<i>Escherichia coli</i>O157:H7 Infections Associated with Contaminated Pork Products — Alberta, Canada, July–October 2014

Honish, Lance; Punja, Nisha; Nunn, S; Nelson, Dale; Hislop, Nyall; Gosselin, G; Stashko, Natisha; Dittrich, D

doi:10.15585/mmwr.mm6552a5

Cited by 27 publications

(7 citation statements)

References 6 publications

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“…A review of the public health database for cases of STEC O157 infections in Alberta for the period 2009 to 2016 yielded a total of 801 cases. Overall, the annual incidence of STEC O157 infections remained stable at around two cases/100,000 persons per year (range 1.71–2.61/100,000), with the exception of 2014, when the third largest STEC outbreak in Canadian history led to the highest incidence seen during the study period (4.6/100,000) [7]. All viable STEC O157 isolates available on culture-confirmed cases (n = 762) were included in the study.…”

Section: Resultsmentioning

confidence: 99%

“…In the late 1980s to early 1990s, the province of Alberta documented one of the highest rates of STEC infections in North America. Local incidence of STEC O157 is now much lower, largely due to improved laboratory detection of cases leading to public health interventions targeting the prevention, detection, and remediation of outbreaks [7]. Herein we report on the updated local epidemiology of STEC O157 in the context of molecular data available on a large collection of clinical isolates from our Alberta STEC surveillance program.…”

Section: Discussionmentioning

confidence: 99%

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Epidemiology of Shiga Toxin-Producing Escherichia coli O157 in the Province of Alberta, Canada, 2009–2016

Lisboa

Szelewicki

Latonas

et al. 2019

Toxins

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Shiga toxin-producing Escherichia coli (STEC) infections are the product of the interaction between bacteria, phages, animals, humans, and the environment. In the late 1980s, Alberta had one of the highest incidences of STEC infections in North America. Herein, we revisit and contextualize the epidemiology of STEC O157 human infections in Alberta for the period 2009–2016. STEC O157 infections were concentrated in large urban centers, but also in rural areas with high cattle density. Hospitalization was often required when the Shiga toxin genotype stx2a stx2c was involved, however, only those aged 60 years or older and infection during spring months (April to June) independently predicted that need. Since the late 1980s, the rate of STEC O157-associated hemolytic uremic syndrome (HUS) in Alberta has remained unchanged at 5.1%, despite a marked drop in the overall incidence of the infection. While Shiga toxin genotypes stx1a stx2c and stx2a stx2c seemed associated with HUS, only those aged under 10 years and infection during spring months were independently predictive of that complication. The complexity of the current epidemiology of STEC O157 in Alberta highlights the need for a One Health approach for further progress to be made in mitigating STEC morbidity.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Epidemiology of Shiga Toxin-Producing Escherichia coli O157 in the Province of Alberta, Canada, 2009–2016

Lisboa

Szelewicki

Latonas

et al. 2019

Toxins

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“…In the same year, an EHEC outbreak in Germany was reported, which infected 4,137 people and 52 people died (Frank et al, 2011 ). In 2014, 119 individuals were infected EHEC O157:H7 via eating infected pork in Canada (Honish et al, 2017 ). Cattle and swine are the most important intermediate natural carriers of EHEC, as well as the major transmission source to humans (Money et al, 2010 ; Pennington, 2010 ).…”

Section: Introductionmentioning

confidence: 99%

The EspF N-Terminal of Enterohemorrhagic Escherichia coli O157:H7 EDL933w Imparts Stronger Toxicity Effects on HT-29 Cells than the C-Terminal

Wang

Hua

et al. 2017

Front. Cell. Infect. Microbiol.

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Enterohemorrhagic Escherichia coli (EHEC) O157:H7 EspF is an important multifunctional protein that destroys the tight junctions of intestinal epithelial cells and promotes host cell apoptosis. However, its molecular mechanism remains elusive. We knocked out the espF sequence (747 bp, ΔespF), N-terminal sequence (219 bp, ΔespFN), and C-terminal sequence (528 bp, ΔespFC) separately using the pKD46-mediated λ Red homologous recombination system. Then, we built the corresponding complementation strains, namely, ΔespF/pespF, ΔespFN/pespFN, and ΔespFC/pespFC by overlap PCR, which were used in infecting HT-29 cells and BALB/C mice. The level of reactive oxygen species, cell apoptosis, mitochondrial trans-membrane potential, inflammatory factors, transepithelial electrical resistance (TER), and animal mortality were evaluated by DCFH-DA, double staining of Annexin V-FITC/PI, JC-1 staining, ELISA kit, and a mouse assay. The wild-type (WT), ΔespF, ΔespF/pespF, ΔespFC, ΔespFC/pespFC, ΔespFN, and ΔespFN/pespFN groups exhibited apoptotic rates of 68.3, 27.9, 64.9, 65.7, 73.4, 41.3, and 35.3% respectively, and mean TNF-α expression levels of 428 pg/mL, 342, 466, 446, 381, 383, and 374 pg/mL, respectively. In addition, the apoptotic rates and TNF-α levels of the WT, ΔespF/pespF, and ΔespFC were significantly higher than that of ΔespF, ΔespFN, ΔespFC/pespFC, and ΔespFN/pespFN group (p < 0.05). The N-terminal of EspF resulted in an increase in the number of apoptotic cells, TNF-α secretion, ROS generation, mitochondria apoptosis, and pathogenicity in BalB/c mice. In conclusion, the N-terminal domain of the Enterohemorrhagic E. coli O157:H7 EspF more strongly promotes apoptosis and inflammation than the C-terminal domain.

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“…The lower intestinal tract of ruminants is considered to be the main natural reservoir of STEC. In most human infections, transmission occurs primarily by ingestion of contaminated food of bovine origin, though few outbreaks have been associated to the consumption of other food products, including pork products contaminated by O157 (CDC, 1995; Williams et al ,2000; MacDonald et al , 2004; Conedera et al , 2007; Trotz-Williams et al , 2012; Honish et al , 2017) and by O111 (Paton et al , 1996). However, the epidemiology and virulence characteristics of STEC carried by on-farm pigs remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Shiga toxin-producing Escherichia coli in slaughtered pigs and pork products

Bardasi¹,

Taddei²,

Fiocchi³

et al. 2017

Ital J Food Safety

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During the years 2015-2016, 83 faecal samples were collected at slaughter from pigs reared in farms located in Central-Northern Italy. During the years 2014-2016 a total of 562 pork products [465 not-readyto-eat (NRTE) and 97 ready-to-eat (RTE) products] were collected from retail outlets, large retailers and processing plants. The samples were analysed according to ISO TS 13136:2012. Out of 83 swine faecal samples, 77 (92.8%) resulted stx-positive by real time polymerase chain reaction (PCR), 5 stx2+ and 1 stx1+ Shiga toxin-producing Escherichia coli (STEC) strains were isolated. Among the 465 NRTE samples, 65 (14.0%) resulted stx-positive by real time PCR and 7 stx2+ STEC strains were isolated. The stx2 gene was detected more frequently than the stx1 gene both in faecal samples (90.4 vs 8.4%) and in NRTE pork products (13.3 vs 1.3%). All the RTE samples included in the analysis resulted stx-negative. Among the samples resulted positive for stx and eae genes, serogroup-associated genes were detected at high frequency: O26 resulted the most frequent in faecal samples (81.3%) and O145 in pork products (88.1%). The O157 serogroup resulted positive in 83.3 and 78.1% of pork products and faecal samples, respectively. Despite the frequent detection by real time PCR of genes indicating the possible presence of STEC strains belonging to the six serogroups, the bacteriological step did not confirm the isolation of any such strains.

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Escherichia coliO157:H7 Infections Associated with Contaminated Pork Products — Alberta, Canada, July–October 2014

Cited by 27 publications

References 6 publications

Epidemiology of Shiga Toxin-Producing Escherichia coli O157 in the Province of Alberta, Canada, 2009–2016

Epidemiology of Shiga Toxin-Producing Escherichia coli O157 in the Province of Alberta, Canada, 2009–2016

The EspF N-Terminal of Enterohemorrhagic Escherichia coli O157:H7 EDL933w Imparts Stronger Toxicity Effects on HT-29 Cells than the C-Terminal

Shiga toxin-producing Escherichia coli in slaughtered pigs and pork products

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