(Something may be lost in translation, which is where Pink Floyd comes in)
This was informed by the Federal office for consumer protection and food safety in Braunschweig, Germany, on Thursday.
It is the in several States product, marketed with the name “Petite Fleur herbs” (“Keiems bloempje met kruiden”) the date of minimum durability 08.11.2018 and the additional indication of “Lot 3603”, as a manufacturer Dischhof/Belgium has been specified.
In the worst case, kidney failure threatening, According to the Schwabacher company in an investigation of the image Verotoxin found E. coli in the cheeses, which are regarded as potential Ehec.
The editor recommends:
“From a consumption of the affected product is strictly not recommended”, the company said.
The Ehec can cause bloody diarrhoea and in severe cases lead to kidney failure, but there are also inconspicuous progressions. The severe course of a disease ends in about two percent of the cases fatal.
In the spring of 2011 had cost the largest German Ehec epidemic 53. In Germany, the disease occurs again and again, every year, about 1000 cases of Ehec are reported cases.
In the PCP Luke (15) died because no one recognized the symptoms – now, his mother warns all.
Don and Ben are back in their respective normal podcasting chairs and talk about the Episode 166 recording in Geneseo, Canadian Thanksgiving, cooking beef and getting together with other food safety nerds. They talk a bunch about risk management decisions and how temperatures get established. The conversation goes to a large Salmonella outbreak in Canada linked to frozen chicken things that look like they are fully cooked. They go back to Thanksgiving talk (American this time) and then how to communicate cooking times/temperatures for products that are supposed to be ready-to-eat (or look ready-to-eat) and what happens if pathogens end up in those products (like frozen ham biscuits). The show ends on some chicken washing talk.
The observable signs was when I fell over while walking.
There’s some white matter degradation, maybe it’s from the booze, maybe it’s from the 50 years of pucks to the head, but I increasingly feel lost, and rely on phone calls with my much wiser children to get me through the day.
In May 2018, five children at Pam Walker’s day care in Tenn. were stricken with E. coli O157.
Kristi L Nelson of Knox News reports that science, public health officials said, sleuthed out the source of the E. coli infection: a goat farm across the road.
But for Walker, there’s been no closure — and she may never get the answers to exactly how a microorganism turned her dream of a bucolic child care center in a farm setting to a weeks-long nightmare.
Meanwhile, the health department was already investigating an E. coli outbreak among 10 children who’d consumed raw milk from a nearby dairy, French Broad Farms. Because it would be so unusual for two different E. coli O157 outbreaks to occur in the same area simultaneously, the health department, in the course of extensive interviews, looked for a link between Kids Place and the dairy. Did any children at the day care drink raw milk? Socialize or swim with anyone in the other group of infected children? Did any person or animal go back and forth between the dairy and the day care? The answers, they found, were no.
“Finding a bacteria that is microscopic, not visible to the naked eye, is really, really challenging,” said health department Director Dr. Martha Buchanan. “You have got to get the right sample at the right spot. And environmental cleaning did happen — the environment had changed when they went back” to sample.
With the positive culture from goat feces, the health department’s investigators determined that bacteria from the goats had somehow gotten into the baby house — and probably would have been present there before cleaning. When the specimens were sent back to the Tennessee Department of Health for DNA comparison with stool samples from the sick children, the DNA “fingerprint” from the goat samples and the Kids Place children were an exact match — but different from the DNA “fingerprint” of the cow feces from the dairy and the children who’d consumed raw milk, which matched each other. That meant, though unusual, that Knox County had two separate E. coli outbreaks in young children happening at the same time.
Finding it in goat feces, however, wasn’t a surprise. Goats, cows, sheep and other “ruminant” animals — animals that have a multichambered stomach and regurgitate and rechew food before digesting it — often carry E. coli in their digestive tracts. They can carry the bacteria, and shed it through their feces, but it typically doesn’t make them sick.
“Given that some of these illnesses have been linked to the goats at your facility, I recommend you no longer keep goats or other ruminant animals on your property, or that those who interact with the goats do not have contact with the children in your care,” Buchanan told Walker in a July 6 letter.
After the outbreak, Walker gave the goat herd to a friend. But the week after the health department informed her of the test results, she and her husband contacted the University of Tennessee College of Veterinary Medicine to have the goats tested again for E. coli. Dr. Marc Caldwell, assistant professor in large animal clinical sciences, remembers the test being requested merely to see if the goats were healthy, but Steve Walker said he wanted to see if this second test also would find a DNA fingerprint match between his goats and the children’s stool samples.
Techs from UTVM swabbed the goats themselves for fecal samples, rather than collecting feces from the ground as the health department did, and sent them to the Nebraska lab for culture. None of the goats tested positive for E. coli, but both herd dogs — also swabbed — did, while the health department’s dog feces samples were negative. It’s unusual, but possible, for dogs to carry E. coli, Caldwell said.
Caldwell said the test doesn’t prove the animals didn’t have E. coli O157 when the health department tested the feces. In fact, it doesn’t prove they didn’t have it that week, since the amount of bacteria shed from an infected animal can depend on heat, stress and other factors, and a certain amount has to be present for the antigen test — which is what the lab used — to show positive.
Escherichia coli are Gram-negative rod-shaped bacteria and part of the normal bacterial flora in the gastrointestinal tract, while diarrhoeagenic E. colipathotypes such as Shiga toxin-producing E. coli (STEC) and enteropathogenic E. coli (EPEC) are able to cause gastrointestinal infections [1]. STEC can lead to a severe disease, such as haemolytic-uraemic syndrome (HUS) [2]. The risk of HUS has been related especially to children under 5 years and to elderly people. HUS is characterised by acute onset of microangiopathic haemolytic anaemia, renal injury and low platelet count.
More than 400 STEC serotypes have been recognised, of which the best-known serotype is O157:H7 [1]. The most common non-O157:H7 serotypes causing human infections are O26, O103, O111 and O145 [3]. The virulence of STEC is largely based on the production of Shiga toxin 1 or 2 and is identified by detecting the presence of stx1 or stx2 genes [1,4]. The virulence of EPEC is caused by its capability to form attaching and effacing (A/E) lesions in the small intestine. This capability requires the presence of virulence genes called the locus of enterocyte effacement (LEE) in a pathogenity island (PAI) that encodes intimin [4]. Unlike STEC, EPEC do not produce Shiga toxin. EPEC are divided into two distinct groups by the presence of EPEC adherence factor plasmid (pEAF) expressing bundle-forming pili (BFP), which is a virulence determinant of typical EPEC (tEPEC) [5]. Thus atypical EPEC (aEPEC) are defined as E. coli that produce A/E lesions but do not express BFP. Typical EPEC are best known as a cause of infantile diarrhoea, especially in developing countries [6]. Diarrhoea-causing aEPEC have been shown to be separate group without a close relation to tEPEC, but some serotypes are genetically related to STEC [5]. The pathogenity of aEPEC has been questioned but their involvement with diarrhoeal outbreaks supports the idea that certain strains are diarrhoeagenic [1,7].
Both STEC and EPEC are transmitted through the faecal-oral route, and outbreaks caused by STEC and aEPEC have been described after ingestion of contaminated food or water [7,8]. STEC is common in ruminants and can be found in foods contaminated by ruminant faeces [9]. Most studies on STEC have focused on the serotype O157:H7, but infections and outbreaks caused by non-O157 strains are increasingly reported in Europe and elsewhere [10–13]. Atypical EPEC strains are found in animals used for food production, such as cattle, sheep, goat, pig and poultry, in contrast to tEPEC that has been found only in humans [1,14].
Since 1995, clinicians and clinical microbiology laboratories have been obliged to report culture-confirmed STEC infections to the Finnish Infectious Disease Registry (FIDR) maintained by the National Institute for Health and Welfare (THL) in Finland. EPEC infections are not reportable. Since PCR instead of culture became the standard for screening of diarrhoeal patients in 2013, the incidence of reported STEC infections has increased in Finland to 1.2–1.8 per 100,000 population between 2013 and 2015 compared with 0.2–0.6 per 100,000 between 2000 and 2012. From 1997 to 2015, six food- or waterborne STEC outbreaks were detected in Finland (Table 1).
Outbreak of multiple strains of non-O157 Shiga toxin-producing and enteropathogenic Escherichia coli associated with rocket salad, Finland, autumn 2016
One of my colleagues from 25 years ago, with his Robert Plant hair, always told me, when he retires, he’s going to do a lot of psychedelics and have huge amps on his cottage porch.
OK.
I’ve done the psychedelic kind of mushrooms once, about 30 years ago in Wainfleet, Ontario, and it ended up with four of us running along the Lake Erie beach, terrified of a dog that wasn’t there.
I’m concerned about quality control.
My friends, not so much, so they broke a window in the cottage I owned.
Researchers from Johns Hopkins University have recommended that psilocybin, the active compound in hallucinogenic mushrooms, be reclassified for medical use, potentially paving the way for the psychedelic drug to one day treat depression and anxiety and help people stop smoking.
The suggestion to reclassify psilocybin from a Schedule I drug, with no known medical benefit, to a Schedule IV drug, which is akin to prescription sleeping pills, was part of a review to assess the safety and abuse of medically administered psilocybin.
Before the Food and Drug Administration can be petitioned to reclassify the drug, though, it has to clear extensive study and trials, which can take more than five years, the researchers wrote.
The analysis was published in the October print issue of Neuropharmacology, a medical journal focused on neuroscience.
The study comes as many Americans shift their attitudes toward the use of some illegal drugs. The widespread legalization of marijuana has helped demystify drug use, with many people now recognizing the medicinal benefits for those with anxiety, arthritis and other physical ailments.
Psychedelics, like LSD and psilocybin, are illegal and not approved for medical or recreational use. But in recent years scientists and consumers have begun rethinking their use to combat depression and anxiety.
“We are seeing a demographic shift, particularly among women,” said Matthew Johnson, an associate professor of psychiatry and behavioral sciences at Johns Hopkins and one of the study’s authors. Among the research he has conducted, he said, “we’ve had more females in our studies.”
Microdosing, or the use of psychedelics in small, managed doses, has become a popular way to try to increase productivity and creative thinking, particularly among the technorati in Silicon Valley. It’s even a plot point in the CBS show “The Good Fight.”
Dr. Johnson said that in 2005, he volunteered to work in the “bad trip” tent at Burning Man, the festival in the Nevada desert known for rampant drug use.
For decades, though, researchers have shunned the study of psychedelics. “In the 1960s, they were on the cutting edge of neuroscience research and understanding how the brain worked,” Dr. Johnson said. “But then it got out of the lab.”
Research stopped, in part, because the use of mind-altering drugs like LSD and mushrooms became a hallmark of hippie counterculture.
The researchers who conducted the new study included Roland R. Griffiths, a professor in the departments of psychiatry and neurosciences at the Johns Hopkins University School of Medicine, who is one of the most prominent researchers on the behavioral and subjective effects of mood-altering drugs. The researchers reviewed data going back to the 1940s.
Dr. Johnson said that the F.D.A. had approved a number of trials of psilocybin. If its use is approved for patients, he said, “I see this as a new era in medicine.”
He added, “The data suggests that psychedelics are powerful behavioral agents.” In legal studies, he said, participants are given a capsule with synthetic psilocybin. (They are not given mushrooms to eat, which is how the drug is most often ingested.)
He warned, though, that psilocybin is not a panacea for everyone. In their analysis, the researchers called for strict controls on its use. There are areas of risk, too, for patients with psychotic disorders and anyone who takes high doses of the drug.
Kathie Grant and Lisa Byrne write in Public Health Matters that in November 2017, supermarket loyalty cards were used to trace the source of a large E coli outbreak affecting mainly men in England. Dr Lisa Byrne leads Public Health England’s surveillance of two key bacteria that lead to food poisoning – E Coli and Listeria. Dr Kathie Grant heads the PHE Gastrointestinal Bacteria Reference Laboratory. The two work together as part of a larger team dedicated to reducing foodborne illness and below tell us how they put the pieces of this puzzle together to find the source.
If you’ve ever had food poisoning you’ll know that feeling of mentally going through everything you ate recently, trying to pinpoint what it was that might have made you ill. It’s our job to do that at a national scale. We bring together lots of different pieces of information from the community and the lab to try to find the source of a food poisoning outbreak and then, working alongside other government agencies, ensure that more people don’t get sick.
We study and monitor many different stomach bugs – some of which you may never have heard of! While stomach bugs are a part of life, PHE works with organisations such as the Food Standards Agency and the Animal and Plant Health Agency to try and prevent them.
Every so often we see a spike in the number of cases. When this happens it is important that we find the link between the cases and the cause of their illness. To do this we need to identify the exact strain of a bug to understand if people have got ill from the exact same source.
Whole Genome Sequencing (WGS) ‒ a relatively new process for showing us the makeup of a bacterium or virus’s genes ‒ has changed the way we can find the cause of an outbreak and stop more people getting ill. You can learn more about the process and how it works in our explainer blog.
Before WGS it could take weeks to identify bacteria and sometimes the bacteria could be missed. This slowed down any investigations as we could not be sure that all the case histories we were taking could be linked to an outbreak – there was a lot of ‘noise’ and false lines of enquiry. With WGS, we can rapidly and accurately identify if bacteria of cases are the same strain and rule out people from our investigation who just happened to be ill at the same time, but with a different illness.
It has also expanded what the word ‘outbreak’ means as we can link cases across several years and different countries, meaning we can more accurately piece together a picture of how something in the food supply chain impacts human health.
Scientists working in the Gastrointestinal Bacteria reference laboratory at Public Health England. The team are processing samples from people who have reported gastrointestinal symptoms, to understand the exact cause of their illness.
Identifying the source of an outbreak is a lot like putting together a jigsaw puzzle, combining multiple pieces of evidence to get the full picture. Sometimes, a common source is obvious, such as when a group of people get ill after eating the same meal, at the same restaurant, on the same day. But other times, we need to use an arsenal of investigative tools, as was the case in a recent E coli outbreak.
In November 2017 our surveillance system alerted us to 12 cases of E coli O157 – (a particular form of E coli), over a six week window. E coliO157 is a relatively rare cause of food poisoning, with only about 700 cases a year, but it can cause a very severe illness. Because of this, any case of E coli O157 identified by doctors and laboratories must be reported to Public Health England. We monitor the number of cases with our surveillance systems to find any patterns.
Very quickly our reference laboratory used WGS which showed that the cases had the identical genetic “fingerprint” and the work began to trace the source of infection. The majority of people who became ill were men, which was unusual as E coli outbreaks are often linked to salad items ‒ traditionally more likely to be eaten by women.
It took a few rounds of interviews – carried out by colleagues in local authorities – to zero in on the potential source of food poisoning, and a picture started to emerge that implicated burgers from a particular retailer.
We asked the supermarket to analyse the loyalty card records of those who had become ill, to help identify the particular burger product the cases had eaten. As you can imagine, there were many different types of burgers supplied by the supermarket and it’s often difficult for people to remember exactly what they ate.
Working with the Food Standards Agency we were able to identify that all the cases had bought a particular brand of burger, leading to a product recall to ensure others didn’t get sick. The recall involved removing all the suspected batches of burgers from the supermarket shelves. The supermarket also contacted people who had bought the burgers, advising them not to eat them and return them for a refund.
Sometimes, as in this case, we can rapidly find what is making people ill and quickly remove it from sale. It’s an exciting role and we get a real sense of satisfaction out of using our skills to help people in this way. Other times it can be more frustrating – some outbreaks remain unsolved and it’s a real worry that people will get sick because we can’t eliminate a threat from food distribution.
The role really keeps us on our toes. Our surveillance systems mean that we have a good sense of patterns of illness across the year and how we can intervene to stop people getting unwell – but changes to food habits can catch us by surprise. For instance, raw milk has become more popular recently, bringing with it all the disease risks you would expect from a product that has come straight from a cow without any treatment to kill off bacteria!
In another case, eight people in the UK were affected while on holiday in Germany that was related to seeds. The seeds were decoratively used as a garnish on salads and were difficult for cases to remember eating. Nearly 1,000 people in Germany got ill in that outbreak and one of the approaches by authorities was to use tourist photos of food to try and identify the common item in meals that could be making people sick.
Solving food borne illness outbreaks can be a real challenge, but by using a variety of the different tools available to us we can quickly intervene to stop people getting ill.
For the past several years I’ve been part of the home food preservation competition at the NC State Fair. Every year, going back decades, people from all over our state bring their pickles, jams and preserves to Raleigh to compete for big prizes – including best in show.
The 2018 competition is tomorrow. A bunch of phenomenal volunteers spent this afternoon looking through recipes and checking processing times. A few products get their pH tested to make sure our judges don’t get botulism.
Last year, Our State covered the completion, and wrote some great stuff. My favorite being,
By 10:30, the hostess cart is operating with smooth efficiency, transporting jars of gherkins and dills, jams and jellies to their appropriate tables. The sugar rush has hit. The bracing smack of brine has loosened tongues. And the atmosphere inside the Education Building has turned bubbly, like a cocktail party. Jar seals are popping (a good sign!), pencils are scribbling (“Let’s make sure we’re thoughtful about giving feedback,” urges Chapman), and entries with rusty lids, stray hairs, or odd-looking weblike things hiding under screw tops are delicately set aside.
Anna Doherty, 19, spent 11 days in intensive care after being struck down with an E. coli infection at the same Egyptian resort where two British tourists died because of E. coli.
After visiting the on-site doctors’ clinic, Anna said she was told she had a water infection and was given an injection and antibiotics.
She began to feel better, but when she returned home to the UK, her condition rapidly deteriorated.
Anna said her family rushed to the Royal Oldham Hospital and she was quickly transferred to The Royal Liverpool Hospital with suspected jaundice.
Doctors in Liverpool originally suspected Anna was suffering from ‘hemolytic uremic syndrome,’ which is commonly caused by a complication from an infection with E coli O157.
They were unable to give a final diagnosis, she said, but believe the previously healthy teenager was struck by a bacterial infection.
Anna told the Manchester Evening News: “It was really scary. I never expected to go away and get this ill.
Tests showed that E. coli was behind the death of two British tourists in a hotel in Egypt’s Red Sea resort of Hurghada, the country’s chief prosecutor said in Sept.
Forensic tests showed that John Cooper, 69, suffered acute intestinal dysentery caused by E. coli, and Susan Cooper, 64, suffered hemolytic-uremic syndrome (HUS), likely because of E. coli, Sadek said.
