the outbreak. STEC O26 infection was identified in 20 children (median age 17 months) with HUS, two of whom reported severe neurological sequelae. No cases in adults were detected. Molecular typing showed that two distinct STEC O26:H11 strains were involved. The case–control study showed an association between STEC O26 infection and consumption of dairy products from two local plants, but not with specific ready-to-eat products. E.coli O26:H11 strains lacking the stx genes were isolated from bulk milk and curd samples, but their PFGE profiles did not match those of the outbreak isolates. This outbreak supports the view that infections with Stx2-producing E. coli O26 in children have a high probability of progressing to HUS and represent an emerging public health problem in Europe.

Plasmids from Shiga Toxin-Producing Escherichia coli Strains with Rare Enterohemolysin Gene ( ehxA ) Subtypes Reveal Pathogenicity Potential and Display a Novel Evolutionary Path

Bacterial plasmids are known to be key agents of change in microbial populations, promoting the dissemination of various traits, such as drug resistance and virulence. This study determined the genetic makeup of virulence plasmids from rare enterohemolysin subtype D and E Shiga toxin-producing E. coli strains. We demonstrated that ehxA subtype D plasmids represent a novel E. coli virulence plasmid, and although subtype D plasmids were derived from nonclinical isolates, they encoded a variety of virulence determinants that are associated with pathogenic E. coli In contrast, subtype E plasmids, isolated from strains recovered from severely ill patients, carry only a few virulence determinants. The results of this study reemphasize the plasticity and vast diversity among E. coli plasmids. This work demonstrates that, although E. coli strains of certain serogroups may not be frequently associated with disease, they should not be underestimated in protecting human health and food safety.

Multi‐country outbreak of Shiga toxin‐producing Escherichia coli infection associated with haemolytic uraemic syndrome

EFSA Supporting PublicationsVolume 13, Issue 4 1017E Technical reportOpen Access Multi-country outbreak of Shiga toxin-producing Escherichia coli infection associated with haemolytic uraemic syndrome European Food Safety Authority and European Centre for Disease Prevention and Control, European Food Safety Authority and European Centre for Disease Prevention and ControlSearch for more papers by this author European Food Safety Authority and European Centre for Disease Prevention and Control, European Food Safety Authority and European Centre for Disease Prevention and ControlSearch for more papers by this author First published: 06 April 2016 https://doi.org/10.2903/sp.efsa.2016.EN-1017Citations: 3 Published date: 6 April 2016 Question number: EFSA-Q-2016-00232 AboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL References Luna-Gierke RE, Wymore K, Sadlowski J, Clogher P, Gierke RW, Tobin-D'Angelo M, et al. Multiple-Aetiology Enteric Infections Involving Non-O157 Shiga Toxin-Producing Escherichia coli - FoodNet, 2001–2010. Zoonoses Public Hlth. 2014 Nov; 61(7): 492– 8. European Centre for Disease Prevention and Control. Escherichia coiifactsheet Stockholm: ECDC; [cited 2016 March 29]. Available from: http://ecdc.europa.eu/en/healthtopics/escherichia_coli/basic_facts/Pages/basic_facts.aspx. Fauci A, Braunwald E, Kasper D, Hauser S, Longo D, Jameson J, et al. Harrison's Principles of internal medicine. MH Medical, editor: McGraw Hill Medical; 2008. 1811– 5 p. EFSA (European Food Safety Authority) and ECDC (European Centre for Disease Prevention and Control). The European Union summary report on trends and sources of zoonoses, zoonotic agents and food-borne outbreaks in 2014. EFSA journal. 13(12): 4329,191. European Centre for Disease Prevention and Control. Surveillance Atlas of Infectious Diseases Stockholm: ECDC; 2016 [cited 2016 March 29]. Available from: http://atlas.ecdc.europa.eu/public/index.aspx. Espie E, Grimont F, Mariani-Kurkdjian P, Bouvet P, Haeghebaert S, Filliol I, et al. Surveillance of hemolytic uremic syndrome in children less than 15 years of age, a system to monitor O157 and non-O157 Shiga toxin-producing Escherichia coli infections in France, 1996–2006. Pediatr Infect Dis J. 2008 Jul; 27(7): 595– 601. Institut de Veille Sanitaire. Epidémie d'infections à E. coli producteurs de Shiga-toxines non 0157 liée à la consommation de camembert au lait cru, nord-ouest de la France, octobre-décembre 20052007 March 30. Available from: http://opac.invs.sante.fr/index.php2lvNnotice_display&id=9416. Ethelberg S, Smith B, Torpdahl M, Lisby M, Boel J, Jensen T, et al. Outbreak of non-O157 Shiga toxin-producing Escherichia coli infection from consumption of beef sausage. Clin Infect Dis. 2009 Apr 15; 48(8): e78– 81. Germinario C, Chironna M, CGallone M, Tafuri S, Desiante F, Calabrese G. Community-wide Outbreak of Haemolytic Uremic Syndrome Associated with Shiga Toxin 2-Producing Escherichia coli O26:H11 in Southern Italy, Summer 2013. Euro Surveill. 2016;(Forthcoming). International Organization for Standardization. ISO/TS 13136:2012 Microbiology of food and animal feed -Real-time polymerase chain reaction (PCR)-based method for the detection of food-borne pathogens -Horizontal method for the detection of Shiga toxin-producing Escherichia coli (STEC) and the determination of O157, O111, O26, O103 and O145 serogroups. Technical Specifications: ISO; 2012. p. 22. Peron E, Zaharia A, Zota L, Severi E, Mârdh O, Usein C, et al. Early findings in outbreak of haemolytic uraemic syndrome among young children caused by Shiga toxin-producing Escherichia coli, Romania, January to February 2016. Eurosurveillance. 2016; 21(11). Jenssen G, Hovland E, Bjerre A, Bangstad H-J, Nygard K, Vold L. Incidence and etiology of hemolytic-uremic syndrome in children in Norway, 1999–2008 - a retrospective study of hospital records to assess the sensitivity of surveillance. BMC Infectious Diseases. 2014; 14(1): 265. Nielsen EM, Andersen MT. Detection and characterization of verocytotoxin-producing Escherichia coli by automated 5' nuclease PCR assay. J Clin Microbiol. 2003 Jul; 41(7): 2884– 93. Citing Literature Volume13, Issue4April 20161017E ReferencesRelatedInformation

Early findings in outbreak of haemolytic uraemic syndrome among young children caused by Shiga toxin-producing Escherichia coli, Romania, January to February 2016.

As at 29 February 2016, 15 cases of haemolytic uraemic syndrome with onset between 25 January and 22 February were reported among children between five and 38 months in Romania, and three of them died. Cases were mostly from southern Romania. Six cases tested positive for Escherichia coli O26 by serology. Fruits, vegetables, meat and dairy products were among the possible common food exposures. Investigations are ongoing in Romania to control the outbreak.

Hypertension and mild chronic kidney disease persist following severe haemolytic uraemic syndrome caused by Shiga toxin-producing Escherichia coli O104:H4 in adults.

Shiga toxin-producing, enteroaggregative Escherichia coli was responsible for the 2011 outbreak of haemolytic uraemic syndrome (HUS). The present single-centre, observational study describes the 1-year course of the disease with an emphasis on kidney function. Outcome data after 1 year are associated with treatment and patient characteristics at onset of HUS. Patients were treated according to a standardized approach of supportive care, including a limited number of plasmapheresis. On top of this treatment, patients with severe HUS (n = 35) received eculizumab, a humanized anti-C5 monoclonal antibody inhibiting terminal complement activation. The per-protocol decision--to start or omit an extended therapy with eculizumab accompanied by azithromycin--separated the patients into two groups and marked Day 0 of the prospective study. Standardized visits assessed the patients' well-being, kidney function, neurological symptoms, haematological changes and blood pressure. Fifty-six patients were regularly seen during the follow-up. All patients had survived without end-stage renal disease. Young(er) age alleviated restoring kidney function after acute kidney injury even in severe HUS. After 1 year, kidney function was affected with proteinuria [26.7%; 95% confidence interval (CI) 13.8-39.6], increased serum creatinine (4.4%, CI 0.0-10.4), increased cystatin C (46.7%, CI 32.1-61.3) and reduced (<90 mL/min) estimated glomerular filtration rate (46.7%, CI 32.1-61.3). Nine of the 36 patients without previous hypertension developed de novo hypertension (25%, CI 10.9-39.1). All these patients had severe HUS. Although shiga toxin-producing Escherichia coli (STEC)-HUS induced by O104:H4 was a life-threatening acute disease, follow-up showed a good recovery of organ function in all patients. Whereas kidney function recovered even after longer duration of dialysis, chronic hypertension developed after severe HUS with neurological symptoms and could not be prevented by the extended therapy.

Molecular typing of VTEC strains isolated from food, feed and animals

Molecular typing of VTEC strains isolated from food, feed and animals