Technology Networks reports that E. coli food poisoning is one of the worst food poisonings, causing bloody diarrhea and kidney damage. But all the carnage might be just an unintended side effect, researchers from UConn Health report in the 27 November issue of Science Immunology. Their findings might lead to more effective treatments for this potentially deadly disease.
Escherichia coli are a diverse group of bacteria that often live in animal guts. Many types of E. coli never make us sick; other varieties can cause traveler’s diarrhea. But swallowing even a few cells of the type of E. coli that makes Shiga toxin can make us very, very ill. Shiga toxin damages blood vessels in the intestines, causing bloody diarrhea. If Shiga toxin gets into the bloodstream it can cause kidney failure.
“This is especially common in children; about 15% of kids with Shiga toxin-producing E. coli infections get kidney disease, and some can suffer long term kidney damage,” says UConn Health immunologist Sivapriya Vanaja.
A group of Shiga toxin-producing E. coli called enterohemorrhagic E. coli, or EHEC, are especially common in the United States. When you hear that a batch of romaine lettuce is being recalled because of a dangerous outbreak of food poisoning, it’s almost certainly due to EHEC.
EHEC normally live in cattle without making them sick. It used to be relatively common to have EHEC outbreaks coming from unhygienically prepared ground meat, but stringent regulations on slaughterhouses have made this less common. Now it’s more likely for EHEC to appear on vegetables grown in fields adjacent to cattle or manure runoff.
But no matter where it comes from, once EHEC bacteria get inside a human, the infection is hard to treat. Antibiotics tend to make it worse—when the bacteria feel themselves dying, they make more Shiga toxin. And EHEC are very good at inhibiting the part of the immune system that normally responds early to this kind of infection, allowing them to grow unchecked in the human gut.
In a study led by Morena Havira, a postdoctoral fellow in Vanaja’s lab, the team wanted to know how EHEC suppresses the immune system. The body normally responds to early stages of E. coli infections by activating an enzyme that kicks off an alarm inside cells. The cell bursts open to release a cloud of warning molecules that call other parts of the immune system to come and fight the bacteria.
But EHEC squashes that early response. To figure out how it does that, Vanaja and her colleagues decided to see which individual gene in EHEC was responsible. They took many different varieties of EHEC from a bacterial mutant library, and infected immune cells with them.
The team found that cells infected with EHEC that was missing the gene for Shiga toxin mustered a higher immune response compared to normal EHEC.
It was surprising. Shiga toxin is very well-studied for its toxic activity; it wasn’t known that it had another function,” Dr. Vanaja says. So Shiga toxin’s stealthy suppression of the immune system may have a link to all the bloody drama that ensues. Spurred on by this exciting observation, they conducted a series of detailed molecular studies, which revealed that Shiga toxin blocks a protein from bursting open the infected cell and alerting the body of infection.
Now that Vanaja and her colleagues know the specific molecular step Shiga toxin interferes with inside the immune cells, they are trying to figure out how, exactly, it blocks it. Once they know that, they may be able to find medicines that prevent toxin from interfering with immune responses.
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I love my shellfish – mussels and scallops (oysters are sorta gross) – but the kid was diagnosed with a shellfish allergy so they’re an occasional lunch while she’s at school.
Health types in the UK report on six cases of diarrhetic shellfish poisoning (DSP) following consumption of mussels in the United Kingdom (UK). The mussels contained high levels of heat-stable okadaic acid (OA)-group toxins. Here we describe the environmental and epidemiological investigation carried out in response to the outbreak.
In June 2019 (day 0), Public Health England South West was notified by the local authority of three diners who were unwell following consumption of mussels in a restaurant 5 days earlier. The local authority had determined that the restaurant had had received a batch recall notice, also 5 days earlier, from the shellfish producer for the mussels because of elevated toxin levels but this was not seen before the mussels were served that day. On day 1, PHE South West received a report from the county neighbouring the first of gastrointestinal illness linked to mussels from the same producer. A multi-agency outbreak control team was therefore convened on day 2 and led by the PHE South West health protection team.
An alert was sent to all health protection teams across England on day 2 asking about any reported cases of gastrointestinal illness following consumption of mussels. Local authorities in areas of product distribution were informed of the identified risk by email. Persons reporting illness who were identified by local authorities as having consumed the affected mussels were asked by PHE to complete a bespoke questionnaire on exposure and clinical data.
A probable case of DSP was defined as an individual with diarrhoea, three or more loose stools in 24 h, or vomiting or abdominal cramps or nausea, with date of onset from 7 days before to 1 day after notification of the outbreak, and time of onset 30 min to 24 h following consumption of mussels harvested from the affected site. Confirmed cases were as probable, but with an absence of pathogens in a stool sample that would otherwise explain illness.
Thirteen individuals reported to have been unwell after consumption of mussels were contacted. Completed questionnaires were received from seven individuals, of which three were confirmed, and three probable cases. The cases ate at four separate venues. One respondent did not meet the case definition as symptom onset was more than 24 h following consumption.
The mean age of cases was 59 years (range: 37–76 years); three were male and three were female. All cases reported eating steamed mussels. Five cases ate mussels as a main course and one as a starter. Reported portion sizes ranged from 11 to 50 mussels.
The mussels were produced in an offshore marine area. A routine shellfish monitoring programme is in place throughout England and Wales, including at the affected site. As a part of this programme, the water column is sampled every 2 weeks from April to September and cell counts of potentially harmful algal species are measured. Shellfish flesh samples are also tested for the presence of selected European Union (EU)-regulated biotoxins every 4 weeks during April to September each year unless phytoplankton counts and/or shellfish toxins are quantified above specified warning limits that require further precautions, including re-testing and closure.
Lipophilic toxin determination, including that for OA-group toxins, is routinely carried out using the method specified in in the EU-Harmonised Standard Operating Procedure for determination of lipophilic marine biotoxins in molluscs by LC-MS/MS [1]. Additional flesh and water samples were taken in advance of the planned sampling date following a report to the local authority from a local fisherman of a red-coloured algal bloom six miles offshore from the production site.
The local authority determined the source of the mussels by questioning venues linked to reports of illness. Subsequently, the shellfish producer provided the outbreak control team with a complete list of all businesses who had received the affected mussels. Mussels from the site were harvested daily from 9 to 5 days before notification of the outbreak for commercial sale. The mussels were not tested by the producer for the presence of toxins. A large volume of mussels was distributed to seafood wholesalers, restaurants and pubs, and subject to the recall notice distributed by the producer 5 days before reports of illness to PHE. A limited number of businesses not linked to any known cases, including wholesalers, retailers, restaurants and pubs, responded to the recall stating they had sold some of the affected produce. No produce was found to still be in circulation at the time of the outbreak response.
Water column and shellfish flesh sampling results are summarised in Table 2. Measured densities of Dinophysis spp. in the water column increased rapidly from being undetectable 16 days before outbreak notification to 1,600 cells per litre 7 days before, coinciding with the time of harvesting of the affected batch and exceeding the England, Wales and Northern Ireland Food Standards Agency trigger level of 100 cells per litre. The level of total OA-group lipophilic toxins in mussel flesh was 338 µg OA equivalents (eq) per kg, following application of measurement uncertainty, 7 days before outbreak notification. This exceeded the maximum permitted limit (MPL) of 160 µg OA eq per kg defined by European Commission (EC) regulation 853/2004 [2]. Toxin concentrations quantified showed that an average of 94% of the OA-group toxins present in the mussels consisted of OA itself, with the remainder being dinophysistoxin 2 (DTX2).
Water column sampling 7 days before outbreak notification did not detect other harmful algal species apart from Pseudo-nitzschia spp., the causative diatom for domoic acid responsible for amnesic shellfish poisoning, at 1,320 cells per litre. This is below the trigger level of 150,000 cells per litre for this species.
Routine shellfish sampling at the same site during the same time period did not detect paralytic shellfish poisoning toxins. Trace levels of yessotoxins were detected, but along with traces of azaspiracids, they were well below regulatory levels. Amnesic shellfish poisoning toxins were below the limit of quantitation (LOQ).
In response to the elevated toxin levels quantified and reported 5 days before outbreak notification, the shellfish bed was immediately closed for harvesting as per standard practice in England. The Food Standards Agency urgently contacted local authorities of places where the affected product had been distributed to ensure that wholesalers and venues had acted upon the recall. Venues were asked whether any product had been frozen, for example in the form of stock, as this would not deactivate the toxin, but there was no evidence this had been done.
Discussion
We report on six cases of DSP associated with consumption of mussels harvested in the South West of England. Without an available validated test for relevant toxins in human samples, the diagnosis was made based on characteristic clinical symptoms, including diarrhoea, abdominal pain, nausea and fever/chills, elevated levels of OA-group toxins in the flesh of mussels from the same batch as those consumed, the absence of faecal pathogens in stool of cases and epidemiological evidence of exposure to the produce.
DSP occurs following consumption of seafood containing high levels of the heat-stable OA-group toxins produced by dinoflagellates including Dinophysis spp., and is characterised by a rapid-onset of self-limiting gastrointestinal illness [3,4]. Recognised outbreaks of DSP are rare. Seventy cases were identified in 2013 following consumption of mussels harvested around the Shetland Islands [5] and 49 cases were identified in 1998 following consumption of UK-harvested mussels in London [6]. Outbreaks have been recorded in recent years in China, the United States, France and Canada [4,7–9].
The lowest-observed-adverse-effect level of OA is 45 to 50 µg OA eq per person [4,10]. In our study, an average main course portion of mussels (500 g in shell) would provide 41 µg OA eq., using a flesh weight yield of 24% [11]. This level of exposure is consistent with DSP as the cause of illness considering variability in portion sizes, flesh yield, body weight and toxin levels at the production site. Individual mussel sizes served were unavailable but would likely vary. Therefore, overall estimated portion weight was used to calculate the exposure dose. A limitation is that body weight (bw) was not recorded for cases and because of this, OA eq per kg bw could not be calculated.
A shellfish biotoxin programme monitoring the occurrence of harmful algal blooms and toxins in classified shellfish production areas in the UK, alongside food business operator checks, remains a robust system to protect population health. Nonetheless, a rapid increase in concentrations of Dinophysis spp. cells within the waters of the production site may have contributed to the outbreak, in tandem with shellfish harvesting occurring before official control results were reported and site closure. Whyte et al. (2014) demonstrated that a similar rapid increase in Dinophysis levels, resulting from a change in prevailing wind direction, occurred in the 2013 Shetland Islands origin outbreak [5]. Transdisciplinary research is required to predict future risk and inform monitoring, particularly given likely changes in the distribution of potentially-toxic species particularly if temperature of ocean water increases [12]. Our investigation suggested that affected produce may have been sold by restaurants and pubs with no known linked cases. Given that DSP is a self-limiting illness that may be under-reported by cases and has low awareness among clinicians, the actual number of persons affected in this outbreak is likely to be higher [13].
This outbreak highlights that clinicians and public health professionals should be aware of algal-derived toxins as a potential cause of illness following seafood consumption, and that the need for effective end-product testing of shellfish to ensure food safety remains.
Outbreak of diarrhetic shellfish poisoning associated with consumption of mussels, United Kingdom, May to June 2019
Earlier this year I ran into a barfblog reader who said, ‘You’re really scared of botulism, aren’t you?’
The question was was related to a few things I had posted about the 24 illnesses and a death linked to an Ohio church potluck dinner. Improperly home canned potatoes were implicated.
I dunno about scared, maybe just in awe. The toxin blocks motor nerve terminals at the myoneural junction, causing paralysis. It starts with the mouth, eyes, face and moves down through the body. It often results in paralysis of the chest muscles and diaphragm, making a ventilator necessary. Months of recovery follow an intoxication.
Maybe I am scared.
Today researchers from the Brookhaven National Laboratories published research in Nature Scientific Reports about how one of the neurotoxins produced by Clostridium botulinum is protected in certain environments – info that can provide insight into vaccination and post-exposure mitigation.
Molecular Assembly of Clostridium botulinum progenitor M complex of type E
Clostridium botulinum neurotoxin (BoNT) is released as a progenitor complex, in association with a non-toxic-non-hemagglutinin protein (NTNH) and other associated proteins. We have determined the crystal structure of M type Progenitor complex of botulinum neurotoxin E [PTC-E(M)], a heterodimer of BoNT and NTNH. The crystal structure reveals that the complex exists as a tight, interlocked heterodimer of BoNT and NTNH. The crystal structure explains the mechanism of molecular assembly of the complex and reveals several acidic clusters at the interface responsible for association at low acidic pH and disassociation at basic/neutral pH. The similarity of the general architecture between the PTC-E(M) and the previously determined PTC-A(M) strongly suggests that the progenitor M complexes of all botulinum serotypes may have similar molecular arrangement, although the neurotoxins apparently can take very different conformation when they are released from the M complex.
When I teach food service folks a certified food protection manager class I often stumble over the pronunciation of ciguatera poisoning (the New York Times says it’s sig-WAH-terra – I’ll go with that). The toxin is produced by a dinoflagellates (usually Gambierdiscus toxicus which lives on algae or dead coral) and is eaten up by sporting fish like barracuda, amber jack and some types of grouper and snapper.
The fish eat the small organisms and overtime bioaccumulate the toxin in their tissue.
Then folks who like fish, eat it and get sick. Even if it’s cooked.
The toxin is pretty heat stable (FAO says that even 20 min of cooking at 158°F/70°C for 20 min was insufficient to fully denature the toxin protein). Ciguatera was responsible for an outbreak aboard a cargo ship earlier this year, leading to a code orange at a Saint John, New Brunswick (that’s in Canada) hospital. Thirteen crew members fell ill within hours of eating toxin-ridden fish.
Elizabeth Radke and colleagues at Florida’s Emerging Pathogens Institute published research earlier this week estimating that ciguatera is a much larger issue than the reported illness disease trackers believe. Public health data show that barracuda, grouper and amberjack caught from subtropical waters in the Bahamas and the Florida Keys are key risk factors.
From the paper:
Our finding that only 7% of diagnosed cases were reported to the FDOH may at first glance be surprising. However, for many notifiable diseases, physicians rely on laboratory reporting of cases, which is not available for ciguatera because of the lack of a diagnostic laboratory test. In addition, because ciguatera is not a communicable disease, physicians may be unaware that it is a notifiable condition in the State of Florida. One survey in Miami-Dade County found that only 47% of physicians knew that ciguatera was notifiable and this is likely to be lower in less endemic parts of the state.
We also found that Hispanics experience the highest rate of ciguatera illness in Florida, possibly due to more frequent consumption of barracuda than non-Hispanics. This may represent an opportunity for targeted, culturally relevant educational messaging after more narrowly identifying high-risk cultural groups.
Know your target audiences, their practices and communicate to them directly.
According to food service provider Sodexo, preliminary laboratory analysis indicates a bacteria on red beats that produces a toxin when stored at room temperature is responsible for the outbreak.
On January 10, 150 children in Lambersart began vomiting and having headaches. After being examined 40 children were diagnosed with “light” poisoning (something may be lost in translation here, but thanks, Amy, for the work, and Luca for the link).
Sodexo says it has changed their beat supplier and is strengthening their regular testing of suppliers.
Food safety inspectors have stopped a shellfish trader in Zeeland from exporting 47 tonnes of mussels after it failed to take action over two food poisoning incidents in England and Switzerland.
A small quantity of the mussels, which were exported to Ireland, are also being recalled, the food safety body NVWA says.
In November, the same company was at the centre of another recall after several people became ill in England after eating mussels containing biotoxins, a poison common in shellfish. Those mussels came from Ireland but had been sold by the Dutch company.
The company was aware of the problem but did not register it with the authorities in time, food safety inspectors say. In December there was a second incident involving mussels in Switzerland. Those mussels, said at the time to be of Danish origin, turned out to be from the same Irish consignment as in the English food poisoning case.
Food inspectors have now effectively closed down the trader pending a full investigation and possible criminal charges.
– Multnomah County, Oregon, health officials, 60 students developed stomach pains, vomiting, and diarrhea after eating beef stroganoff.
– C. perfringens spores often survive cooking but are not a problem until the food is held at an improper temperature.
– These spores can germinate into cells which then can multiply to food poisoning levels if food is held between 41°F and 135°F for more than four hours.Foodsafetyinfosheet-10-28-15
– Use a tip sensitive digital thermometer to measure temperature and monitor throughout service and cooling.
Scientists at Lawrence Livermore National Laboratory have been crafting a high-tech fabric for the military made out of tiny carbon nanotubes — hollow structures that stay breathable in hot weather yet are small enough to block out pathogens. For an extra layer of safety, they’re planning to add a special coating that will block out even the smallest toxins, such as anthrax spores and other chemical and biological warfare agents.
The technology is still in the concept stages, but the research has already received funding from the U.S. Defense Threat Reduction Agency
Francesco Fornasiero, a chemical engineer at the Bay Area lab, told the Los Angeles Times, “We developed membranes which have pores that are made only of carbon nanotubes. These pores have walls that are extremely small. The smoothness of this wall and the hydrophobicity [ability to repel water] are together responsible for the extremely rapid transport rates observed for both gases and liquids.”
Bill Stanley, an 83-year-old six-term county commissioner from North Carolina, had breakfast at the Crowne Plaza Hotel in Northeast Portland last July.
According to a state outbreak investigation, was one of seven people sickened after breakfast that morning at. All of them ate eggs benedict. An eighth person, who ordered eggs benedict but had the hollandaise sauce on the side and didn’t consume it, felt fine.
No one else got sick, pointing to the hollandaise sauce as the culprit.
Oregon heath officials couldn’t test it for pathogens, however. The hotel threw it away after breakfast service.
But lab tests confirmed that Stanley — and another person hospitalized in the outbreak — were sickened by a strain of Staphylococcus aureus, a bacterium commonly found on the skin and in the noses of healthy people. Certain strains produce toxins that can spark quick and acute gastrointestinal symptoms.
The same strain was found in a nasal swab of one of the food workers at Crowne Plaza.
Dr. Mathieu Tourdjman, lead Oregon epidemiologist investigating the outbreak, said the sauce became toxic because it was not kept hot enough.
Unlike many other pathogens, the toxins produced by Staph cannot be killed by cooking. The only way to prevent foodborne Staph infections is by thorough hand washing and proper cooking. Food safety advocates recommend keeping cooked food warm at 140 degrees Fahrenheit or more.
The temperature of the hollandaise sauce was not monitored by kitchen staff at Crowne Plaza, Tourdjman found.
The outbreak shocked the hotel, according to general manager Ziggy Lopuszynski, who said the hotel has taken the hollandaise sauce off the menu.
Stanley is suing for medical expenses of nearly $14,000 and $26,000 in noneconomic damages. The hotel has balked at the settlement.
One of my great laments about Manhattan (Kansas) has been the lack of sushi. In the past few years, however, sushi has appeared on campus, in grocery stores and a Japanese restaurant is expected to open in Aggieville. Today during our regular pilgrimage to a Dillon’s grocery store (owned by Kroger), the "Sushi" sign was prominently displayed out front. While thinking to myself, "that might make a nice lunch today,"once inside the store I changed my mind. I snapped this picture (right) of an unattended rice container and decided not to buy sushi there because of the potential risk.
While most people presume that the greatest risk for foodborne illness in sushi comes from the raw fish, I’ve learned from living with Doug that rice is too often the culprit. When held at improper temperatures or temperature abused, Bacillus cereus, a soil dwelling bacterium, can germinate in the rice and create toxins. Although only responsible for 2-5% of foodborne illness, B. cereus can result in nausea, vomiting and diarrhea. Diarrhea onset usually occurs between 8 and 16 hours after consumption but nausea and vomiting can occur from 1 to 5 hours after consumption. This is one of the few foodborne illnesses with symptom onset soon after consumption.
Last year when one of my students told me he got sick from eating sushi on campus, he blamed himself for eating raw fish. He was rather surprised when I told him the rice was more likely to blame.
Escherichia coli are a diverse group of bacteria that often live in animal guts. Many types of E. coli never make us sick; other varieties can cause traveler’s diarrhea. But swallowing even a few cells of the type of E. coli that makes Shiga toxin can make us very, very ill. Shiga toxin damages blood vessels in the intestines, causing bloody diarrhea. If Shiga toxin gets into the bloodstream it can cause kidney failure.
the hollandaise sauce on the side and didn’t consume it, felt fine. .jpg)