Known impossibles

There are a number of known knowns say food safety types and they insist that we follow their sometimes impracticable or impossible advice. But is scientific opinion always right?

Impossible hand washing advice


The ever important hand wash (Photo: Marmotto)

They want us to wash our hands for an impossible 20 seconds. It doesn’t sound much but you stand there with cold hands since it might take more than 20 seconds for the warm water to flow through the long pipe.

Well, Health Canada is a little more sensible reducing the washing time to 15 seconds but insisting it should be warm water. However, contrary to popular belief scientific studies have shown that using warm instead of cold water has no effect on reducing the microbial load on hands. Scientific results also show that soap is more effective than water only and drying with a paper towel is preferable to using hand driers for removing the bugs on your hands.

So the practical recommendation? Above all wash your hands before preparing food with a method you feel comfortable with.

Impossible fruit and vegetable advice

They want us to eat 2 portions of fruits and 5-6 portions of vegetables per day. Translated to weight that would be 300 grams of fruit and 450 grams of vegetables or a full 750 grams in total on a daily basis. Are they mad, there will be no place for anything else.

However, to be fair a meta study showed that a diet with more than five servings of fruit and vegetables reduces a person’s risk of developing conditions such as heart disease and diabetes. But according to the Australian Bureau of Statistics, in 2014-15, while half of Australians aged 18 years and over met the guidelines for recommended daily serves of fruit (2 or more serves), only 7% met the guidelines for serves of vegetables (5-6 or more serves). A paltry one in twenty adults met both guidelines.

See what I am saying? And the situation is similar in many other countries. So the practical recommendation? Sure, try to increase your consumption of fruit and vegetables. An extra leaf of lettuce and a tomato on your lunch sandwich might help.

Impossible rule change for dropped food


A dropped slice of chocolate cake might be rescued.

And now we cannot follow the 5-second rule any longer, that is if you drop a piece of food on the floor but pick it up within 5 seconds you are safe to still eat it. What a waste of food. Just imagine you drop a nice slice of chocolate cake on the floor but pick it up immediately before the dog can take it and you still have to throw it away. No way I would say and by the way chocolate is dangerous for dogs so you have to be quick anyway.

Though scientists have backed up the new advice. They experimented with different food and contact surface types and concluded that the 5-second rule is a significant oversimplification of what actually happens when bacteria transfer from a surface to food. Bacteria can actually contaminate the food instantaneously. The scientists demonstrated that the 5-second rule was relevant in the sense that longer contact time resulted in more bacterial transfer, but factors like the nature of the food and the surface it falls on are of equal or greater importance.

And the practical recommendation? Obviously it doesn’t help to be quick, the bugs will still beat you. But you might wash off a hard surface and scrape off a little bit of the chocolate cake before eating the rest. If the food is still to be heated there is no problem. But a buttered sandwich surface down might be best to put in the garbage bin.

Impossible fiddling with temperature probes

They also say that when you prepare your hamburgers you cannot rely on your visual senses anymore. That is colour, firmness and smell are not considered sufficient. You have to use a digital thermometer and make sure that the centre of the hamburger reaches 71ºC. You have to fiddle with the thermometer tip sticking it into the side of the burger to reach all the way to the middle while at the same time avoiding getting your fingers burnt. And you have to do it for each burger separately.

Scientists explain that heat-induced denaturation of myoglobin, responsible for the characteristic dull-brown colour of cooked meats, is influenced by a multitude of factors. The interactions between these factors critically influence the internal cooked colour and can confuse the consumers who often wrongly perceive cooked colour to be a reliable indicator for doneness and safety. But there are some hope. Another scientific study agreed that colour alone was a misleading guide for the core temperature of a hamburger. However, when including texture of the meat and clarity of the meat juice in the judgement the situation improved.

And the practical recommendation? It might pay off to invest in a meat thermometer but once familiar with the cooking time needed to reach the recommended core temperature a bit more flexibility might be possible. As long as you promise to not eat rare or medium-rare hamburgers.

Impossible cross-contamination prevention


Use different cutting boards to avoid cross-contamination. 

And there’s more. You are not allowed to keep the same cutting board and utensils you just used to cut your raw chicken for subsequently preparing your vegetables to eat without further heating. Come on, the food will be cold before you have done all the washing up.

Well, I am sorry to say that scientists are unequivocal on this point. You just have to use different utensils for raw and cooked meat and utensils that have been in contact with raw meat can never be used for produce that will be consumed without further heating.

Known unknowns and unknown unknowns

For all the food safety rules for known knowns, there is little said for the known unknowns that we might worry more about.

What about the bisphenol A in our food packaging material and cash register receipts? There have been several reports of damaging endocrine effects on unborn babies, but this science is still controversial so you’re on your own on this one.

And of course nothing can be said about unknown unknowns.

Acrylamide, a carcinogen, has been present in some heated foods since time memorial following the invention of fire. But it was not until the late 20th century that it was detected by a coincidence. Since then there have been many attempts to reduce its presence in food.

What else is lurking around? That is impossible to say so better relax. Overall, a balanced diet is the best protection for a healthy life. Stay sufficiently safe to stay healthy might be the best motto!

Campylobacter in the headlines

Chicken a time bomb for campylobacteriosis (Photo: Eyal Bairey)

Chicken a time bomb for campylobacteriosis (Photo: Eyal Bairey)

You’re a brave soul, you’ve just bought raw chicken to cook for dinner. You tremble a bit when you start opening the meat tray, but with gloves on and mouth protection you feel relatively safe. The difficulty is not to spill any fluid on the kitchen bench and to make sure that the cutting board and utensils used are promptly put into the dishwasher. With a sigh of relief everything is in hand, chicken in the frying pan and gloves in the garbage bin. You can’t be sure but the next few days will prove if you’ve been successful and protected the family from campylobacteriosis.

Leading cause of gastroenteritis

Campylobacteriosis is a leading cause of human gastroenteritis in the developed world and has been estimated to cost the society around US$4 billion annually in the USA alone. As the name of the disease implies, it is caused by Campylobacter species, literally curved rods, a reflection of the Greek meaning of the name and the way they look. Campylobacter jejuni is the dominating species causing 90% of human campylobacteriosis, with most of the rest caused by Campylobacter coli, both ubiquitous in nature and found in the gut of farm animals where they thrive at temperatures between 37 to 42℃ causing very few ill effects.

Most people who become ill with campylobacteriosis get diarrhoea, cramping, abdominal pain, and fever within two to five days after exposure to the organism. Foodborne illness caused by Campylobacter can be severely debilitating, but is rarely life-threatening. The diarrhoea may be bloody and can be accompanied by nausea and vomiting. The illness typically lasts about one week. On rare occasions there are some long-term consequences of this infection, called sequelae, beginning several weeks after the diarrheal illness. Some people develop arthritis. Others develop a rare disease called Guillain-Barré syndrome that affects the nerves of the body resulting in paralysis and requiring intensive medical care. It is estimated that approximately one in every 1,000 reported Campylobacter illnesses leads to Guillain-Barré syndrome.

Chicken the most common source

Only 500 Campylobacter organisms needed to get ill (Photo: ARS)

Only 500 Campylobacter organisms needed to get ill (Photo: ARS)

Chicken meat is the most common source of campylobacteriosis in most countries. It only takes less than 500 Campylobacter organisms to make you sick. Even one drop of juice from raw chicken meat can carry enough Campylobacter to infect a person. The most common way of getting infected is to cut raw poultry meat on a cutting board, and then use the unwashed cutting board or utensils to prepare vegetables or other raw or lightly cooked foods. The Campylobacter organisms from the raw meat thus get onto the other foods through cross-contamination. So now you can see that the precautions suggested above is not completely crazy.

Finding Campylobacter bugs on chicken carcasses is nothing new, what is new is the recent publicity in the UK. There was no publicity ten years ago when around 1,000 raw poultry products were purchased from butcher shops, supermarkets, and specialty stores in New South Wales and South Australia and Campylobacter was found on 87.8 and 93.2% of the carcasses in the respective state. As a matter of fact the then Minister put the lid on the findings and they were later only allowed to be published in a scientific journal without much attention. Although the UK Food Standards Agency tried to do the same, they had to relent to public pressure. Now we know that following six months of testing, an average of 70% of supermarket chickens proved positive for Campylobacter on samples of skin in the UK supermarkets. Admittedly, the number of bugs on each carcass can be quite low, but in the UK case they found that 18% of the nearly 2,000 chickens tested contained the highest levels of Campylobacter that easily can make people sick.

Possible to reduce contamination

This is just not good enough. New Zealand has been affected most badly by campylobacteriosis. In the early 1980s campylobacteriosis became a notifiable disease in New Zealand and evolution of the disease could be followed. At a peak in 2006 the disease affected around 350 people out of every 100,000 of the population. That year a number of voluntary and regulatory interventions to reduce Campylobacter contamination of poultry were introduced by government and industry. And two years later the rate of the disease had more than halved. This apparent success proved that it is possible to produce chicken meat with a much reduced Campylobacter contamination rate.

Let’s demand that the chicken sold irrespective of country should be free of Campylobacter to the extent possible. It is ridiculous the way that farmers have been pressured to reduce costs and take shortcuts to be competitive. It is time for the whole industry to shape up and invest in sustainable production practices. It might make chicken slightly more expensive but it will save money in the long run for the society as a whole.

The fight for your attention

Cravings for a doughnut might be blamed on the microbiome (Photo: Makoto Satsukawa)

Cravings for a doughnut might be blamed on the microbiome (Photo: Makoto Satsukawa)

You’re working along doing your usual stuff and suddenly you feel a hunger pang. And you don’t just feel hungry, you crave fatty food. If you had a Krispy Kreme doughnut ready you would gulp it down. But fortunately there is none within reach. There are conflicting signals and you change your mind. Now you have a craving for sugar and you stretch for the Coke. You know you shouldn’t but you still do it. What’s happening here?

Your microbiome at work

You remember the microbiome we have written about in previous blogs, the 100 trillion bacteria in your gut that outnumber your own cells about 100-fold? They help breaking down your food, fighting off infections and nurturing your immune system. It’s a lovely, invisible garden that play a crucial role in your well-being. However, even if it sounds like science fiction, it seems they are not content with limiting their activity to the gut, but may very well affect both your cravings and mood to get you to eat what they want.

Bacterial species vary in the nutrients they need. What that means is that some for instance prefer fat, and others sugar. The creepy part is that they not only vie with each other for the food they need to try to retain a niche within the digestive tract, they also try to make sure that you select the food they need. Different species of microbes thrive on different kinds of food. If they can prompt us to eat more of the food they depend on, they can multiply.

Researchers in reviewing the recent scientific literature concluded that microbes in the microbiome influence human eating behaviour and dietary choice to favour consumption of the particular nutrients they grow best on, rather than simply passively living off whatever nutrients you choose to send their way. There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals, and others not. Of course it makes sense for them, but the question is how they have the means to influence what you eat.

Signalling systems at work

While it is unclear exactly how this occurs, the research team believes this diverse community of microbes may influence our decisions by releasing signaling molecules into our gut. This alone might not send any red flags, but because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence your physiologic and even your own behavioural responses.

Research suggests that gut bacteria may be affecting your eating decisions in part by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain. Microbes have the capacity to alter the neural signals in the vagus nerve, changing taste receptors, producing toxins to make you feel bad, and releasing chemical rewards to make you feel good.

Who is the puppet master?

Who is the puppet master? (Photo: Luc De Leeuw)

Who is the puppet master? (Photo: Luc De Leeuw)

Fortunately, it’s not a one-way street. In turn your own diet choice will have a huge impact on the microbial population in your gut. It’s a whole ecosystem, and it’s evolving on the time scale of minutes. You can influence the composition of the microbiome by deliberately change what you eat, with measurable changes in the microbiome within 24 hours of a diet change.

This may be accomplished through food and supplement choices, by ingesting specific bacterial species in the form of probiotics, or by killing targeted species with antibiotics. Because the microbiome is easily manipulated by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota might offer a possible approach to otherwise difficult problems of obesity and unhealthy eating. Optimising the balance of power among bacterial species in our gut might allow us to fight obesity and live more healthier lives.

We are only beginning to scratch the surface of the importance of the microbiome for human health. Targeting the microbiome could open up possibilities for preventing a variety of diseases from obesity and diabetes to cancers of the digestive tract. Although it is early days, it might pay off to attempt to be in charge of what you eat, now when you know the sneaky impact of your own bugs. Try to be your own puppet master.

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Be kind to your gut microbiota

The gut microbiota important for well being (Photo: Wikimedia)

The gut microbiota is important for our well being (Photo: Wikimedia)

We have written about it before, but to be honest you might not want to know the details of what is inside your gut. I can tell you, though, that it is very important for your well being. In case you got curious, it is called the gut microbiota, a mix of maybe 100 trillion microorganisms, and can weigh up to 2 kilograms that you carry around with you on a daily basis.

Why not deduct it when you next step on the scale? It should be fair enough.

One third of our gut microbiota is common to most people, while two thirds are specific to each one of us. That is to say that the microbiota in your intestine is like an individual identity card. Not that anyone will use it as such, I wouldn’t think.

A most complex ecosystem

The large number of different microbial communities that can be found in the human gut and their impact on human health and disease is a most exciting new area of research. The gut microbiota contains a vast number of microorganisms from all three domains of life, including bacteria, fungi, and viruses. These interact in a complex way to contribute to our well being. It has long been a dark corner of missing knowledge, but the application of advanced DNA sequencing technology has been of an immense help in starting to better identifying the inhabitants.

The microorganisms in the gut can be broadly divided into prokaryotes (bacteria and archaea), bacteriophages (viruses that infect prokaryotes), eukaryotic viruses, and the meiofauna (microscopically small benthic invertebrates that live in both marine and fresh water environments — primarily fungi and protozoa). Of these, bacteria have been the most extensively studied. The gastrointestinal tract is now considered one of the most complex microbial ecosystems on earth and understanding how the multiple communities interact presents both opportunities and challenges.

Competitive pressure

And there is a life and death fight between the different kinds of inhabitants. It has long been known that the bacteria in the gut play an important role in both health and disease. It is also now becoming clear that the non-bacterial microbiota interacts in a complex way with the bacterial microbiota to contribute to these processes. The most common viruses in the gut are the bacteriophages. They infect and destroy bacterial cells and also have the ability to transfer genetic material from one bacterium to another, with potentially profound implications for health and disease.

There is a predator–prey relationship between bacteriophages and bacteria that can change the composition of the bacterial microbiota in conditions such as inflammatory bowel diseases. Bacteriophages induce immune responses in bacteria and transmit genomic material into bacteria that may alter their function. It makes them extremely important and we have only started to scratch the surface of understanding what they do.

There is also a fight between fungi and bacteria. Decreases in fungal diversity have been shown to be associated with an increase in healthy bacterial colonisation following probiotic therapy, suggesting niche competition between fungi and bacteria.

But there are disturbing signs

Antibiotics are valuable, potentially life-saving tools that have significantly reduced human morbidity and mortality. Unfortunately, antibiotics may also have unintended consequences from their off-target effects that may increase the risk of many long-term conditions. Recently,  a possible link has been detected between antibiotic use in childhood and weight gain—with disruption to the normal gut microbiota considered the most likely cause.

It has also been suggested that over-use of antibiotic therapy might be fueling the dramatic increase in conditions such as obesity, type-1 diabetes, inflammatory bowel disease, allergies and asthma, which have more than doubled in prevalence in many populations. There is evidence that microbiota resilience decreases with each subsequent course of antibiotics and that, once disrupted, the normal microbiota may never recover completely or it may be replaced by resistant organisms.

So be kind to your gut microbiota

Low-fat yoghurt good for health claim researchers

Probiotics in fermented food can restore the gut microbiota

Take good care of your gut microbiota. The food you eat can have a profound effect.

Many studies have demonstrated the beneficial effects of prebiotics and probiotics on our gut microbiota. Serving as “food” for beneficial bacteria, prebiotics help improve the functioning of microbiota while allowing the growth and activity of beneficial bacteria.

Present in some fermented products such as yoghurt, probiotics help gut microbiota keep its balance, integrity and diversity. Although authorities are still to be convinced of the cause and effect of individual preparations on the growth of beneficial bacteria to award any of them a health claim status.

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Foodborne hepatitis E infection

The ever important hand wash (Photo: Marmotto)

The ever important hand wash (Photo: Marmotto)

So you’ve heard of the hepatitis A virus? Then you probably know that hepatitis is the name of an inflammation of the liver. Hepatitis A is a foodborne disease usually spread by the fecal-oral route, disgusting as it sounds. Hand washing anyone? It is transmitted person-to-person by ingestion of contaminated food or water or through direct contact with an infectious person. Tens of millions of individuals worldwide are estimated to become infected with the hepatitis A virus each year. The infection is self-limited and doesn’t result in chronic infection or chronic liver disease. However, 10–15% of patients might experience a relapse of symptoms during the six months after acute illness. Acute liver failure from hepatitis A is rare. A vaccine is available and vaccination is often recommended when visiting countries with poor hygiene conditions.

And hepatitis B virus? This can be found in blood and body fluids, such as semen and vaginal fluids, so it can be spread during unprotected sex or by sharing needles to inject drugs.  The disease has caused epidemics in parts of Asia and Africa, and it is endemic in China. About a third of the world population has been infected at one point in their lives, including 350 million who are chronic carriers. National and regional prevalence ranges from over 10% in Asia to under 0.5% in the USA and northern Europe.  According to the World Health Organization (WHO), an estimated 600,000 people die every year related to the infection. But most people infected with hepatitis B are able to fight off the virus and fully recover from the infection within a couple of months. The infection can be unpleasant to live with, but usually causes no lasting harm. A vaccine is available, which is recommended for people in high-risk groups, such as injecting drug users.

What about hepatitis C, you might be familiar with that disease as well? The hepatitis C virus is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment and transfusions. The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer or life-threatening dilation of blood vessels in the oesophagus or stomach called varices. Hepatitis C is the leading reason for liver transplantation, though the virus usually recurs after transplantation. No vaccine against hepatitis C is available.

You can almost forget about hepatitis D virus. It is only present in people already infected with hepatitis B, since it needs the presence of the hepatitis B virus to be able to survive in the body. So the worry is more the hepatitis B virus.

Now this blog was supposed to deal with the hepatitis E virus, a less commonly known variety of the hepatitis family of five virus strains. Hepatitis E infection is very similar to the hepatitis A disease and it is also a foodborne disease. Symptoms of hepatitis E are usually flu-like causing fever, abdominal pain, nausea, muscle and joints aches and loss of appetite. Jaundice is very common in hepatitis E infection, but it is possible to have the disease and not show any symptoms. It is a self-limited disease in most cases, that is it usually requires no medical treatment and will eventually be healed by the bodies immune system. However, during the duration of the infection (usually several weeks), the disease severely impairs a person’s ability to work, care for family members, and obtain food. Hepatitis E occasionally develops into an acute, severe liver disease, and is fatal in about 2% of all cases. Pregnant women, especially those in the third trimester, suffer an elevated mortality rate from the disease of around 20%.

Hepatitis E is prevalent in most developing countries, and common in any country with a hot climate. It is widespread in Southeast Asia, northern and central Africa, India, and Central America. It is spread mainly through fecal contamination of water supplies or food, while person-to-person transmission is uncommon. The hepatitis E virus causes around 20 million infections a year. These result in around three million acute illnesses and around 57,000 deaths annually. The virus is a major cause of illness and of death in the developing world and disproportionate cause of deaths among pregnant women.

Sausages might carry the hepatitis E virus (Photo: mharvey75)

Sausages might carry the hepatitis E virus (Photo: mharvey75)

And the reason for highlighting this disease in a food safety blog? Well, hepatitis E is increasingly being seen in developed nations, with reports of cases in the UK, USA and Japan. Once considered very rare, cases have risen by nearly 40 per cent in a year in the UK. The disease is actually thought to be a zoonosis in that both deer and swine have been implicated as the source of human infections. An investigation by the Animal Health and Veterinary Laboratories Agency in the UK found hepatitis E in 49% of pigs in Scotland. But an even higher prevalence has been reported in other British studies. A limited Hungarian study found the virus in 39% of investigated farms, while the virus was detected in a majority of Chinese pig farms and in more than half of slaughter pigs.

So it shouldn’t be a surprise that the hepatitis E virus has now been found in pork sausages in the UK. The zoonoses report published in September 2013 by the Department for Environment, Food, and Rural Affairs says 10 per cent of sausages sampled were found to contain the virus. Sausages are regarded as particularly dangerous as they often contain liver meat and traces of pig’s blood as well as a casing from the animal’s intestine. To kill the virus, sausages have to be cooked at 70°C for at least 20 minutes.  Most people would not cook sausages for that long. At temperatures of 60°C the virus can survive for at least an hour. Scientists have also warned about the acute risk of hepatitis E from the French delicacy figatellu – a smoked pigs liver sausage produced in Corsica – which is often eaten raw.

So a new food safety scare to add to an already long list. If you’re an avid sausage consumer you might think about vaccination against the hepatitis E virus, but you have to think again. Since hepatitis E is still rare in the developed world there has been no economic incentive to commercialise an earlier developed successful vaccine. The only country to have a preventative vaccine approved for use is China.

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Campylobacter – the bad bug on chicken

If you are eating chicken, I can only hope you cooked it well. Surely you washed your hands after touching the raw chicken. And the most important, you didn’t use the same cutting board and knife to prepare vegetables to be eaten without further heating. If you didn’t follow those simple rules you might regret it in a few days time. I’ll tell you why.

Common food poisoning

The twisted Campylobacter (Photo: Wikimedia)

The twisted Campylobacter (Photo: Wikimedia)

Campylobacter is a twisted bacteria, actually literally since this is the meaning of the name and the way it looks. It is the most frequently reported bacterial zoonosis in many countries. Most people who become ill with campylobacteriosis get diarrhea, cramping, abdominal pain, and fever within two to five days after exposure to the organism. The diarrhea may be bloody and can be accompanied by nausea and vomiting. The illness typically lasts about one week.

On rare occasions there are some long-term consequences of this infection beginning several weeks after the diarrheal illness. Some people develop arthritis. Others develop a rare disease called Guillain-Barré syndrome that affects the nerves of the body resulting in paralysis and requiring intensive medical care. It is estimated that approximately one in every 1,000 reported campylobacter illnesses leads to Guillain-Barré syndrome.

The drop in the ocean

With that out of the way I hope you are sufficiently alerted to continue reading.

Chicken meat is the most common source of campylobacter in most countries. But you always cook chicken well you say. But here’s the thing, it only takes less than 500 campylobacter organisms to make you sick. Even one drop of juice from raw chicken meat can carry enough campylobacter to infect a person! One way to become infected is to cut raw poultry meat on a cutting board, and then use the unwashed cutting board or utensil to prepare vegetables or other raw or lightly cooked foods. The campylobacter organisms from the raw meat get onto the other foods. And you get sick.

This has been known for a long time but not much has been done about it. In Denmark some years ago, a study of food handling behaviour showed that young males after leaving home had the riskiest kitchen practices. Maybe they had no interest in the home economics topic at school.

New Zealand has been affected most badly by campylobacteriosis. And they had to do something. In the early 1980s campylobacteriosis became a notifiable disease in New Zealand and evolution of the disease could be followed. At a peak in 2006 the disease affected around 350 people out of every 100,000 of the population. That year a number of voluntary and regulatory interventions to reduce campylobacter contamination of poultry was introduced by government and industry. And two years later the rate of the disease had more than halved. This apparent success proved that it is possible to produce chicken meat with a much reduced campylobacter contamination rate.

So what is the rest of the world doing?

Chicken commonly carry Campylobacter (Photo: Jack Letourneau)

Chicken commonly carry Campylobacter (Photo: Jack Letourneau)

Campylobacteriosis is estimated by the Centers for Disease Control and Prevention to affect over 1.3 million persons every year in the USA, killing around 76 persons. In 2011, campylobacter was found on 47% of raw chicken samples bought in grocery stores and tested through the National Antimicrobial Resistance Monitoring System. That year USDA established performance standards to limit campylobacter contamination of whole broiler chickens in processing plants. However, the effect of USDA’s action is uncertain since campylobacteriosis continued to increase in the following year by 14%.

The European Food Safety Authority has calculated that the actual number of cases of campylobacteriosis is around nine million each year in the European Union. This would amount to a cost of around €2.4 billion a year to public health systems and to lost productivity. But firm action at the EU level is still wanting.

Some individual EU countries have introduced counter measures. For example, in Denmark, ‘campylobacter-free’ chicken meat can be marketed at a premium price, providing that it comes from flocks that meet required monitoring standards. So the young male adults in Denmark might now be on safer ground.

In January 2013, the UK’s Food Standards Agency warned that two-thirds of all raw chicken bought from UK shops was contaminated with campylobacter, affecting an estimated half a million people annually and killing approximately 100. A campylobacter risk management programme has been developed to reduce levels of campylobacter in chicken. A target has been set for the industry to reduce the numbers of the most contaminated birds in UK poultry houses from 27% to 10% by 2015. It is estimated that achievement of this target could mean a reduction in campylobacter food poisoning of up to 30%.

The cost of action

Money talks (Photo:

Money talks (Photo:

Of course it is a cost involved in reducing campylobacter contamination of chicken in the first place. In a Dutch study, industry data on campylobacter contamination of chicken carcasses were collected from 16 plants. Based on these data, the risk for consumers of campylobacteriosis was calculated per plant and per year, using a published risk assessment model. As a baseline scenario, a critical limit of 1,000 campylobacter organisms per gram of breast-and neck-skin was modelled, with the model predicting a reduction in consumer risk of around 70%.

Economic analysis suggested that implementing such a limit would be highly cost-effective from a societal point of view. The costs to the Dutch poultry industry were estimated in the order of €2 million per year whereas the benefits to the Dutch economy were in the order of €9 million per year.

Who should bear the cost?

So isn’t it time that the chicken industry carried responsibility for the product they sell? Why should it be the consumer’s responsibility to treat chicken meat as a potential time bomb? I just ask the question. Over to the industry. The New Zealand experience has shown what is possible. It’s only a matter of money.

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The dark force in gaining weight

A variety of microbes colonise the gastrointestinal system

A variety of microbes colonise the gastrointestinal system

You better know your Smithiis from your Bacteroidetes and Firmicutes or you might start gaining weight. I guess this statement will require quite a lot of explanation. Can I just assume that you know that you carry a lot of microorganisms in your gastrointestinal system? As a matter of fact the number of microbes easily outnumber your own cells. It is believed that the gut microflora contains somewhere around one million million cells (trillion if you are American or billion if you are continental European, confusing I know but big numbers anyway) and weighs between 1 to 2 kilograms. It consists of around 500 different types of microorganisms, many we have not been able to grow outside the gut.

Just so you know, we are born with a sterile gut but very quickly pick up the crucial microorganisms. Within days bugs have colonised the colon in particular with the initial composition dependent on the birth method and food delivery method (natural birth or cesarian section, breast or bottle to be precise).

Why do we carry so many bugs?

The fact that we quickly colonise the colon with beneficial bugs is very important. We actually will live in a symbiotic relationship with our friendly bugs, that is we are mutually beneficial to each other. Our friends fulfil a host of useful functions, including digestion of left-over energy in food, stimulating cell growth, hindering the growth of harmful microorganisms, training the immune system to respond only to disease causing bacteria, and defending against some diseases. Without gut microflora, the human body would be unable to use some of the undigested carbohydrates we consume. However, because some types of gut flora have enzymes that human cells lack they can break down left-over polysaccharides. These include certain starches, fibre, oligosaccharides and sugars that the body failed to digest and absorb.

The bacteria ferment the left-over carbohydrates into short chain fatty acids including acetic acid, propionic acid and butyric acid. These materials provide a major source of useful energy and nutrients for humans. The bugs also help the body to absorb essential dietary minerals such as calcium, magnesium and iron. Evidence also indicates that bacteria enhance the absorption and storage of lipids and produce and then facilitate absorption of necessary vitamins like vitamin K.

This is all good to an extent, because we don’t want to waste food. And we would without the gut microflora. It has been shown in laboratory experiments that animals raised in a sterile environment and lacking gut flora need to eat 30% more calories just to remain the same weight as their normal counterparts. Unfortunately, the gut flora is in a constant state of change and the important balance between microbes can be disturbed. An excess of some of the bugs can make digestion too efficient, and in here lies the problem.

The problem bug

In 2009, a large human study concerning obesity and gut flora was conducted. It was found that obesity disorders could be the result of an imbalance in the gut flora, which could have serious consequences such as cardiovascular disease, type-2 diabetes, and colon cancer. However, a recent study by a different group took the science one step further finding that overweight people may be more likely to harbour a certain type of intestinal microbe. This microbe may contribute to weight gain by helping other organisms to digest certain nutrients, making even more calories available.

The dark force that seems to cause weight gain is called Methanobrevibacter smithii (the Smithii from the initial sentence). The more M. smithii bugs you have, the more you are likely to weigh. As is implied by the name of the organism it produces methane when digesting food. A way of detecting the presence of the organism is to test the amount of methane and hydrogen in the breath – elevated levels indicate the presence of the bug. The scientists found that people with the highest readings on the breath test were more likely to be heavier and have more body fat, and they suspect that M. smithii may be at least partly responsible for their obesity.

This type of organism may have been useful thousands of years ago, when people ate more roughage and needed all the help they could get to squeeze every last calorie out of their food. But modern diets are much richer and the need less. It thus seems that our external environment is changing faster than our internal environment can cope.

As a curiosity M. smithii was also found in higher numbers in anorexic patients. On the surface this seems to be an anomaly. However, it is believed that this may be due to an adaptive attempt by the gut microflora towards optimal use of the low caloric diet of anorexic patients.

A possible future solution

A future pill might help weight loss (Photo: fantasyhealthball)

A future pill might help weight loss (Photo: fantasyhealthball)

Question is should we just accept our fate and let the bugs grow as they want? Maybe not since scientists are trying to figure out if it would be possible to help people lose weight by selectively killing off the guilty bug. They are fully aware that to just kill gut bacteria in general could be a disaster. Studies have already shown that taking antibiotics can alter the balance of microbes in a bad way, causing stomach upset, possibly allowing deadly infections to take hold and, perhaps, even allowing a takeover by the obesity-generating bugs. However, a future selective pill targeting our Smithii might be a possibility for losing weight.

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Deadly bug in sprouts

SummarySeed sprouting provides an ideal environment with optimal temperature and humidity for bacterial growth. Once the bugs are there they are very difficult to remove from fresh sprouts. A German case study shows the serious impact of sprout contamination with a particularly nasty bug that can cause diarrhoea, kidney disease and death.

On 21 May 2011, Germany reported an outbreak of Shiga-toxin producing Escherichia coli (STEC), serotype O104:H4. At the conclusion of the outbreak at least 4,300 cases of diarrhoeal disease, 773 cases of haemolytic uraemic syndrome (HUS) and 50 deaths across Europe linked to the outbreak in Germany had been reported to the European Centre for Disease Prevention and Control (ECDC). In addition, outside the EU eight cases of STEC and five cases of HUS, including one death had been reported in the USA, Canada and Switzerland through the international health regulations (IHR), all with recent travel history to Germany.

The clinical onset of the last outbreak-related case in Germany was 4 July 2011. The Robert Koch Institute (RKI) in Germany announced the end of the E. coli outbreak on 26 July 2011 after more than two months of intensive investigative activities.

Sprouted seeds

Early case-control studies conducted by the RKI demonstrated that clinical disease was associated with the consumption of fresh salad vegetables. The high proportion of adult women among cases, was consistent with fresh salad vegetables as the source of infection. This led to a false warning about some Spanish grown vegetables causing havoc for some Spanish growers. Later, a detailed cohort study demonstrated an association with sprouted seeds. Epidemiological studies on an associated French outbreak also implicated sprouted seeds as the outbreak vehicle.

A tracing back and tracing forward study showed that most of the clusters could be attributed to consumption of sprouted seeds from one producer in Germany. Investigation of the production site showed no evidence of environmental contamination. This left the seeds used for the sprout production as the prime suspect vehicle of infection. Fenugreek seeds were found to be common to both outbreaks and that a specific consignment of fenugreek seeds imported from Egypt was the most likely link between the outbreaks.

Import ban

A ban on imports into the EU of Egyptian fenugreek seeds and certain other sprouting seeds was imposed in July 2011 after the European Food Safety Authority said this was the most likely cause of the E. coli outbreaks.

The European Commission’s Food and Veterinary Office (FVO) visited Egypt in August 2011 and found that Egypt did not differentiate between seeds for sprouting and seeds for planting. The trace-back exercise found that three implicated lots were produced in upper Egypt by the same farmer in separate farms grown under organic conditions.

The Egyptian investigation found no evidence of STEC O104:H4 presence, although there was plenty of potential for contamination from human populations and animals, and problems with analytical methods. The FVO said Egypt must ensure that seeds produced specifically for sprouting must comply with hygiene rules and microbiological criteria.

Given an exchange of information with the Egyptian authorities and new measures to prevent contamination, the ban on fenugreek imports from Egypt was lifted on 31 March 2012.

Rare strain

The published data for STEC O104:H4 are scarce as this is a very rare serogroup infecting humans in Europe and globally. According to the information reported to ECDC, there were 10 reported cases of STEC O104:H4 infection in the EU Member States and Norway during 2004-2010. Five of the 10 cases between 2004 and 2010 were related to travel to Afghanistan (2008), Egypt (2010), Tunisia (2009, 2010) and Turkey (2009).

In addition to those cases reported to ECDC, a review of the scientific literature revealed that STEC O104:H4 has been isolated twice in Germany in 2001 and once in Korea in 2005. The German isolates differed from the 2011 outbreak strain.

Inherent problems in sprout production

The preparation of fresh sprouted seeds rarely includes a step where bacterial contamination is eliminated. Hence, food preparation of fresh sprouted seeds is based on the understanding that they are sold as ready-to-eat, i.e. safe to eat as is, or following only minimal preparation. For fresh produce, this assumes and relies on a production process which prevents contamination and an ability to detect contamination when it occurs. These conditions have proven not to be satisfied in this case.