Enteropathogenic Escherichia coli O157 strains from Brazil.
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SUBMITTER: Blank TE
PROVIDER: S-EPMC2873750 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The number of diarrhea cases caused by atypical enteropathogenic Escherichia coli (aEPEC) has been increasing worldwide. Here, we report the draft whole-genome sequences of 10 aEPEC strains isolated in Brazil. These sequences will provide an important source for future studies concerning aEPEC pathogenicity and genetic markers of potentially virulent strains.
| S-EPMC6284090 | biostudies-literature
Project description: Not available
| S-EPMC130765 | biostudies-literature
Project description:BackgroundAtypical enteropathogenic Escherichia coli (aEPEC) are one of the most frequent intestinal E. coli pathotypes isolated from diarrheal patients in Brazil. Isolates of aEPEC contain the locus of enterocyte effacement, but lack the genes of the bundle-forming pilus of typical EPEC, and the Shiga toxin of enterohemorrhagic E. coli (EHEC). The objective of this study was to evaluate the phylogeny and the gene content of Brazilian aEPEC genomes compared to a global aEPEC collection.MethodologySingle nucleotide polymorphism (SNP)-based phylogenomic analysis was used to compare 106 sequenced Brazilian aEPEC with 221 aEPEC obtained from other geographic origins. Additionally, Large-Scale BLAST Score Ratio was used to determine the shared versus unique gene content of the aEPEC studied.Principal findingsPhylogenomic analysis demonstrated the 106 Brazilian aEPEC were present in phylogroups B1 (47.2%, 50/106), B2 (23.6%, 25/106), A (22.6%, 24/106), and E (6.6%, 7/106). Identification of EPEC and EHEC phylogenomic lineages demonstrated that 42.5% (45/106) of the Brazilian aEPEC were in four of the previously defined lineages: EPEC10 (17.9%, 19/106), EPEC9 (10.4%, 11/106), EHEC2 (7.5%, 8/106) and EPEC7 (6.6%, 7/106). Interestingly, an additional 28.3% (30/106) of the Brazilian aEPEC were identified in five novel lineages: EPEC11 (14.2%, 15/106), EPEC12 (4.7%, 5/106), EPEC13 (1.9%, 2/106), EPEC14 (5.7%, 6/106) and EPEC15 (1.9%, 2/106). We identified 246 genes that were more frequent among the aEPEC isolates from Brazil compared to the global aEPEC collection, including espG2, espT and espC (P<0.001). Moreover, the nleF gene was more frequently identified among Brazilian aEPEC isolates obtained from diarrheagenic patients when compared to healthy subjects (69.7% vs 41.2%, P<0.05).ConclusionThe current study demonstrates significant genomic diversity among aEPEC from Brazil, with the identification of Brazilian aEPEC isolates to five novel EPEC lineages. The greater prevalence of some virulence genes among Brazilian aEPEC genomes could be important to the specific virulence strategies used by aEPEC in Brazil to cause diarrheal disease.
| S-EPMC7289442 | biostudies-literature
Project description:Epithelial cell migration is an essential response to enteric pathogens such as enteropathogenic Escherichia coli (EPEC). This study aimed to investigate the effects of EPEC infection on intestinal epithelial cell migration in vitro, as well as the involvement of type III secretion system (T3SS) and Rho GTPases. Crypt intestinal epithelial cells (IEC-6) were infected with EPEC strains (E2348/69, ΔescF, and the LDI001 strain isolated from a malnourished Brazilian child) and commensal E. coli HS. Wound migration and cell death assays were performed at different time-points. Transcription and expression of Rho GTPases were evaluated using real-time PCR and western blotting. Overall, EPEC E2348/69 reduced migration and increased apoptosis and necrosis levels compared to EPEC LDI001 and E. coli HS strains. Moreover, EPEC LDI001 impaired cell migration at a higher level than E. coli HS and increased necrosis after 24 hours compared to the control group. The different profiles of virulence genes between the two wild-type EPEC strains, characterized by the absence of espL and nleE genes in the LDI001, might explain the phenotypic results, playing significant roles on cell migration impairment and cell death-related events. Moreover, the type III secretion system is determinant for the inhibition of intestinal epithelial cell migration by EPEC 2348/69, as its deletion prevented the effect. Active Rac1 concentrations were increased in E2348/69 and LDI001-infected cells, while the T3SS-deficient strain did not demonstrate this activation. This study contributes with valuable insight to characterize the mechanisms involved in the impairment of intestinal cell migration induced by EPEC.
| S-EPMC6065879 | biostudies-literature
Project description:In August 2016, an outbreak of Shiga toxin-producing Escherichia coli (STEC) and enteropathogenic E. coli (EPEC) with 237 cases occurred in the Helsinki metropolitan area, Finland. Gastroenteritis cases were reported at 11 events served by one catering company. Microbiological and epidemiological investigations suggested rocket salad as the cause of the outbreak. STEC ONT:H11 and EPEC O111:H8 strains isolated from food samples containing rocket were identical to the patient isolates. In this outbreak, the reported symptoms were milder than considered before for STEC infection, and the guidelines for STEC control measures need to be updated based on the severity of the illness. Based on our experience in this outbreak, national surveillance criteria for STEC have been updated to meet the practice in reporting laboratories covering both PCR-positive and culture-confirmed findings. We suggest that EPEC could be added to the national surveillance since diagnostics for EPEC are routinely done in clinical laboratories.
| S-EPMC6124187 | biostudies-literature
Project description:Escherichia coli O157:H7, a food-borne pathogen, causes hemorrhagic colitis and the hemolytic-uremic syndrome. A putative virulence factor of E. coli O157:H7 is a 60-MDa plasmid (pO157) found in 99% of all clinical isolates and many bovine-derived strains. The well characterized E. coli O157:H7 Sakai strain (Sakai) and its pO157-cured derivative (Sakai-Cu) were compared for phenotypic differences. Sakai-Cu had enhanced survival in synthetic gastric fluid, did not colonize cattle as well as wild-type Sakai, and had unchanged growth rates and tolerance to salt and heat. These results are consistent with our previous findings with another E. coli O157:H7 disease outbreak isolate ATCC 43894 and its pO157-cured (43894-Cu). However, despite the essentially sequence identical pO157 in these strains, Sakai-Cu had changes in antibiotic susceptibility and motility that did not occur in the 43894-Cu strain. This unexpected result was systematically analyzed using phenotypic microarrays testing 1,920 conditions with Sakai, 43894, and the plasmid-cured mutants. The influence of the pO157 differed between strains on a wide number of growth/survival conditions. Relative expression of genes related to acid resistance (gadA, gadX, and rpoS) and flagella production (fliC and flhD) were tested using quantitative real-time PCR and gadA and rpoS expression differed between Sakai-Cu and 43894-Cu. The strain-specific differences in phenotype that resulted from the loss of essentially DNA-sequence identical pO157 were likely due to the chromosomal genetic diversity between strains. The O157:H7 serotype diversity was further highlighted by phenotypic microarray comparisons of the two outbreak strains with a genotype 6 bovine E. coli O157:H7 isolate, rarely associated with human disease.
| S-EPMC2951829 | biostudies-literature
Project description:Alongside the well-characterized enterohemorrhagic Escherichia coli (EHEC) O157:H7, serogroup O157 comprises sorbitol-fermenting typical and atypical enteropathogenic E. coli (EPEC/aEPEC) strains that carry the intimin-encoding gene eae but not Shiga toxin-encoding genes (stx). Since little is known about these pathogens, we characterized 30 clinical isolates from patients with hemolytic uremic syndrome (HUS) or uncomplicated diarrhea with respect to their flagellin gene (fliC) type and multilocus sequence type (MLST). Moreover, we applied whole-genome sequencing (WGS) to determine the phylogenetic relationship with other eae-positive EHEC serotypes and the composition of the rfbO157 region. fliC typing resulted in five fliC types (H7, H16, H34, H39, and H45). Isolates of each fliC type shared a unique ST. In comparison to the 42 HUS-associated E. coli (HUSEC) strains, only the stx-negative isolates with fliCH7 shared their ST with EHEC O157:H7/H(-) strains. With the exception of one O157:H(-) fliCH16 isolate, HUS was exclusively associated with fliCH7. WGS corroborated the separation of the fliCH7 isolates, which were closely related to the EHEC O157:H7/H(-) isolates, and the diverse group of isolates exhibiting different fliC types, indicating independent evolution of the different serotypes. This was also supported by the heterogeneity within the rfbO157 region that exhibited extensive recombinations. The genotypic subtypes and distribution of clinical symptoms suggested that the stx-negative O157 strains with fliCH7 were originally EHEC strains that lost stx The remaining isolates form a distinct and diverse group of atypical EPEC isolates that do not possess the full spectrum of virulence genes, underlining the importance of identifying the H antigen for clinical risk assessment.
| S-EPMC4844722 | biostudies-literature
Project description:The ability of Escherichia coli O157:H7 to induce cellular damage leading to disease in humans is related to numerous virulence factors, most notably the stx gene, encoding Shiga toxin (Stx) and 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 (nonmotile) 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 atypical enteropathogenic E. coli (aEPEC). However, they had phenotypic characteristics similar to those of 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 effacement region, and plasmids. Core genome phylogenetic analysis using a gene-by-gene typing approach showed that the sorbitol-fermenting (SF) stx-negative isolates clustered together with an SF STEC isolate and that one non-sorbitol-fermenting (NSF) stx-negative isolate clustered together with NSF STEC isolates. Therefore, these stx-negative isolates were thought either to have lost the Stx phage or to be a progenitor of STEC O157:H7/NM. As detection of STEC infections is often based solely on the identification of the presence of stx genes, these may be misdiagnosed in routine laboratories. Therefore, an improved diagnostic approach is required to manage identification, strategies for treatment, and prevention of transmission of these potentially pathogenic strains.
| S-EPMC4609726 | biostudies-literature
Project description:The virulence plasmid of Escherichia coli O157 strain EDL933 carries a 10-kb putative virulence gene designated toxB. Little is known about the distribution of this gene among E. coli O157 strains or its presence in other enterohemorrhagic E. coli (EHEC) and enteropathogenic E. coli (EPEC) strains. We developed PCR and hybridization tools for the detection of the entire toxB sequence and investigated its presence in a collection of EHEC O157 strains and other EHEC and EPEC strains belonging to different serogroups and isolated from different sources. The EHEC O157 strains reacted with all of the PCR primers and probes used, thus indicating the presence of a complete toxB gene regardless of the human or bovine origin of the isolates. Similar positive reactions were observed for about 50% of the EHEC O26 strains tested and a few other EHEC and EPEC strains. However, the size of the DNA fragments hybridizing with the toxB probes differed from that of the positive fragments from EHEC O157, suggesting a polymorphism in the toxB genes present in the different E. coli serogroups. Moreover, several EHEC and EPEC strains belonging to different serogroups reacted with only some of the genetic tools used, suggesting either the existence of major variants of toxB or the presence of fragments of the gene. Southern blotting analysis showed that toxB sequences were located on large plasmids in EHEC and EPEC O26 as well.
| S-EPMC1233992 | biostudies-literature
Project description:BackgroundWe recently observed an association of resistance with a certain enteropathogenic Escherichia coli (EPEC) serotypes and identified a conjugative plasmid, similar to plasmid pED208, that was conserved among archival O111:H2/NM and O119:H2 strains of diverse geographical origin. In this study, we sought to determine the prevalence and distribution of this plasmid among a collection of EPEC isolates from Brazil, as well as to study the susceptibilities of these isolates to antimicrobial agents.ResultsResistance was more commonly seen in typical EPEC than atypical strains. The most prevalent resistances were to ampicillin, tetracycline, streptomycin and the sulfonamides. Markers for the EPEC conjugative multiresistance plasmid, were detected in 21 (30%) of typical but only 4 (5%) of atypical strains (p = 0.001, Chi-squared test). This plasmid, previously reported from only O111 and O119 strains was found in O55 and O127 strains and was associated with the presence of class 1 integrons.ConclusionOur data suggest a limited but expanding host range for the EPEC resistance plasmid.
| S-EPMC2828443 | biostudies-literature