scholarly journals Distribution of Pathogenicity Islands OI-122, OI-43/48, and OI-57 and a High-Pathogenicity Island in Shiga Toxin-Producing Escherichia coli

2013 ◽  
Vol 79 (11) ◽  
pp. 3406-3412 ◽  
Author(s):  
Wenting Ju ◽  
Jinling Shen ◽  
Magaly Toro ◽  
Shaohua Zhao ◽  
Jianghong Meng
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Phylogenetic Trees ◽  
Virulence Genes ◽  
Severe Disease ◽  
Strong Association ◽  
Pathogenicity Island ◽  
Pathogenicity Islands ◽  
Content Type ◽  
High Pathogenicity

ABSTRACTPathogenicity islands (PAIs) play an important role in Shiga toxin-producingEscherichia coli(STEC) pathogenicity. The distribution of PAIs OI-122, OI-43/48, and OI-57 and a high-pathogenicity island (HPI) were determined among 98 STEC strains assigned to seropathotypes (SPTs) A to E. PCR and PCR-restriction fragment length polymorphism assays were used to identify 14 virulence genes that belonged to the four PAIs and to subtypeeaeandstxgenes, respectively. Phylogenetic trees were constructed based on the sequences ofpagCamong 34 STEC strains andihaamong 67 diverse pathogenicE. coli, respectively. Statistical analysis demonstrated that the prevalences of OI-122 (55.82%) and OI-57 (82.35%) were significantly greater in SPTs (i.e., SPTs A, B, and C) that are frequently associated with severe disease than in other SPTs.terC(62.5%) andureC(62.5%) in OI-43/48 were also significantly more prevalent in SPTs A, B, and C than in SPTs D and E. In addition, OI-122, OI-57, and OI-43/48 and their associated virulence genes (exceptiha) were found to be primarily associated witheae-positive STEC, whereas HPI occurred independently of theeaepresence. The strong association of OI-122, OI-43/48, and OI-57 witheae-positive STEC suggests in part that different pathogenic mechanisms exist betweeneae-positive andeae-negative STEC strains. Virulence genes in PAIs that are associated with severe diseases can be used as potential markers to aid in identifying highly virulent STEC.

scholarly journals Molecular Profiling of Escherichia coli O157:H7 and Non-O157 Strains Isolated from Humans and Cattle in Alberta, Canada

2014 ◽  
Vol 53 (3) ◽  
pp. 986-990 ◽  
Author(s):  
Linda Chui ◽  
Vincent Li ◽  
Patrick Fach ◽  
Sabine Delannoy ◽  
Katarzyna Malejczyk ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Virulence Genes ◽  
Molecular Profiling ◽  
Surveillance Program ◽  
Escherichia Coli O157 ◽  
Significant Determinant ◽  
Content Type ◽  
Virulence Markers ◽  
Almost All

Virulence markers in Shiga toxin-producingEscherichia coli(STEC) and their association with diseases remain largely unknown. This study determines the importance of 44 genetic markers for STEC (O157 and non-O157) from human clinical cases and their correlation to disease outcome. STEC isolated from a cattle surveillance program were also included. The virulence genes tested were present in almost all O157:H7 isolates but highly variable in non-O157 STEC isolates. Patient age was a significant determinant of clinical outcome.

scholarly journals Association of Clustered Regularly Interspaced Short Palindromic Repeat (CRISPR) Elements with Specific Serotypes and Virulence Potential of Shiga Toxin-Producing Escherichia coli

2013 ◽  
Vol 80 (4) ◽  
pp. 1411-1420 ◽  
Author(s):  
Magaly Toro ◽  
Guojie Cao ◽  
Wenting Ju ◽  
Marc Allard ◽  
Rodolphe Barrangou ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Virulence Genes ◽  
Genetic Relatedness ◽  
Average Length ◽  
Content Type ◽  
Virulence Potential ◽  
Short Palindromic Repeat ◽  
K 12 ◽  
Potential Pathogenicity

ABSTRACTShiga toxin-producingEscherichia coli(STEC) strains (n= 194) representing 43 serotypes andE. coliK-12 were examined for clustered regularly interspaced short palindromic repeat (CRISPR) arrays to study genetic relatedness among STEC serotypes. A subset of the strains (n= 81) was further analyzed for subtype I-Ecasand virulence genes to determine a possible association of CRISPR elements with potential virulence. Four types of CRISPR arrays were identified. CRISPR1 and CRISPR2 were present in all strains tested; 1 strain also had both CRISPR3 and CRISPR4, whereas 193 strains displayed a short, combined array, CRISPR3-4. A total of 3,353 spacers were identified, representing 528 distinct spacers. The average length of a spacer was 32 bp. Approximately one-half of the spacers (54%) were unique and found mostly in strains of less common serotypes. Overall, CRISPR spacer contents correlated well with STEC serotypes, and identical arrays were shared between strains with the same H type (O26:H11, O103:H11, and O111:H11). There was no association identified between the presence of subtype I-Ecasand virulence genes, but the total number of spacers had a negative correlation with potential pathogenicity (P< 0.05). Fewer spacers were found in strains that had a greater probability of causing outbreaks and disease than in those with lower virulence potential (P< 0.05). The relationship between the CRISPR-cassystem and potential virulence needs to be determined on a broader scale, and the biological link will need to be established.

scholarly journals Diverse Virulence Gene Content of Shiga Toxin-Producing Escherichia coli from Finishing Swine

2014 ◽  
Vol 80 (20) ◽  
pp. 6395-6402 ◽  
Author(s):  
Marion Tseng ◽  
Pina M. Fratamico ◽  
Lori Bagi ◽  
Sabine Delannoy ◽  
Patrick Fach ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Virulence Genes ◽  
Genetic Relatedness ◽  
Virulence Gene ◽  
Health Concern ◽  
Limited Information ◽  
Content Type ◽  
Genes Encoding ◽  
Critical Public Health

ABSTRACTShiga toxin-producingEscherichia coli(STEC) infections are a critical public health concern because they can cause severe clinical outcomes, such as hemolytic uremic syndrome, in humans. Determining the presence or absence of virulence genes is essential in assessing the potential pathogenicity of STEC strains. Currently, there is limited information about the virulence genes carried by swine STEC strains; therefore, this study was conducted to examine the presence and absence of 69 virulence genes in STEC strains recovered previously from finishing swine in a longitudinal study. A subset of STEC strains was analyzed by pulsed-field gel electrophoresis (PFGE) to examine their genetic relatedness. Swine STEC strains (n= 150) were analyzed by the use of a high-throughput real-time PCR array system, which included 69 virulence gene targets. Three major pathotypes consisted of 16 different combinations of virulence gene profiles, and serotypes were determined in the swine STEC strains. The majority of the swine STEC strains (n= 120) belonged to serotype O59:H21 and carried the same virulence gene profile, which consisted of 9 virulence genes:stx2e,iha,ecs1763,lpfAO113,estIa(STa),ehaA,paa,terE, andureD. Theeae,nleF, andnleH1-2genes were detected in one swine STEC strain (O49:H21). Other genes encoding adhesins, includingiha, were identified (n= 149). The PFGE results demonstrated that swine STEC strains from pigs raised in the same finishing barn were closely related. Our results revealed diverse virulence gene contents among the members of the swine STEC population and enhance understanding of the dynamics of transmission of STEC strains among pigs housed in the same barn.

scholarly journals The emerging importance of Shiga toxin-producing Escherichia coli other than serogroup O157 in England

2021 ◽  
Vol 70 (7) ◽  
Author(s):  
Bhavita Vishram ◽  
Claire Jenkins ◽  
David R. Greig ◽  
Gauri Godbole ◽  
Kevin Carroll ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Severe Disease ◽  
Descriptive Analysis ◽  
Fold Increase ◽  
Surveillance Data ◽  
Bloody Diarrhoea ◽  
Content Type ◽  
Emerging Risk ◽  
Pcr Targeting

Introduction. Shiga toxin-producing Escherichia coli (STEC) can cause severe disease and large outbreaks. In England, the incidence and clinical significance of STEC serogroups other than O157 (non-O157) is unknown due to a testing bias for detection of STEC O157. Since 2013, the implementation of PCR to detect all STEC serogroups by an increasing number of diagnostic laboratories has led to an increase in the detection of non-O157 STEC. Hypothesis/Gap statement. Due to a bias in testing methodologies to select for STEC serogroup O157 in frontline diagnostic laboratories in most countries, very little surveillance data have been previously generated on non-O157 STEC. Aim. Five years (2014–2018) of STEC national surveillance data were extracted and descriptive analysis undertaken to assess disease severity of non-O157 STEC strains. Methods. Data from 1 January 2014 to 31 December 2018 were extracted from the National Enhanced Surveillance System for STEC and analysed. Results. The implementation of Gastrointestinal Polymerase Chain Reaction (GI-PCR) has resulted in a four-fold increase in the detection of non-O157 STEC cases between 2014 and 2018. There were 2579 cases infected with 97 different non-O157 serogroups. The gender distribution was similar amongst STEC O157 and non-O157 STEC cases with 57 and 56 % of cases being female respectively, but a significantly higher proportion of cases (P <0.001) under 5 years of age was observed among STEC O157 (22 %) cases compared to non-O157 STEC (14 %). The most common non-O157 serogroups were O26 (16 %), O146 (11 %), O91 (10 %), O128 (7 %), O103 (5 %) and O117 (3 %). Overall, rates of bloody diarrhoea were highest in O26 (44 %) and O103 (48 %) cases and lowest in STEC O117 cases (17 %). Strains harbouring Shiga toxin stx1a caused the highest proportion of diarrhoea (93 %) and caused the same level of bloody diarrhoea as stx2a (39 %). However, stx2a caused the highest proportion of vomiting (46 %), hospitalisation (49 %) and considerably more HUS (29 %) than other stx profiles. Conclusion. The implementation of PCR targeting stx at diagnostic laboratories has shown that non-O157 STEC, most notably STEC O26, are an emerging risk to public health.

scholarly journals The Gene tia, Harbored by the Subtilase-Encoding Pathogenicity Island, Is Involved in the Ability of Locus of Enterocyte Effacement-Negative Shiga Toxin-Producing Escherichia coli Strains To Invade Monolayers of Epithelial Cells

2017 ◽  
Vol 85 (12) ◽  
Author(s):  
Roslen Bondì ◽  
Paola Chiani ◽  
Valeria Michelacci ◽  
Fabio Minelli ◽  
Alfredo Caprioli ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Shiga Toxin ◽  
Cultured Cells ◽  
Pathogenicity Island ◽  
Content Type ◽  
Cell Monolayers ◽  
E Coli ◽  
Enterocyte Effacement ◽  
K 12

ABSTRACT Locus of enterocyte effacement (LEE)-negative Shiga toxin (Stx)-producing Escherichia coli (STEC) strains are human pathogens that lack the LEE locus, a pathogenicity island (PAI) involved in the intimate adhesion of LEE-positive strains to the host gut epithelium. The mechanism used by LEE-negative STEC strains to colonize the host intestinal mucosa is still not clear. The cell invasion determinant tia, previously described in enterotoxigenic E. coli strains, has been identified in LEE-negative STEC strains that possess the subtilase-encoding pathogenicity island (SE-PAI). We evaluated the role of the gene tia, present in these LEE-negative STEC strains, in the invasion of monolayers of cultured cells. We observed that these strains were able to invade Caco-2 and HEp-2 cell monolayers and compared their invasion ability with that of a mutant strain in which the gene tia had been inactivated. Mutation of the gene tia resulted in a strong reduction of the invasive phenotype, and complementation of the tia mutation with a functional copy of the gene restored the invasion activity. Moreover, we show that the gene tia is overexpressed in bacteria actively invading cell monolayers, demonstrating that tia is involved in the ability to invade cultured monolayers of epithelial cells shown by SE-PAI-positive E. coli, including STEC, strains. However, the expression of the tia gene in the E. coli K-12 strain JM109 was not sufficient, in its own right, to confer to this strain the ability to invade cell monolayers, suggesting that at least another factor must be involved in the invasion ability displayed by the SE-PAI-positive strains.

scholarly journals Virulence Genes in Expanded-Spectrum-Cephalosporin-Resistant and -Susceptible Escherichia coli Isolates from Treated and Untreated Chickens

2015 ◽  
Vol 60 (3) ◽  
pp. 1874-1877 ◽  
Author(s):  
S. Baron ◽  
S. Delannoy ◽  
S. Bougeard ◽  
E. Larvor ◽  
E. Jouy ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Antimicrobial Resistance ◽  
Virulence Factors ◽  
Shiga Toxin ◽  
Virulence Genes ◽  
Phylogenetic Groups ◽  
Content Type ◽  
E Coli ◽  
Heat Stable ◽  
Intestinal Infections

This study investigated antimicrobial resistance, screened for the presence of virulence genes involved in intestinal infections, and determined phylogenetic groups ofEscherichia coliisolates from untreated poultry and poultry treated with ceftiofur, an expanded-spectrum cephalosporin. Results show that none of the 76 isolates appeared to be Shiga toxin-producingE. colior enteropathogenicE. coli. All isolates were negative for the major virulence factors/toxins tested (ehxA,cdt, heat-stable enterotoxin [ST], and heat-labile enterotoxin [LT]). The few virulence genes harbored in isolates generally did not correlate with isolate antimicrobial resistance or treatment status. However, some of the virulence genes were significantly associated with certain phylogenetic groups.

scholarly journals Molecular Profiling of Shiga Toxin-Producing Escherichia coli and Enteropathogenic E. coli Strains Isolated from French Coastal Environments

2016 ◽  
Vol 82 (13) ◽  
pp. 3913-3927 ◽  
Author(s):  
C. Balière ◽  
A. Rincé ◽  
S. Delannoy ◽  
P. Fach ◽  
M. Gourmelon
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Virulence Gene ◽  
Coastal Environment ◽  
Pathogenicity Islands ◽  
Content Type ◽  
E Coli ◽  
Gene Profiles ◽  
Genes Encoding ◽  
High Level

ABSTRACTShiga toxin-producingEscherichia coli(STEC) and enteropathogenicE. coli(EPEC) strains may be responsible for food-borne infections in humans. Twenty-eight STEC and 75 EPEC strains previously isolated from French shellfish-harvesting areas and their watersheds and belonging to 68 distinguishable serotypes were characterized in this study. High-throughput real-time PCR was used to search for the presence of 75E. colivirulence-associated gene targets, and genes encoding Shiga toxin (stx) and intimin (eae) were subtyped using PCR tests and DNA sequencing, respectively. The results showed a high level of diversity between strains, with 17 unique virulence gene profiles for STEC and 56 for EPEC. Seven STEC and 15 EPEC strains were found to display a large number or a particular combination of genetic markers of virulence and the presence ofstxand/oreaevariants, suggesting their potential pathogenicity for humans. Among these, an O26:H11stx1aeae-β1 strain was associated with a large number of virulence-associated genes (n= 47), including genes carried on the locus of enterocyte effacement (LEE) or other pathogenicity islands, such as OI-122, OI-71, OI-43/48, OI-50, OI-57, and the high-pathogenicity island (HPI). One O91:H21 STEC strain containing 4stxvariants (stx1a,stx2a,stx2c, andstx2d) was found to possess genes associated with pathogenicity islands OI-122, OI-43/48, and OI-15. Among EPEC strains harboring a large number of virulence genes (n, 34 to 50), eight belonged to serotype O26:H11, O103:H2, O103:H25, O145:H28, O157:H7, or O153:H2.IMPORTANCEThe speciesE. coliincludes a wide variety of strains, some of which may be responsible for severe infections. This study, a molecular risk assessment study ofE. colistrains isolated from the coastal environment, was conducted to evaluate the potential risk for shellfish consumers. This report describes the characterization of virulence gene profiles andstx/eaepolymorphisms ofE. coliisolates and clearly highlights the finding that the majority of strains isolated from coastal environment are potentially weakly pathogenic, while some are likely to be more pathogenic.

scholarly journals Improving Detection of Shiga Toxin-Producing Escherichia coli by Molecular Methods by Reducing the Interference of Free Shiga Toxin-Encoding Bacteriophages

2014 ◽  
Vol 81 (1) ◽  
pp. 415-421 ◽  
Author(s):  
Pablo Quirós ◽  
Alexandre Martínez-Castillo ◽  
Maite Muniesa
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Virulence Genes ◽  
Molecular Methods ◽  
Culture Methods ◽  
Content Type ◽  
Low Protein ◽  
Phage Dna ◽  
Stool Samples ◽  
Efficiency And Reliability

ABSTRACTDetection of Shiga toxin-producingEscherichia coli(STEC) by culture methods is advisable to identify the pathogen, but recovery of the strain responsible for the disease is not always possible. The use of DNA-based methods (PCR, quantitative PCR [qPCR], or genomics) targeting virulence genes offers fast and robust alternatives. However, detection ofstxis not always indicative of STEC becausestxcan be located in the genome of temperate phages found in the samples as free particles; this could explain the numerous reports of positivestxdetection without successful STEC isolation. An approach based on filtration through low-protein-binding membranes and additional washing steps was applied to reduce free Stx phages without reducing detection of STEC bacteria. River water, food, and stool samples were spiked with suspensions of phage 933W and, as a STEC surrogate, a lysogen harboring a recombinant Stx phage in whichstxwas replaced bygfp. Bacteria were tested either by culture or by qPCR forgfpwhile phages were tested using qPCR targetingstxin phage DNA. The procedure reduces phage particles by 3.3 log10units without affecting the recovery of the STEC population (culturable or assessed by qPCR). The method is applicable regardless of phage and bacteria densities and is useful in different matrices (liquid or solid). This approach eliminates or considerably reduces the interference of Stx phages in the detection of STEC by molecular methods. The reduction of possible interference would increase the efficiency and reliability of genomics for STEC detection when the method is applied routinely in diagnosis and food analysis.

scholarly journals A Genomic Island, Termed High-Pathogenicity Island, Is Present in Certain Non-O157 Shiga Toxin-Producing Escherichia coli Clonal Lineages

1999 ◽  
Vol 67 (11) ◽  
pp. 5994-6001 ◽  
Author(s):  
H. Karch ◽  
S. Schubert ◽  
D. Zhang ◽  
W. Zhang ◽  
H. Schmidt ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Wide Spectrum ◽  
Pathogenicity Island ◽  
Immunoblot Analysis ◽  
Ecological Niches ◽  
Pathogenic Potential ◽  
Integrase Gene ◽  
E Coli ◽  
High Pathogenicity

ABSTRACT Shiga toxin-producing Escherichia coli (STEC) strains cause a wide spectrum of diseases in humans. In this study, we tested 206 STEC strains isolated from patients for potential virulence genes including stx, eae, and enterohemorrhagicE. coli hly. In addition, all strains were examined for the presence of another genetic element, the high-pathogenicity island (HPI). The HPI was first described in pathogenic Yersiniaspecies and encodes the pesticin receptor FyuA and the siderophore yersiniabactin. The HPI was found in the genome of distinct clonal lineages of STEC, including all 31 eae-positive O26:H11/H− strains and 7 of 12 eae-negative O128:H2/H− strains. In total, the HPI was found in 56 (27.2%) of 206 STEC strains. However, it was absent from the genome of all 37 O157:H7/H−, 14 O111:H−, 13 O103:H2, and 13 O145:H− STEC isolates, all of which were positive for eae. Polypeptides encoded by the fyuA gene located on the HPI could be detected by using immunoblot analysis in most of the HPI-positive STEC strains, suggesting the presence of a functional yersiniabactin system. The HPI in STEC was located next to the tRNA gene asnT. In contrast to the HPI of other pathogenic enterobacteria, the HPI of O26 STEC strains shows a deletion at its left junction, leading to a truncated integrase geneint. We conclude from this study that theYersinia HPI is disseminated among certain clonal subgroups of STEC strains. The hypothesis that the HPI in STEC contributes to the fitness of the strains in certain ecological niches rather than to their pathogenic potential is discussed.

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