Hamburger safety videos: Who’s the bullshitter, UK or US?

How can two different countries come up with two different recommendations – yet equally cheesy videos – on the basics of hamburger food safety?

Value assumptions in risk assessments.

My guess would be the UK Food Standards Agency thinks consumers can’t handle thermometers so they provide misguided and meaningless risk messages. And when talking about steaks, they don’t talk about needle- or blade tenderized steaks, in which the outside is pushed into the inside.

The U.S. Department of Agriculture gets the science right, but fails to expand beyond the simplistic cook-chill-clean-separate mantra and doesn’t mention sourcing food from safe sources, like the World Health Organization does.

I provide information. You decide.


I don’t see color, it doesn’t matter: UK hamburger edition

Don’t burger up your bank holiday.

Get it? Don’t bugger it up? Burger it up?

barfblog.Stick It InThose bureaucrats at UK’s Food Standards Agency are really yukking it up, focused on stupid jokes rather than evidence-based communications.

FSA has long been in its own undersirable class when talking about food safety risks, and class is so very important to the Brits.

FSA is great is talking at people rather than talking with people (a huge difference, like educating versus providing information).

FSA’s idea of risk communication is to commission a meaningless survey – people lie, especially about food and drink – which found that despite 71% of people stating that they are concerned about food poisoning, over a third (36%) of Brits would eat a burger that isn’t fully cooked through. More than one in 10 said that they actually prefer burgers cooked this way.  When cooking them at home 81% of those admit to undercooking them. So we at the FSA are encouraging all those who are getting their barbecues out this weekend to ensure they cook their burgers all the way through – until steaming hot throughout, there’s no pink meat in the middle and the juices run clear.

Those scientifically meanginless terms – steaming hot, no pink – have featured prominently in FSA foodsafetytalk for years, with steaming hot replacing piping hot.

Lead FSA policy thingy said something that is not worth repeating because it ignores the risks associated with needle-tenderized steaks.

And we’ve been over this so many times before.

The BBC repeated the advice verbatium in its latest version of PR blowjobs rather than something resembling journalism.

Use a thermometer and stick it in.

And now this.


2 students at UK school sickened with E. coli O157

Paul Cargill of the Daily Record writes that a Perth Academy pupil is recovering at home after being struck down by E. coli O157.

The sixth year pupil’s mother, who did not want her son to be named, told the PA he was doing well after coming down with the stomach bug following an expedition which was organised through the school.

Duke of Edinburgh Gold Award tripIt is understood that at least one other Perth Academy pupil took ill with the same strain of the bug after returning from a Duke of Edinburgh Gold Award trip, which took place two weeks ago.

The two boys did not return to school this week as expected and the mother who talked to the PA yesterday, confirmed her son was being kept off school to recover.

Consultant in public health medicine Dr Daniel Chandler told the PA: “We can confirm that NHS Tayside and Perth and Kinross Council are together investigating a small number of linked cases of E coli O157 infection.

“Those affected have received appropriate medical treatment and advice.

“Possible sources are currently being investigated and control measures have been put in place to prevent further spread.”

How can that be if the source is unknown? Maybe person-to-person transmission can be limited, but there did it come from originally?

‘Timing couldn’t have been better’ 40 sickened with E. coli O157 at Richey reunion

It was supposed to be unforgettable, but for some who attended the Richey, Montana, Centennial last month, it was unforgettable for the wrong reasons.

Richey1Around 40 people from 10 states reported they had been infected with E. coli O157.

At least seven were hospitalized, and six Montana counties have been affected.

“If you had to have a foodborne outbreak, the timing couldn’t have been better,” says Jennifer Fladager, Dawson Co. Emergency Preparedness Coordinator.

Fladager had relatives who attended the celebration. She says staff members were prepared for this outbreak.

“We were aquatically trained and prepared for something like this. It’s rather ironic, we were just at a public health summer institute and we went over how to properly conduct case interviews with foodborne illness,” says Fladager.

Investigators say they have nearly completed their investigation and are working with the caterer to determine how the meal became contaminated.

It’s all over now: Another UK E. coli O157 mystery with hundreds sick

There’s a reason the Britain’s contribution to global cuisine is mushy peas and mad cow disease.

mushy.peasI get the UK is a small island, sinking in all kinds of animal shit, but tell us what you are doing for on-farm food safety?

And don’t answer with some bogus certification scheme.

Beginning in December 2010, a subtype of E. coli O157, began sickening Brits and resulted in over 250 sick with 80 hospitalizations, four with hemolytic uremic syndrome, and one death.

Dr. Andrew Wadge, chief scientist at the Food Standards Agency was reported as saying “This outbreak is a timely reminder that it is essential to wash all fruits and vegetables, including salad, before you eat them, unless they are labeled ‘ready to eat’, to ensure that they are clean. It is also important to wash hands thoroughly as well as clean chopping boards, knives and other utensils after preparing vegetables to prevent cross contamination.”

This advice is of limited use. Maybe a 1-log reduction use.

But it blames consumers.

The outbreak was linked to the handling of raw leeks and potatoes, and a public warning was given – reportedly months after a guidance had been issued the food industry on reducing the risk of E. coli cross-contamination.

In Nov. 2015, the BBC reported the number of people infected with E. coli across England rose by more than 1,000 over the previous year.

Public Health England figures show there were 39,604 from September 2014 to September 2015, compared with 38,291 for the same period the year before.

Another mysterious affliction.

Now, once again, the PhD health types are baffled by an outbreak of E. coli O157 in the UK that has sickened at least 161.

Those same health-thingies do say the likely cause of the outbreak was imported mixed salad leaves.

The last recorded case of the bug was on July 5 and now PHE has declared the outbreak over.

People are being urged to remove any loose soil before storing vegetables and thoroughly wash all vegetables and salads that will be eaten raw unless they have been pre-prepared and are labelled ‘ready to eat’.

Because the Brits have a long history of blaming consumers for something that should be controlled on the farm.

It wasn’t us: Cheese firm ‘blamed’ for E. coli outbreak slams ‘untrue’ claims

Jane Bradley of The Scotsman reports that Humphrey Errington, owner of Errington Cheeses, which manufactures Dunsyre Blue cheese, says it was “untrue” the cheese was the likely source of an E. coli O157 outbreak last month. said that all Dunsyre Blue had tested negative for E.coli and claimed that most of the people who had been diagnosed with the illness and not eaten any blue cheese. Health Protection Scotland said on Friday that the number of people with the infection had risen to 19.

“Health Protection Scotland’s claim that the 19 ill people had consumed Dunsyre Blue is untrue according to the data which they themselves have released; of the 19 ill people, seven may have eaten blue cheese (not necessarily Dunsyre Blue); some never ate any blue cheese.

“We can now say with absolute confidence that, following comprehensive tests and the examination of them by an independent expert microbiologist, there is no evidence whatever for any link to the recent outbreak of illness; the government agency tests have all also proved negative.

“We have to conclude that the HPS/FSS position is based on a malicious prejudice against raw milk cheese, and that this threatens not just our business but the reputation of the whole British artisan cheese industry, one of the great success stories of recent years.”

A spokeswoman for Health Protection Scotland said that Dunsyre Blue “remains the most likely source of this outbreak,” adding, “Based on the detailed information available to the multi-agency team, Dunsyre Blue cheese remains the most likely source of this outbreak, with confirmed cases becoming unwell between July 2 and 15. It would not be appropriate to respond in more detail at present as investigations have not yet concluded. However a formal outbreak report will be produced by the Incident Management Team after the investigation is declared over.”

Fancy food ain’t safe food: 19 sick with E. coli in UK from Dunsyre Blue cheese

Another case of E. coli has been confirmed in an outbreak believed to be linked to blue cheese made in Lanarkshire, 16 people were diagnosed with the strain of E. coli O157 with the number of those affected rising to 18 earlier this month.

Health Protection Scotland (HPS) confirmed on Friday that another case has been diagnosed.

The cases developed symptoms between July 2 and 15.

HPS has been working with Foods Standards Scotland (FSS), NHS boards and local authority environmental health teams to investigate and manage this outbreak.

All patients, the majority of whom live in Scotland, are recovering at home, HPS said.

Officials are advising that – as a precaution – Dunsyre Blue cheese purchased between mid-May and the end of July with the batch codes C22 or D14 should not be eaten.

We’re all hosts on a viral planet, plants too

I studied Verticillium in tomato plants in my aborted MSc degree.

Journalism was more fun, and my hands were black from the printing press instead of green (yes, I am that old).

tomato.cmvLaurel Hamers of Science News writes that instead of destroying its leafy hosts, one common plant virus takes a more backhanded approach to domination. It makes infected plants more attractive to pollinators, ensuring itself a continued supply of virus-susceptible plant hosts for generations to come.

The strategy might be a way for the virus to discourage resistance from building up in the plant population, University of Cambridge biologist John Carr and colleagues report online August 11 in PLOS Pathogens.

“It looks like the pathogen is cheating a little bit —but in a way that helps its host,” says Carr.

Plants give off cocktails of volatile chemicals that send signals to pollinators, predators and other plants. Carr and his team found that tomato plants infected with cucumber mosaic virus gave off a different cocktail of these chemicals than non-infected plants — and that bumblebees preferred the infected plants’ brew.

That’s a small consolation for plants that have been stunted and blemished by cucumber mosaic virus. When infected tomato plants relied on self-fertilization, they produced fewer seeds on their own than their healthy counterparts. But when bumblebees helped out, infected plants’ seed production matched healthy ones.

The virus benefits, too, Carr says. By ensuring that sick plants can still reproduce, “those genes enabling susceptibility to the virus will stay in the population.” And plants that are resistant to the virus can’t gain the foothold that they could if all the sick plants died too soon.

The team also found that cucumber mosaic virus changes plants’ chemicals by disrupting their natural defenses against disease.

Normally, plants can identify when bits of foreign genetic material (like those from a virus) have worked their way inside. Specialized silencing enzymes snap into action and chop up the foreign invaders. But a cucumber mosaic virus protein called 2b disrupts this process by binding to the silencing molecules so that they can’t do their job, Carr and his colleagues found.

That lets the virus infect the plant more easily— and it also changes the way the plant turns its genes on and off. When the researchers tested a virus that didn’t have the gene for the 2b protein, the infected plants didn’t shift the chemicals they gave off like the plants infected with the fully functioning virus did.

The link between the 2b protein and volatile production is a major finding that could help scientists to better understand how viruses manipulate their hosts, says Andrew Stephenson, a biologist at Penn State University who wasn’t involved in the work.

But further research is needed to convincingly show that the increased pollination is really a fitness benefit for the plant, Stephenson says. Even though the infected plants produced more seeds, those seeds could be smaller and less likely to germinate, he says. And the shift in chemical production could lure aphids (which transmit the virus from plant to plant) just as much as bumblebees.  

Rockmelon safety hard to grasp

Contrary to what Australians are being told, cantaloupe – er, rockmelon – is a known source of foodborne illness and many scientists have investigated the many ways nasty bacteria get on or in the melon; along with potential treatments.

red.dirt.melonsIn this paper, researchers from the U.S. Department of Agriculture report surface structure and biochemical characteristics of bacteria and produce play a major role in how and where bacteria attach, complicating decontamination treatments.

Whole cantaloupe rind surfaces were inoculated with Salmonella, Escherichia coli O157:H7, and Listeria monocytogenes at 107 CFU/ml. Average population size of Salmonella, Escherichia coli O157:H7, and L. monocytogenes recovered after surface inoculation was 4.8 ± 0.12, 5.1 ± 0.14, and 3.6 ± 0.13 log CFU/cm2, respectively. Inoculated melons were stored at 5 and 22°C for 7 days before washing treatment interventions. Intervention treatments used were (i) water (H2O) at 22°C, (ii) H2O at 80°C, (iii) 3% hydrogen peroxide (H2O2) at 22°C, and (iv) a combination of 3% H2O2 and H2O at 80°C for 300 s. The strength of pathogen attachment (SR value) at days 0, 3, and 7 of storage was determined, and then the efficacy of the intervention treatments to detach, kill, and reduce transfer of bacteria to fresh-cut pieces during fresh-cut preparation was investigated. Populations of E. coliO157:H7 attached to the rind surface at significantly higher levels (P < 0.05) than Salmonella and L. monocytogenes, but Salmonella exhibited the strongest attachment (SR value) at all days tested. Washing with 3% H2O2 alone led to significant reduction (P < 0.05) of bacteria and caused some changes in bacterial cell morphology. A combination treatment with H2O and 3% H2O2 at 8°C led to an average 4-log reduction of bacterial pathogens, and no bacterial pathogens were detected in fresh-cut pieces prepared from this combination treatment, including enriched fresh-cut samples.

The results of this study indicate that the microbial safety of fresh-cut pieces from treated cantaloupes was improved at day 6 of storage at 5°C and day 3 of storage at 10°C.

Effect of hydrogen peroxide in combination with minimal thermal treatment for reducing bacterial populations on cantaloupe rind surfaces and transfer to fresh cut pieces


Ukuku, Dike O.1; Mukhopadhyay, Sudarsan2; Geveke, David2; Olanya, Modesto2; Niemira, Brendan2

1: U.S. Department of Agriculture, Agricultural Research Service, Eastern Regional Research Center, 600 East Mermaid Lane, Wyndmoor, Pennsylvania 19038, USA;, Email: 2: U.S. Department of Agriculture, Agricultural Research Service, Eastern Regional Research Center, 600 East Mermaid Lane, Wyndmoor, Pennsylvania 19038, USA

Journal of Food Protection, August 2016, Number 8, Pages 1316-1324, DOI:

Cattle be shedding STECs

Shiga toxin-producing Escherichia coli (STEC) is an important foodborne pathogen that can cause hemorrhagic colitis and hemolytic-uremic syndrome. Cattle are the primary reservoir for STEC, and food or water contaminated with cattle feces is the most common source of infections in humans.

beef.cattleConsequently, we conducted a cross-sectional study of 1,096 cattle in six dairy herds (n = 718 animals) and five beef herds (n = 378 animals) in the summers of 2011 and 2012 to identify epidemiological factors associated with shedding.

Fecal samples were obtained from each animal and cultured for STEC. Multivariate analyses were performed to identify risk factors associated with STEC positivity. The prevalence of STEC was higher in beef cattle (21%) than dairy cattle (13%) (odds ratio [OR], 1.76; 95% confidence interval [CI], 1.25, 2.47), with considerable variation occurring across herds (range, 6% to 54%). Dairy cattle were significantly more likely to shed STEC when the average temperature was >28.9°C 1 to 5 days prior to sampling (OR, 2.5; 95% CI, 1.25, 4.91), during their first lactation (OR, 1.8; 95% CI, 1.1, 2.8), and when they were <30 days in milk (OR, 3.9; 95% CI, 2.1, 7.2). These data suggest that the stress or the negative energy balance associated with lactation may result in increased STEC shedding frequencies in Michigan during the warm summer months.

Future prevention strategies aimed at reducing stress during lactation or isolating high-risk animals could be implemented to reduce herd-level shedding levels and avoid transmission of STEC to susceptible animals and people.

STEC shedding frequencies vary considerably across cattle herds in Michigan, and the shedding frequency of strains belonging to non-O157 serotypes far exceeds the shedding frequency of O157 strains, which is congruent with human infections in the state. Dairy cattle sampled at higher temperatures, in their first lactation, and early in the milk production stage were significantly more likely to shed STEC, which could be due to stress or a negative energy balance. Future studies should focus on the isolation of high-risk animals to decrease herd shedding levels and the potential for contamination of the food supply.

Factors associated with Shiga toxin-producing Escherichia coli shedding by dairy and beef cattle

Cristina Venegas-Vargasa*, Scott Hendersona,b, Akanksha Khareb*,Rebekah E. Moscib, Jonathan D. Lehnertb*, Pallavi Singhb,Lindsey M. Ouelletteb*, Bo Norbya, Julie A. Funka, Steven Rustc, Paul C. Bartletta,Daniel Groomsa and Shannon D. Manningb

aDepartment of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, USA

bDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA

cDepartment of Animal Science, Michigan State University, East Lansing, Michigan, USA

Applied and Environmental Microbiology, August 2016, Volume 82, Number 16, Pages 5049-5056, doi:10.1128/AEM.00829-16