Food as a Vehicle for Transmission of Shiga Toxin–Producing Escherichia coli

2007 ◽  
Vol 70 (10) ◽  
pp. 2426-2449 ◽  
Author(s):  
MARILYN C. ERICKSON ◽  
MICHAEL P. DOYLE
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Cetylpyridinium Chloride ◽  
The United States ◽  
Influential Factors ◽  
Sodium Chlorite ◽  
Processing Plant ◽  
E Coli ◽  
Wide Range ◽  
Alfalfa Sprouts

Contaminated food continues to be the principal vehicle for transmission of Escherichia coli O157:H7 and other Shiga toxin–producing E. coli (STEC) to humans. A large number of foods, including those associated with outbreaks (alfalfa sprouts, fresh produce, beef, and unpasteurized juices), have been the focus of intensive research studies in the past few years (2003 to 2006) to assess the prevalence and identify effective intervention and inactivation treatments for these pathogens. Recent analyses of retail foods in the United States revealed E. coli O157:H7 was present in 1.5% of alfalfa sprouts and 0.17% of ground beef but not in some other foods examined. Differences in virulence patterns (presence of both stx1 and stx2 genes versus one stx gene) have been observed among isolates from beef samples obtained at the processing plant compared with retail outlets. Research has continued to examine survival and growth of STEC in foods, with several models being developed to predict the behavior of the pathogen under a wide range of environmental conditions. In an effort to develop effective strategies to minimize contamination, several influential factors are being addressed, including elucidating the underlying mechanism for attachment and penetration of STEC into foods and determining the role of handling practices and processing operations on cross-contamination between foods. Reports of some alternative nonthermal processing treatments (high pressure, pulsed-electric field, ionizing radiation, UV radiation, and ultrasound) indicate potential for inactivating STEC with minimal alteration to sensory and nutrient characteristics. Antimicrobials (e.g., organic acids, oxidizing agents, cetylpyridinium chloride, bacteriocins, acidified sodium chlorite, natural extracts) have varying degrees of efficacy as preservatives or sanitizing agents on produce, meat, and unpasteurized juices. Multiple-hurdle or sequential intervention treatments have the greatest potential to minimize transmission of STEC in foods.

scholarly journals A Toxic Environment: a Growing Understanding of How Microbial Communities Affect Escherichia coli O157:H7 Shiga Toxin Expression

2020 ◽  
Vol 86 (24) ◽  
Author(s):  
Erin M. Nawrocki ◽  
Hillary M. Mosso ◽  
Edward G. Dudley
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Microbial Interactions ◽  
Severe Illness ◽  
Content Type ◽  
E Coli ◽  
Wide Range ◽  
Lambdoid Prophage

ABSTRACT Enterohemorrhagic Escherichia coli (EHEC) strains, including E. coli O157:H7, cause severe illness in humans due to the production of Shiga toxin (Stx) and other virulence factors. Because Stx is coregulated with lambdoid prophage induction, its expression is especially susceptible to environmental cues. Infections with Stx-producing E. coli can be difficult to model due to the wide range of disease outcomes: some infections are relatively mild, while others have serious complications. Probiotic organisms, members of the gut microbiome, and organic acids can depress Stx production, in many cases by inhibiting the growth of EHEC strains. On the other hand, the factors currently known to amplify Stx act via their effect on the stx-converting phage. Here, we characterize two interactive mechanisms that increase Stx production by O157:H7 strains: first, direct interactions with phage-susceptible E. coli, and second, indirect amplification by secreted factors. Infection of susceptible strains by the stx-converting phage can expand the Stx-producing population in a human or animal host, and phage infection has been shown to modulate virulence in vitro and in vivo. Acellular factors, particularly colicins and microcins, can kill O157:H7 cells but may also trigger Stx expression in the process. Colicins, microcins, and other bacteriocins have diverse cellular targets, and many such molecules remain uncharacterized. The identification of additional Stx-amplifying microbial interactions will improve our understanding of E. coli O157:H7 infections and help elucidate the intricate regulation of pathogenicity in EHEC strains.

How Does Escherichia coli O157:H7 Testing in Meat Compare with What We Are Seeing Clinically?

2000 ◽  
Vol 63 (6) ◽  
pp. 819-821 ◽  
Author(s):  
DAVID W. K. ACHESON
Keyword(s):  
United States ◽  
Escherichia Coli ◽  
Shiga Toxin ◽  
Food Supply ◽  
The United States ◽  
Escherichia Coli O157 ◽  
Current Policy ◽  
E Coli ◽  
Different Types ◽  
Uremic Syndrome

Escherichia coli O157:H7 is but one of a group of Shiga toxin-producing E. coli (STEC) that cause both intestinal disease such as bloody and nonbloody diarrhea and serious complications like hemolytic uremic syndrome (HUS). While E. coli O157: H7 is the most renowned STEC, over 200 different types of STEC have been documented in meat and animals, at least 60 of which have been linked with human disease. A number of studies have suggested that non-O157 STEC are associated with clinical disease, and non-O157 STEC are present in the food supply. Non-O157 STEC, such as O111 have caused large outbreaks and HUS in the United States and other countries. The current policy in the United States is to examine ground beef for O157:H7 only, but restricting the focus to O157 will miss other important human STEC pathogens.

scholarly journals Molecular Characterization of Shiga Toxin-Producing Escherichia coli Strains Isolated in Poland

2016 ◽  
Vol 65 (3) ◽  
pp. 261-269 ◽  
Author(s):  
Aleksandra Januszkiewicz ◽  
Waldemar Rastawicki
Keyword(s):  
Escherichia Coli ◽  
Virulence Factors ◽  
Shiga Toxin ◽  
Virulence Gene ◽  
Virulence Determinants ◽  
E Coli ◽  
Heat Stable ◽  
Food Borne ◽  
Wide Range ◽  
Uremic Syndrome

Shiga toxin-producing Escherichia coli (STEC) strains also called verotoxin-producing E. coli (VTEC) represent one of the most important groups of food-borne pathogens that can cause several human diseases such as hemorrhagic colitis (HC) and hemolytic – uremic syndrome (HUS) worldwide. The ability of STEC strains to cause disease is associated with the presence of wide range of identified and putative virulence factors including those encoding Shiga toxin. In this study, we examined the distribution of various virulence determinants among STEC strains isolated in Poland from different sources. A total of 71 Shiga toxin-producing E. coli strains isolated from human, cattle and food over the years 1996 – 2010 were characterized by microarray and PCR detection of virulence genes. As stx1a subtype was present in all of the tested Shiga toxin 1 producing E. coli strains, a greater diversity of subtypes was found in the gene stx2, which occurred in five subtypes: stx2a, stx2b, stx2c, stx2d, stx2g. Among STEC O157 strains we observed conserved core set of 14 virulence factors, stable in bacteria genome at long intervals of time. There was one cattle STEC isolate which possessed verotoxin gene as well as sta1 gene encoded heat-stable enterotoxin STIa characteristic for enterotoxigenic E. coli. To the best of our knowledge, this is the first comprehensive analysis of virulence gene profiles identified in STEC strains isolated from human, cattle and food in Poland. The results obtained using microarrays technology confirmed high effectiveness of this method in determining STEC virulotypes which provides data suitable for molecular risk assessment of the potential virulence of this bacteria.

Verotoxigenic Escherichia coli Infection: U.S. Overview†

1997 ◽  
Vol 60 (11) ◽  
pp. 1466-1471 ◽  
Author(s):  
PHILLIP I. TARR ◽  
THOMAS E. BESSER ◽  
DALE D. HANCOCK ◽  
WILLIAM E. KEENE ◽  
MARCIA GOLDOFT
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Public Health Problem ◽  
The United States ◽  
Human Populations ◽  
Molecular Fingerprinting ◽  
Dna Encoding ◽  
E Coli ◽  
Escherichia Coli Infection ◽  
Toxigenic Strains

Escherichia coli O157:H7 remains a public health problem in the United States despite a dramatic increase in the awareness of, and concern about, foodborne infections since the 1993 multistate E. coli O157:H7 epidemic. Although surveillance data can be difficult to interpret, the incidence of endemic disease caused by this organism is probably not increasing, and might be decreasing, at least in selected populations. With increased recognition of E. coli O157:H7 infection has come the investigation of increasing number of outbreaks, leading to the recognition of many “new” vehicles, including some foods not traditionally associated with enteric infections, such as dry-cured salami and lettuce. Molecular fingerprinting techniques are being used to track the transmission of E. coli O157:H7 through human populations. Analysis of DNA encoding virulence factors and surface antigens suggests that diarrheagenic E. coli have evolved by acquiring large DNA fragments, with subsequent chromosomal recombination. Some Shiga toxin–producing E. coli other than E. coli O157:H7 are no doubt pathogens, but the majority of these toxigenic strains found in food are probably not virulent. More research is needed to define the characteristics that render selected Shiga toxin–producing organisms harmful to humans.

Desiccation and Thermal Resistance of Escherichia coli O121 in Wheat Flour

2019 ◽  
Vol 82 (8) ◽  
pp. 1308-1313 ◽  
Author(s):  
QUINCY J. SUEHR ◽  
NATHAN M. ANDERSON ◽  
SUSANNE E. KELLER
Keyword(s):  
Escherichia Coli ◽  
Thermal Resistance ◽  
Wheat Flour ◽  
Shiga Toxin ◽  
Salmonella Enteritidis ◽  
Thermal Inactivation ◽  
The United States ◽  
Inactivation Kinetics ◽  
E Coli ◽  
D Values

ABSTRACT Non-O157 Shiga toxin–producing Escherichia coli infections have recently been associated with wheat flour on two separate accounts in the United States and Canada. However, there is little information regarding the thermal resistance and longevity of non-O157 Shiga toxin–producing Escherichia coli during storage in low-moisture environments. The objectives of this study were to determine the thermal inactivation kinetics of E. coli O121 in wheat flour and to compare the thermal inactivation rates with those of other pathogens. Wheat flour, inoculated with E. coli O121, was equilibrated at 25°C to a water activity of 0.45 in a humidity-controlled conditioning chamber. Inoculated samples were treated isothermally at 70, 75, and 80°C, and posttreatment population survivor ratios were determined by plate counting. D- and z-values calculated with a log-linear model, were compared with those obtained in other studies. At 70, 75, and 80°C, the D-values for E. coli O121 were 18.16 ± 0.96, 6.47 ± 0.50, and 4.58 ± 0.40 min, respectively, and the z-value was 14.57 ± 2.21°C. Overall, E. coli O121 was observed to be slightly less thermally resistant than what has been previously reported for Salmonella Enteritidis PT30 in wheat flour as measured under the same conditions with the same methods.

Behavior of Non-O157 Shiga Toxin–Producing Escherichia coli, Enteroinvasive E. coli, Enteropathogenic E. coli, and Enterotoxigenic E. coli Strains on Alfalfa Sprouts

2013 ◽  
Vol 76 (8) ◽  
pp. 1429-1433 ◽  
Author(s):  
CARLOS A. GÓMEZ-ALDAPA ◽  
ESMERALDA RANGEL-VARGAS ◽  
M. del REFUGIO TORRES-VITELA ◽  
ANGÉLICA VILLARRUEL-LÓPEZ ◽  
JAVIER CASTRO-ROSAS
Keyword(s):  
Escherichia Coli ◽  
Seed Germination ◽  
Shiga Toxin ◽  
Practical Significance ◽  
E Coli ◽  
Alfalfa Sprouts ◽  
Alfalfa Seeds

Data about the behavior of non-O157 Shiga toxin–producing Escherichia coli (non-O157 STEC), enteroinvasive E. coli (EIEC), enterotoxigenic E. coli (ETEC), and enteropathogenic E. coli (EPEC) on seeds and alfalfa sprouts are not available. The behavior of STEC, EIEC, ETEC, and EPEC was determined during germination and sprouting of alfalfa seeds at 20 ± 2°C and 30 ± 2°C and on alfalfa sprouts at 3 ± 2°C. When alfalfa seeds were inoculated with STEC, EIEC, ETEC, or EPEC strains, all these diarrheagenic E. coli pathotypes (DEPs) grew during germination and sprouting of seeds, reaching counts of approximately 5 and 6 log CFU/g after 1 day at 20 ± 2°C and 30 ± 2°C, respectively. However, when the sprouts were inoculated after 1 day of seed germination and stored at 20 ± 2°Cor30 ± 2°C, no growth was observed for any DEP during sprouting at 20 ± 2°Cor 30 ± 2°C for 9 days. Refrigeration reduced significantly (P < 0.0.5) the number of viable DEPs on sprouts after 20 days in storage; nevertheless, these decreases have no practical significance for the safety of the sprouts.

scholarly journals Differential Binding of Escherichia coli O157:H7 to Alfalfa, Human Epithelial Cells, and Plastic Is Mediated by a Variety of Surface Structures

2005 ◽  
Vol 71 (12) ◽  
pp. 8008-8015 ◽  
Author(s):  
Alfredo G. Torres ◽  
Cecelia Jeter ◽  
William Langley ◽  
Ann G. Matthysse
Keyword(s):  
Escherichia Coli ◽  
Biofilm Formation ◽  
Food Poisoning ◽  
The United States ◽  
Surface Proteins ◽  
E Coli ◽  
Alfalfa Sprouts ◽  
K 12 ◽  
Plant Surfaces

ABSTRACT Escherichia coli O157:H7 carried on plant surfaces, including alfalfa sprouts, has been implicated in food poisoning and outbreaks of disease in the United States. Adhesion to cell surfaces is a key component for bacterial establishment and colonization on many types of surfaces. Several E. coli O157:H7 surface proteins are thought to be important for adhesion and/or biofilm formation. Therefore, we examined whether mutations in several genes encoding potential adhesins and regulators of adherence have an effect on bacterial binding to plants and also examined the role of these genes during adhesion to Caco-2 cells and during biofilm formation on plastic in vitro. The genes tested included those encoding adhesins (cah, aidA1, and ompA) and mediators of hyperadherence (tdcA, yidE, waaI, and cadA) and those associated with fimbria formation (csgA, csgD, and lpfD2). The introduction of some of these genes (cah, aidA1, and csg loci) into an E. coli K-12 strain markedly increased its ability to bind to alfalfa sprouts and seed coats. The addition of more than one of these genes did not show an additive effect. In contrast, deletion of one or more of these genes in a strain of E. coli O157:H7 did not affect its ability to bind to alfalfa. Only the absence of the ompA gene had a significant effect on binding, and the plant-bacterium interaction was markedly reduced in a tdcA ompA double mutant. In contrast, the E. coli O157:H7 ompA and tdcA ompA mutant strains were only slightly affected in adhesion to Caco-2 cells and during biofilm formation. These findings suggest that some adhesins alone are sufficient to promote binding to alfalfa and that they may exist in E. coli O157:H7 as redundant systems, allowing it to compensate for the loss of one or more of these systems. Binding to the three types of surfaces appeared to be mediated by overlapping but distinct sets of genes. The only gene which appeared to be irreplaceable for binding to plant surfaces was ompA.

Source Tracking of Escherichia coli O157:H7 and Salmonella Contamination in the Lairage Environment at Commercial U.S. Beef Processing Plants and Identification of an Effective Intervention†

2008 ◽  
Vol 71 (9) ◽  
pp. 1752-1760 ◽  
Author(s):  
TERRANCE M. ARTHUR ◽  
JOSEPH M. BOSILEVAC ◽  
DAYNA M. BRICHTA-HARHAY ◽  
NORASAK KALCHAYANAND ◽  
DAVID A. KING ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Gel Electrophoresis ◽  
The United States ◽  
Pulsed Field Gel Electrophoresis ◽  
Processing Plant ◽  
Escherichia Coli O157 ◽  
Pulsed Field ◽  
E Coli ◽  
Beef Processing ◽  
Processing Plants

Transportation from the feedlot and lairage at the processing plant have been identified as potential sources of Escherichia coli O157:H7 and Salmonella hide contamination. The objective of this study was to perform a comprehensive tracking analysis of E. coli O157:H7 and Salmonella associated with beef cattle from the feedlot through processing. Cattle (n = 581) were sampled in a feedlot, then transported in multiple lots to three commercial, fed beef processing plants in the United States, where they were sampled again. Samples were collected from the tractor trailers prior to loading cattle and from the lairage environment spaces prior to entry of the study cattle. Pathogen prevalence on cattle hides increased on every lot of cattle between exiting the feedlot and beginning processing. Prior to loading cattle, E. coli O157:H7 was found in 9 (64%) of 14 tractor trailers. E. coli O157:H7 was detected in over 60% of the samples from each lairage environment area, while Salmonella was detected in over 70% of the samples from each lairage environment area. E. coli O157:H7 and Salmonella isolates (n 3,645) were analyzed using pulsed-field gel electrophoresis. The results of the pulsed-field gel electrophoresis tracking indicate that the transfer of bacteria onto cattle hides that occurs in the lairage environments of U.S beef processing plants accounts for a larger proportion of the hide and carcass contamination than does the initial bacterial population found on the cattle exiting the feedlot. Finally, the results of this study indicate that hide wash cabinets are effective in removing contamination derived from the lairage environment.

Growth and Enrichment Medium for Detection and Isolation of Shiga Toxin–Producing Escherichia coli in Cattle Feces

2008 ◽  
Vol 71 (5) ◽  
pp. 927-933 ◽  
Author(s):  
HUSSEIN S. HUSSEIN ◽  
LAURIE M. BOLLINGER ◽  
MARK R. HALL
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Brain Heart Infusion ◽  
Toxin Production ◽  
Detection Methods ◽  
African Green Monkey Kidney ◽  
Potassium Tellurite ◽  
E Coli ◽  
Cattle Feces ◽  
Wide Range

Detection methods of Shiga toxin–producing Escherichia coli (STEC) in cattle feces varied in using enrichment media containing different antibiotic combinations. To examine efficacy of a new detection method for STEC, three O157:H7 (ATCC 43889, 43890, and 43895) and 41 non-O157:H7 (members of the O1, O15, O26, O86, O103, O111, O125, O127, O128, O136, O146, O153, O158, O165, O166, and O169 serogroups) isolates were tested. These isolates were grown in tryptic soy broth for 6 h, and their concentrations were determined before inoculation of tubes containing 1 g of cattle feces (sterile [experiment 1; evaluating growth] and fresh [experiment 2; evaluating enrichment]) to simulate the high and low levels of STEC shedding by cattle (105 versus 102 CFU/g feces, respectively). Eight STEC isolates (the three O157:H7 and five non-O157:H7 selected at random) were tested at a very low level (10 CFU/g feces). The feces were incubated in 50 ml of brain heart infusion broth containing potassium tellurite, novobiocin, and vancomycin (2.5, 20, and 40 mg/liter, respectively) and cefixime (50 μg/liter) at 37°C for 12 h and tested for STEC (VTEC [verotoxin-producing E. coli]–Screen assay [agglutination immunoassay]). Potential STEC isolates were recovered, characterized biochemically, serotyped, and tested for toxin production using Vero (African green monkey kidney) cell toxicity assay and agglutination immunoassay. In both experiments, all the STEC isolates used for fecal inoculation were recovered at the concentrations tested. Our medium supported growth of and enrichment for a wide range of STEC isolates.

scholarly journals Origin and Evolution of Hybrid Shiga Toxin-Producing and Uropathogenic Escherichia coli Strains of Sequence Type 141

2019 ◽  
Vol 58 (1) ◽  
Author(s):  
Noble Selasi Gati ◽  
Barbara Middendorf-Bauchart ◽  
Stefan Bletz ◽  
Ulrich Dobrindt ◽  
Alexander Mellmann
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
The United States ◽  
Sequence Type ◽  
Comparative Genomic ◽  
Trna Genes ◽  
Ancestral Reconstruction ◽  
Content Type ◽  
E Coli ◽  
Tract Infections

ABSTRACT Hybrid Shiga toxin-producing Escherichia coli (STEC) and uropathogenic E. coli (UPEC) strains of multilocus sequence type 141 (ST141) cause both urinary tract infections and diarrhea in humans and are phylogenetically positioned between STEC and UPEC strains. We used comparative genomic analysis of 85 temporally and spatially diverse ST141 E. coli strains, including 14 STEC/UPEC hybrids, collected in Germany (n = 13) and the United States (n = 1) to reconstruct their molecular evolution. Whole-genome sequencing data showed that 89% of the ST141 E. coli strains either were STEC/UPEC hybrids or contained a mixture of virulence genes from other pathotypes. Core genome analysis and ancestral reconstruction revealed that the ST141 E. coli strains clustered into two lineages that evolved from a common ancestor in the mid-19th century. The STEC/UPEC hybrid emerged ∼100 years ago by acquiring an stx prophage, which integrated into previously unknown insertion site between rcsB and rcsD, followed by the insertion of a pathogenicity island (PAI) similar to PAI II of UPEC strain 536 (PAI II536-like). The two variants of PAI II536-like were associated with tRNA genes leuX and pheU, respectively. Finally, microevolution within PAI II536-like and acquisition of the enterohemorrhagic E. coli plasmid were observed. Our data suggest that intestinal pathogenic E. coli (IPEC)/extraintestinal pathogenic E. coli (ExPEC) hybrids are widespread and that selection pressure within the ST141 E. coli population led to the emergence of the STEC/UPEC hybrid as a clinically important subgroup. We hypothesize that ST141 E. coli strains serve as a melting pot for pathogroup conversion between IPEC and ExPEC, contrasting the classical theory of pathogen emergence from nonpathogens and corroborating our recent phenomenon of heteropathogenicity among pathogenic E. coli strains.

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