Escherichia coli encoding Shiga toxin subtype Stx2f causing human infections in England, 2015–2022 (original) (raw)
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The Journal of Infectious Diseases, 2002
Shiga toxin (Stx)-producing Escherichia coli (STEC) from patients with hemolytic-uremic syndrome (HUS), patients with diarrhea without HUS, or asymptomatic subjects were genotyped to assess associations between stx 2 variants and clinical manifestations of infection. Neither stx 2d nor stx 2e was found in 268 STEC isolates from patients with HUS. Of 262 STEC isolates from patients with diarrhea, stx 2d was found in 41 (15.6%; P , .000001), and stx 2e was found in 12 (4.6%; P ¼ .0004). The stx 2c genotype frequency was similar among isolates from patients with HUS (3.7%) and diarrhea (5.0%). The frequencies of stx 2c , stx 2d , and stx 2e among 96 STEC isolates from asymptomatic subjects were comparable to those among isolates from patients with diarrhea. None of the 626 STEC isolates contained stx 2f . All stx 2d -positive or stx 2e -positive STEC isolates were eae negative and originated from subjects older than those with STEC isolates with stx 2c . stx 2c -positive STEC isolates can cause HUS, but the presence of stx 2d or stx 2e may predict a milder disease with a minimal risk of HUS.
PLoS ONE, 2014
Shiga toxin-producing Escherichia coli (STEC) cause infections in humans ranging from asymptomatic carriage to bloody diarrhoea and haemolytic uremic syndrome (HUS). Here we present whole genome comparison of Norwegian non-O157 STEC strains with the aim to distinguish between strains with the potential to cause HUS and less virulent strains. Whole genome sequencing and comparisons were performed across 95 non-O157 STEC strains. Twenty-three of these were classified as HUS-associated, including strains from patients with HUS (n = 19) and persons with an epidemiological link to a HUS-case (n = 4). Genomic comparison revealed considerable heterogeneity in gene content across the 95 STEC strains. A clear difference in gene profile was observed between strains with and without the Locus of Enterocyte Effacement (LEE) pathogenicity island. Phylogenetic analysis of the core genome showed high degree of diversity among the STEC strains, but all HUS-associated STEC strains were distributed in two distinct clusters within phylogroup B1. However, non-HUS strains were also found in these clusters. A number of accessory genes were found to be significantly overrepresented among HUS-associated STEC, but none of them were unique to this group of strains, suggesting that different sets of genes may contribute to the pathogenic potential in different phylogenetic STEC lineages. In this study we were not able to clearly distinguish between HUS-associated and non-HUS non-O157 STEC by extensive genome comparisons. Our results indicate that STECs from different phylogenetic backgrounds have independently acquired virulence genes that determine pathogenic potential, and that the content of such genes is overlapping between HUS-associated and non-HUS strains. Citation: Haugum K, Johansen J, Gabrielsen C, Brandal LT, Bergh K, et al. (2014) Comparative Genomics to Delineate Pathogenic Potential in Non-O157 Shiga Toxin-Producing Escherichia coli (STEC) from Patients with and without Haemolytic Uremic Syndrome (HUS) in Norway. PLoS ONE 9(10): e111788.
International Journal of Medical Microbiology, 2018
Since 2015, the Swiss Federal Office of Public Health registered an increase of notifications of STEC, probably due to the adoption of culture independent stx screening tests in diagnostic laboratories. This study aimed to identify the serotypes and virulence genes of 120 STEC isolated from human clinical stx positive specimens during 2017 in order to estimate any changes in serotype distribution and toxin profiles of STEC compared to the time span 2010-2014. Culturing of STEC from stool samples was achieved using the streak plate technique on MacConkey agar. We performed O and H serotyping by PCR and by micro array. Virulence genes were identified and subtyped using molecular methods, including stx1 and stx2 subtypes, and the intimin encoding gene, eae. STEC were recovered from 27.5% of the stx positive samples. STEC O157:H7 accounted for 7.5% of all isolates, and STEC O80:H2, O91:H10/H14/H21, O103:H2/H11, and O26:H11 accounted for 36.9% of the non-O157 strains. Forty-five isolates with stx1 variants, 47 with stx2 variants and 28 isolates with both stx1 and stx2 variants were identified. Forty (33.3% of all isolates) carried the subtypes associated with high pathogenic potential, stx2a, stx2c, or stx2d. The eae gene for intimin was detected in 54 strains (45% of all strains). Compared to 2010-2014, our data show that the proportion of the so called "top five" serogroups, STEC O26, O111, O103, and O157 declined from 53.7% to 28.3% in 2017. The proportion of isolates with stx2a, stx2c, or stx2d decreased from 50.5% to 33.3%. We also observed an increase of STEC harbouring the low pathogenic subtypes stx2b and stx2e from 12.6% to 29.2%, and of eae negative STEC from 29.5% in 2010-2014 to 55% in 2017. Simultaneously, there was a sharp increase of the patients' median age from 24 years to 46.5 years. Clinical manifestations in the patients included abdominal pain without diarrhea (22.3%), diarrhea (77.7%), and the haemolytic-uremic syndrome (HUS) (7.4%). Our data show that a greater number and a wider range of STEC serotypes are detected by culture-independent testing, with implications for public health services.
Eurosurveillance
The first documented British outbreak of Shiga toxin-producing Escherichia coli (STEC) O55:H7 began in the county of Dorset, England, in July 2014. Since then, there have been a total of 31 cases of which 13 presented with haemolytic uraemic syndrome (HUS). The outbreak strain had Shiga toxin (stx) subtype 2a associated with an elevated risk of HUS. This strain had not previously been isolated from humans or animals in England. The only epidemiological link was living in or having close links to two areas in Dorset. Extensive investigations included testing of animals and household pets. Control measures included extended screening, iterative interviewing and exclusion of cases and high risk contacts. Whole genome sequencing (WGS) confirmed that all the cases were infected with similar strains. A specific source could not be identified. The combination of epidemiological investigation and WGS indicated, however, that this outbreak was possibly caused by recurrent introductions from a local endemic zoonotic source, that a highly similar endemic reservoir appears to exist in the Republic of Ireland but has not been identified elsewhere, and that a subset of cases was associated with human-to-human transmission in a nursery.
Scientific Reports, 2019
Hybrid E. coli pathotypes are representing emerging public health threats with enhanced virulence from different pathotypes. Hybrids of Shiga toxin-producing and enterotoxigenic E. coli (steC/eteC) have been reported to be associated with diarrheal disease and hemolytic uremic syndrome (HUs) in humans. Here, we identified and characterized four clinical STEC/ETEC hybrids from diarrheal patients with or without fever or abdominal pain and healthy contact in Sweden. Rare stx2 subtypes were present in STEC/ETEC hybrids. Stx2 production was detectable in stx2a and stx2e containing strains. Different copies of ETEC virulence marker, sta gene, were found in two hybrids. Three sta subtypes, namely, sta1, sta4 and sta5 were designated, with sta4 being predominant. The hybrids represented diverse and rare serotypes (O15:H16, O187:H28, O100:H30, and O136:H12). Genome-wide phylogeny revealed that these hybrids exhibited close relatedness with certain ETEC, STEC/ETEC hybrid and commensal E. coli strains, implying the potential acquisition of Stx-phages or/and ETEC virulence genes in the emergence of STEC/ETEC hybrids. Given the emergence and public health significance of hybrid pathotypes, a broader range of virulence markers should be considered in the E. coli pathotypes diagnostics, and targeted follow up of cases is suggested to better understand the hybrid infection. Escherichia coli strains isolated from intestinal diseases have been grouped into at least six main pathotypes on the basis of epidemiological evidence, phenotypic traits, clinical features, and specific virulence factors 1. The well-described intestinal pathotypes of diarrheagenic E. coli (DEC) are Shiga toxin-producing E. coli (STEC), enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enteroaggregative E. coli (EAEC), enteroinvasive E. coli (EIEC), and diffusely adherent E. coli (DAEC). The virulence-associated genes that are unique to a pathotype have been used as molecular markers to define the pathotype of E. coli strains. STEC, defined by the production of phage-encoded Shiga toxins (Stxs), poses a significant public health concern as it can cause a wide spectrum of symptoms ranging from asymptomatic carriage to severe diarrhea, as well as bloody diarrhea and hemolytic uremic syndrome (HUS) 1. Stxs are classified into two major families, Stx1 and Stx2 (encoded by stx1 and stx2) on the basis of toxin neutralization assays and sequence analysis 2. The Stx1/Stx2
Frontiers in Cellular and Infection Microbiology, 2022
Shiga toxin-producing Escherichia coli (STEC) belonging to the O26 serogroup represent an important cause of Hemolitic Uremic Syndrome (HUS) in children worldwide. The localization of STEC virulence genes on mobile genetic elements allowed the emergence of clones showing different assets of this accessory genomic fraction. A novel O26 STEC clone belonging to Sequence Type (ST) 29 and harboring stx2a, ehxA and etpD plasmid-borne genes has emerged and spread in Europe since the mid-1990s, while another ST29 clone positive for stx2d and lacking plasmid-borne virulence genes was recently described as emerging in France. In Italy, O26 has been the most frequently detected STEC serogroup from HUS cases since the late 1990s. In this study we describe the genomic characterization and population structure of 144 O26 STEC strains isolated from human sources in Italy in the period 1989-2020. A total of 89 strains belonged to ST21, 52 to ST29, two to ST396 and one to ST4944. ST29 strains starte...
PLOS ONE, 2018
To generate hypotheses on possible sources of Shiga toxin-producing Escherichia coli (STEC) serogroup O80 associated hemolytic-uremic syndrome (HUS), we explored differences in factors associated with STEC O80 associated HUS, compared with STEC O157 or STEC of other serogroups, in France during 2013-16. STEC was isolated from 153/521 (30%) reported HUS cases: 45 serogroup O80, 46 O157 and 62 other serogroups. Median ages were 1.1 years, 4.0 years and 1.8 years, respectively. O80 infected patients were less likely to report ground beef consumption (aOR [adjusted Odds Ratio] 0.14 95% CI [Confidence Interval] 0.02-0.80) or previous contact with a person with diarrhea or HUS (aOR 0.13 95%CI 0.02-0.78) than patients infected with STEC O157. They were also less likely to report previous contact with a person presenting with diarrhea/HUS than patients infected with other serogroups (aOR 0.13 95%CI 0.02-0.78). STEC O80 spread all over France among young children less exposed to known risk factors of O157 or other STEC infections, suggesting the existence of different reservoirs and transmission patterns.
Journal of clinical microbiology, 2015
The ability of Escherichia coli O157:H7 to induce cellular damage leading to disease in humans is related to numerous virulence factors, most notably stx gene encoding Shiga toxin (Stx), carried by a bacteriophage. Loss of the Stx encoding bacteriophage may occur during infection or culturing of the strain. Here, we collected stx-positive and stx-negative variants of E. coli O157:H7/NM (non-motile) isolates from patients with gastrointestinal complaints. Isolates were characterized by whole genome sequencing (WGS) and their virulence properties and phylogenetic relationship were determined. Because of the presence of the eae gene but lack of the bfpA gene, the stx-negative isolates were considered as atypical enteropathogenic E. coli (aEPEC). However, they had similar phenotypic characteristics as the Shiga toxin producing E. coli (STEC) isolates and belonged to the same sequence type ST11. Furthermore, EPEC and STEC isolates shared similar virulence genes, the locus of enterocyte e...