In August 2018, Public Health England (PHE) was made aware of five probable cases of Shiga toxin‐producing Escherichia coli (STEC) O157:H7 among individuals reporting participation in a mud‐based obstacle race. An additional four cases, identified via routine whole‐genome sequencing, were subsequently linked to the same event. Two of the nine cases were due to secondary household transmission.
Despite an agreement between the event organizers and the local authority, to ensure that all livestock were removed from the site 28 days before the event, sheep were observed grazing on some of the routes taken by the runners 2 days prior to the race taking place. A retrospective review of incidents reported to PHE between 2015 and 2018 identified 41 cases of gastroenteritis associated with muddy assault course events. Of these, 25 cases were due to infection with STEC O157:H7, of which all but one were associated with outbreaks.
Due to the environment in which such events take place, it is impossible to entirely remove the risk of exposure to potentially pathogenic zoonoses. However, race organizers should ensure that livestock are removed from the course 28 days before the event. They should also ensure that participants are made aware of the risk of contracting gastrointestinal disease from the environment, and to stress the importance of hand hygiene post‐event and the risk of secondary transmission, particularly to children who are at risk of developing haemolytic uraemic syndrome.
An outbreak of shiga toxin-producing Escherichia coli O157:H7 linked to a mud-based obstacle course, England, August 2018
Consumers should immediately stop using any of the affected pet food products and contact the retailer where they purchased the affected product for a full refund or exchange.
As of June 12, 2020, the company has been made aware of 4 reports of illnesses in Canada – in people.
Consumers are advised to always wash hands, surfaces and utensils thoroughly with soap and water after feeding, handling or cleaning up after pets. Clean surfaces that come into contact with pet food or ill pets.
One of daughter Sorenne’s daily tasks is to give stress-reducing wet food to our neurotic cat, and she absolutely knows to wash her hands after handling the food.
Scott Weese over at the Worms and Germs blog writes that while people were presumably not eating the pet food (I wouldn’t presume that), there is the potential for cross-contamination of human food when handling raw pet food, as well as potential for exposure to pathogens through things like contact with pet food bowls and pet feces.
While most dogs and cats that eat raw diets are fine, and most owners don’t get sick, it’s clear that feeding raw diet or raw animal-based treats (e.g. pig ears) is associated with risks to the pet and any human contacts. I’d rather people not feed raw diets to their pets, particularly when the pet or household members are very young, elderly, pregnant or have compromised immune systems. If none of those risk factors are present and someone wants to feed a raw diet, I’d still rather they didn’t, but there are some things that can reduce the risks, as outlined on the Worms & Germs infosheet on raw diets available on our Resources – Pets page.
Oh, and don’t go to the company’s website for accurate information about risk and risk mitigation. They bury some good prevention recommendations in a pile of often out-of-context dialogue to try to deflect any concerns and the typical raw diet misinformation. Some other raw pet food companies are up front about the risks and prevention measures – I have a lot more confidence in companies like that.
Outbreaks of E. coli illness sickened 188 people last year who ate romaine lettuce in three separate outbreaks.
There have been so many outbreaks going back to spinach in 2006, and beyond that, my favorite salad now is a Greek salad – without the lettuce.
If the Leafy Greens Marketing Association was as rigorous as its press releases maintain this would be minimized.
Instead, between 2009 and 2018, federal authorities identified 40 food-borne outbreaks of E. coli in the U.S. “with a confirmed or suspected link to leafy greens,” the FDA said.
Investigators concluded the most recent outbreaks were centered on ranches and fields owned by the same grower and that were located downslope from public land where cattle grazed.
So if LGMA is doing internal audits, why didn’t they notice this dude?
Because it’s PR not gumshoes, people out in the field.
We figured out 20 years ago that gumshoes are required.
The U.S. Food and Drug Administration published the findings of an investigation into the contamination of romaine lettuce implicated in three outbreaks of E. coli O157:H7 during the Fall of 2019.
The investigation was conducted at several farms identified in the outbreak tracebacks, as well as at other businesses and public access areas and resulted in several key findings:
Each of these three outbreaks, identified in the report as Outbreaks A, B and C was caused by distinctly different strains of E. coli O157:H7 as determined by whole genome sequencing (WGS) analysis;
Traceback investigations of multiple illness sub-clusters and supply chain information identified a common grower with multiple ranches/fields which supplied romaine lettuce during the timeframe of interest to multiple business entities associated with all three outbreaks.
The same strain of E. coli O157:H7 that caused Outbreak A was found in two different brands of fresh-cut salads containing romaine lettuce in 2019;
This same outbreak strain of E. coli O157:H7 in Outbreak A was detected in a fecal–soil composite sample taken from a cattle grate on public land less than two miles upslope from a produce farm with multiple fields tied to the outbreaks by the traceback investigations;
Other strains of Shiga toxin-producing E.coli (STEC), while not linked to any of the outbreaks, were found in closer proximity to where romaine lettuce crops were grown, including two samples from a border area of a farm immediately next to cattle grazing land in the hills above leafy greens fields and two samples from on-farm water drainage basins.
These findings, together with the findings from earlier leafy greens outbreaks dating back to 2013, suggest that a potential contributing factor has been the proximity of cattle—a persistent source of E. coli O157:H7 and other STEC—to the produce fields identified in traceback investigations.
Because of the reoccurring nature of outbreaks associated with leafy greens, the FDA recently released a 2020 Leafy Greens STEC Action Plan, which outlines a three-pronged approach for tackling this problem. It describes the FDA’s plans for working with industry, federal partners, state and local regulators, academia and others to address the safety of leafy greens by advancing work in three areas: prevention, response, and addressing knowledge gaps.
Outbreak investigation of E. coli: Romaine from Salinas, California (November 2019)
Tahini is a common food product in the Mediterranean area that is used as a main ingredient in variety of ready-to-eat foods. The objective of the current study was to investigate the inhibitory effect of thyme oil (TO) or cinnamon oil (CO) on E. coli O157:H7 viability in tahini and diluted tahini at different storage temperatures.
Addition of 2.0% CO to tahini reduced E. coli O157:H7 numbers by 1.38, 1.79 or 2.20 log10 CFU/mL at 10, 25 or 37 °C, respectively, by 28d. In diluted tahini at 10 °C, no viable cells of E. coli O157:H7 by 21d were detected when 1.0% CO was used. However, at 25 and 37 °C, no viable cells were detected by 14d when CO was added at 0.5% level. Addition of 2.0% TO to tahini, resulted in 1.82, 2.01 or 1.65 log10 CFU/mL reduction in E. coli O 157:H7 numbers was noted at 37, 25 or 10 °C, respectively, by 28d. In diluted tahini, TO at 0.5% or 1.0% induced complete reduction in the viability of E. coli O157:H7 by 28d storage at 37 or 25 °C. At 10 °C, a 3.02 log10 CFU/mL reduction was observed by 28d compared to the initial inoculation level in samples treated with 2.0% TO.
Inhibitory effect of thyme and cinnamon essential oils against e. coli O157:H7 in tahini, 08 May 2020
Food Science and Technology
Anas Al-Nabulsi, Tareq Osaili, Amin Olaimat, Weam Almarsi, Murad Al-Holy, Ziad Jaradat, Mutamed Ayyash, Saddam Awaisheh, Richard Holley
Escherichia coli O157:H7 (EcO157) infections have been recurrently associated with produce. The physiological state of EcO157 cells surviving the many stresses encountered on plants is poorly understood. EcO157 populations on plants in the field generally follow a biphasic decay in which small subpopulations survive over longer periods of time. We hypothesized that these subpopulations include persister cells, known as cells in a transient dormant state that arise through phenotypic variation in a clonal population.
Using three experimental regimes (with growing, stationary at carrying capacity, and decaying populations), we measured the persister cell fractions in culturable EcO157 populations after inoculation onto lettuce plants in the laboratory. The greatest average persister cell fractions on the leaves within each regime were 0.015, 0.095, and 0.221%, respectively. The declining EcO157 populations on plants incubated under dry conditions showed the largest increase in the persister fraction (46.9-fold). Differential equation models were built to describe the average temporal dynamics of EcO157 normal and persister cell populations after inoculation onto plants maintained under low relative humidity, resulting in switch rates from a normal cell to a persister cell of 7.7 × 10−6 to 2.8 × 10−5 h−1. Applying our model equations from the decay regime, we estimated model parameters for four published field trials of EcO157 survival on lettuce and obtained switch rates similar to those obtained in our study. Hence, our model has relevance to the survival of this human pathogen on lettuce plants in the field. Given the low metabolic state of persister cells, which may protect them from sanitization treatments, these cells are important to consider in the microbial decontamination of produce.
IMPORTANCE Despite causing outbreaks of foodborne illness linked to lettuce consumption, E. coli O157:H7 (EcO157) declines rapidly when applied onto plants in the field, and few cells survive over prolonged periods of time. We hypothesized that these cells are persisters, which are in a dormant state and which arise naturally in bacterial populations. When lettuce plants were inoculated with EcO157 in the laboratory, the greatest persister fraction in the population was observed during population decline on dry leaf surfaces. Using mathematical modeling, we calculated the switch rate from an EcO157 normal to persister cell on dry lettuce plants based on our laboratory data. The model was applied to published studies in which lettuce was inoculated with EcO157 in the field, and switch rates similar to those obtained in our study were obtained. Our results contribute important new knowledge about the physiology of this virulent pathogen on plants to be considered to enhance produce safety.
Formation of Escherichia coli O157:H7 persister cells in the lettuce phyllosphere and application of differential equation models to predict their prevalence on lettuce plants in the field
08 November 2019
Applied and Environmental Microbiology
Daniel S. Munther, Michelle Q. Carter, Claude V. Aldric, Renata Ivanek, Maria T. Brandl
I love Mondays in Australia because it’s Sunday in the U.S., football and hockey are on TV for background, the kid is at school when not in France, and I write (Sorenne painting in France).
Fourteen years ago, me and Chapman went on a road trip to Prince George (where Ben thought he would be eaten by bears) to Seattle, then to Manhattan, Kansas, where in the first week I met a girl, got a job, and then spinach happened.
Leafy greens are still covered in shit.
I am drowning in nostalgia, but things haven’t changed, and, as John Prine wrote, all the news just repeats itself.
Same with relationships.
Former U.S. Food and Drug Administration food safety chief, David Acheson, writes that on October 31, 2019, FDA announced a romaine lettuce E. coli O157:H7 outbreak for which the active investigation had ended and the outbreak appeared to be over. As such FDA stated there was no “current or ongoing risk to the public” and no avoidance of the produce was recommended.
Since that announcement, however, I have seen a number of articles condemning FDA and CDC. Why? Because the traceback investigation of the outbreak began in mid-September when CDC notified FDA of an illness cluster that had sickened 23 people across 12 states. So why the delay in announcing it to the public?
Despite the critical (and rather self-serving; always self-serving) stance on the “inexcusable” delay taken by a prominent foodborne illness attorney and his Food Safety “News” publication – which blasted a headline FDA “hid” the outbreak – my stance, having been an FDA official myself involved in outbreak investigations, is that the delay was practical and sensible.
Why? As FDA states right in its announcement:
When romaine lettuce was identified as the likely source, the available data indicated that the outbreak was not ongoing and romaine lettuce eaten by sick people was past its shelf life and no longer available for sale.
Even once romaine was identified as the likely cause, no common source or point of contamination was identified that could be used to further protect the public.
During the traceback investigation, the outbreak strain was not detected in any of the samples collected from farms, and there were no new cases.
Thus, neither FDA nor CDC identified any actionable information for consumers.
So, if it is not in consumers’ best interest to publicize an issue that no longer exists, why should they be driven away from a healthy food alternative? Why should unfounded unease be generated that will damage the industry, providing no benefit for consumers but ultimately impacting their pockets? There is just no upside to making an allegation without information. We’ve seen the impact on consumers and the industry when an announcement of a suspected food turns out to be incorrect; specifically “don’t eat the tomatoes” when it turned out to be jalapeno and serrano peppers. Having learned from such incidents, FDA’s approach is: If we don’t have a message that will help protect the public, then there is no message to be imparted.
So, rather than condemn FDA and CDC, I would commend them for getting the balance correct. And, perhaps, instead of any condemning, we should be working together to get the answers faster, to get outbreak data through better, faster, more efficient and coordinated traceability. Our entire system is too slow – a topic we have discussed many times in these newsletters.
The public and the scientific community need to be informed to prevent additional people from barfing.
I also rarely eat lettuce of any sort because it is overrated and the hygiene controls are not adequate.
Greek salad without lettuce is my fave.
Going public: Early disclosure of food risks for the benefit of public health
NEHA, Volume 79.7, Pages 8-14
Benjamin Chapman, Maria Sol Erdozaim, Douglas Powell
Often during an outbreak of foodborne illness, there are health officials who have data indicating that there is a risk prior to notifying the public. During the lag period between the first public health signal and some release of public information, there are decision makers who are weighing evidence with the impacts of going public. Multiple agencies and analysts have lamented that there is not a common playbook or decision tree for how public health agencies determine what information to release and when. Regularly, health authorities suggest that how and when public information is released is evaluated on a case-by-case basis without sharing the steps and criteria used to make decisions. Information provision on its own is not enough. Risk communication, to be effective and grounded in behavior theory, should provide control measure options for risk management decisions. There is no indication in the literature that consumers benefit from paternalistic protection decisions to guard against information overload. A review of the risk communication literature related to outbreaks, as well as case studies of actual incidents, are explored and a blueprint for health authorities to follow is provided.
AIMS: The aim of this study was to evaluate the microbiological quality of commercially prepared ready-to-eat (RTE) sushi by enumerating aerobic mesophilic bacteria (AMB) and thermotolerant coliforms (TC) and detecting Escherichia coli and Salmonella ssp. An isolate was identified as E. coli O157:H7 which was evaluated for its virulence and antimicrobial resistance profiling as well as its ability to form biofilms on stainless steel.
METHODS AND RESULTS: There were four sampling events in seven establishments, totalling 28 pools of sushi samples. Mean AMB counts ranged between 5·2 and 7·7 log CFU per gram. The enumeration of TC varied between 2·1 and 2·7 log MPN per gram. Salmonella ssp. were not detected, and one sample was positive for E. coli and was identified as E. coli O157:H7. To the best of our knowledge, this is the first report of E. coli O157:H7 in sushi samples in the world literature. This isolate presented virulence genes stx1, stx2, eae and hlyA. It was also susceptible to 14 antimicrobials tested and had the ability to form biofilms on stainless steel.
CONCLUSIONS: There is a need to improve the good hygiene practices adopted in establishments selling sushi in the city of Pelotas, Brazil. In addition, the isolated E. coli O157:H7 carries a range of important virulence genes being a potential risk to consumer health, as sushi is a RTE food. This isolate also presents biofilm formation ability, therefore, may trigger a constant source of contamination in the production line of this food.
SIGNIFICANCE AND IMPACT OF THE STUDY: The increase in the consumption of sushi worldwide attracts attention regarding the microbiological point of view, since it is a ready-to-eat food. To our knowledge, this was the first time that E. coli O157:H7 was identified in sushi samples.
First report of Escherichia coli O157:H7 in ready-to-eat sushi