I recently received an e-mail from Paul Hench, who writes for http://www.mastersinpublichealth.net/, a website dedicated to providing students with the information and tools needed in order to pursue their Masters in Public Health.
Paul has included Safe Food in his top 50 list of food safety blogs. Though unofficial, this list puts Safe Food alongside blogs that I regard as important sources of information and opinion and it's gratifying to see this recognition. The list will be a valuable resource, not just for PH students, but for all those interested in food safety.
I have not yet searched the whole list and therefore cannot endorse these blogs, but you may care to check them out for yourself. Goto:
http://www.mastersinpublichealth.net/top-50-food-safety-blogs/
Saturday, September 10, 2011
Wednesday, August 24, 2011
Natural mercury in fish
Most of the posts on this blog are about bacterial food poisoning, so this post is a change on two counts.
Mercury contamination of fish is usually associated with industrial pollution of rivers and estuaries. William Ray, of Radio New Zealand, today reported that experts have suggested that the levels of mercury in trout in waterways around Totorua are so high, people should limit their intake to one trout per month. (I wish I could catch so many!).
Rotorua is one of New Zealand's most famous geothermal areas and the experts have suggested that the mercury is from natural hydrothermal sources. However, it appears that runoff from farms in the area may also be involved. The nutrients washed into the rivers and lakes cause algal blooms, which lower the dissolved oxygen content of the water. This in turn allows transfer of mercury from mud into the water, from whence it enters the food chain.
Perhaps the most infamous mercury poisoning occurred in the Japanese city of Minamata, which gave the name Chisso-Minamata disease to the resulting neurological syndrome. The Chisso Corporation chemical factory released methyl mercury into the Minamata Bay and this highly toxic compound was accumulated by fish and shellfish.
The Rotorua trout have also accumulated mercury, but Dr. Ngaire Phillips from the National Institute of Water and Atmospheric Research points out that the recommendation for consumption of no more than one trout per month is based on a lifetime consumption.
Mercury contamination of fish is usually associated with industrial pollution of rivers and estuaries. William Ray, of Radio New Zealand, today reported that experts have suggested that the levels of mercury in trout in waterways around Totorua are so high, people should limit their intake to one trout per month. (I wish I could catch so many!).
Rotorua is one of New Zealand's most famous geothermal areas and the experts have suggested that the mercury is from natural hydrothermal sources. However, it appears that runoff from farms in the area may also be involved. The nutrients washed into the rivers and lakes cause algal blooms, which lower the dissolved oxygen content of the water. This in turn allows transfer of mercury from mud into the water, from whence it enters the food chain.
Perhaps the most infamous mercury poisoning occurred in the Japanese city of Minamata, which gave the name Chisso-Minamata disease to the resulting neurological syndrome. The Chisso Corporation chemical factory released methyl mercury into the Minamata Bay and this highly toxic compound was accumulated by fish and shellfish.
The Rotorua trout have also accumulated mercury, but Dr. Ngaire Phillips from the National Institute of Water and Atmospheric Research points out that the recommendation for consumption of no more than one trout per month is based on a lifetime consumption.
Saturday, August 13, 2011
Listeria and bacon recall
I was just scanning the news and did a double take. An Ontario company, Aliments Prince, S.E.C., has just recalled 380,000 lbs of bacon because of possible contamination with Listeria monocytogenes. That's a lot of bacon!
It seemed to me that this was excessively cautious. L. monocytogenes should not be found in a food product that has been processed in such a way that the bacteria should not survive, but the organism can occasionally be found in foods that have not been given a listericidal process. So green leafy vegetables and other raw foods may occasionally contain L. monocytogenes. The bacteria can be found in many parts of the environment, such as surface water, soil and decaying vegetation, and it's not surprising to find it turning up sometimes in raw foods.
On closer reading, it turns out that the FSIS found a sample of cooked diced bacon from Aliments Prince contained the bacteria. This is a whole new ball game - the product could be expected to be consumed without further heating and thus could put at risk susceptible consumers. See my post "Listeria Hysteria" for further information.
The company has done the right thing. We can't avoid occasional low levels of contamination of raw foods by L. monocytogenes, but something has gone seriously wrong when we find it in cooked foods. Either the process given was too mild, or, much more likely, the product has been recontaminated post processing.
It seemed to me that this was excessively cautious. L. monocytogenes should not be found in a food product that has been processed in such a way that the bacteria should not survive, but the organism can occasionally be found in foods that have not been given a listericidal process. So green leafy vegetables and other raw foods may occasionally contain L. monocytogenes. The bacteria can be found in many parts of the environment, such as surface water, soil and decaying vegetation, and it's not surprising to find it turning up sometimes in raw foods.
On closer reading, it turns out that the FSIS found a sample of cooked diced bacon from Aliments Prince contained the bacteria. This is a whole new ball game - the product could be expected to be consumed without further heating and thus could put at risk susceptible consumers. See my post "Listeria Hysteria" for further information.
The company has done the right thing. We can't avoid occasional low levels of contamination of raw foods by L. monocytogenes, but something has gone seriously wrong when we find it in cooked foods. Either the process given was too mild, or, much more likely, the product has been recontaminated post processing.
Tuesday, August 9, 2011
Haemolytic Uraemic Syndrome
In the wake of infection by Shigatoxin producing Escherichia coli (STEC), some patients develop Haemolytic Uraemic Syndrome (HUS). The recent outbreak of O104:H4 STEC in Europe resulted in an unusually high proportion of patients going on to develop the syndrome, some of whom succumbed to the infection.
Drew Falkenstein, an associate of Marler Clark law firm in Seattle, has written a very well informed article on HUS. Rather than write another, I suggest that interested readers follow the link to Drew's posting on Food Poison Journal.
Drew Falkenstein, an associate of Marler Clark law firm in Seattle, has written a very well informed article on HUS. Rather than write another, I suggest that interested readers follow the link to Drew's posting on Food Poison Journal.
Wednesday, July 20, 2011
Hello, how are you, is it seeds you're looking for?
It's all over, bar the shouting. Or is it?
As at 30th June, 2011, there were 50 reported deaths from the Escherichia coli O104:H4 outbreak centred in Germany. Cases of illness have been reported from 16 countries, not all victims having travelled to Germany. This suggests that there may have been some person-to-person infection, though in at least one case, there appears to be none of these links.
Thankfully, the number of cases reported is dropping, the outbreak following a classic curve of increasing number of cases, followed by a decrease once reporting shows that there is an outbreak under way and information and preventative measures become available.
European scientists and government sources have suggested that fenugreek seeds imported from Egypt in either 2009 or 2010 are implicated in the outbreaks in Germany and Bordeaux. Epidemiological investigations do link these particular sprout seeds with the outbreaks. But a link is not proof.
Not surprisingly, the Egyptians have objected to their seeds being blamed for the outbreak. I have some sympathy with them - as far as I am aware, O104:H4 has not been isolated from any seed samples. If these seeds are the source, then we have another problem on our hands.
If the seeds were imported to Germany and France, and perhaps other countries, the implication is that any E. coli O104:H4 present in the seeds survived for between two and three years before the sprouting process allowed them to multiply and cause the outbreak. This raises a number of questions: is this strain of E. coli particularly hardy, so that it can survive for years in dry seeds? Were all the infected seeds exported from Egypt? If not, were there any O104:H4 cases in Egypt between 2009 and the present? If there were cases, why have we not heard about it?
I don't believe that we have heard the last of this by a long chalk.
As at 30th June, 2011, there were 50 reported deaths from the Escherichia coli O104:H4 outbreak centred in Germany. Cases of illness have been reported from 16 countries, not all victims having travelled to Germany. This suggests that there may have been some person-to-person infection, though in at least one case, there appears to be none of these links.
Thankfully, the number of cases reported is dropping, the outbreak following a classic curve of increasing number of cases, followed by a decrease once reporting shows that there is an outbreak under way and information and preventative measures become available.
European scientists and government sources have suggested that fenugreek seeds imported from Egypt in either 2009 or 2010 are implicated in the outbreaks in Germany and Bordeaux. Epidemiological investigations do link these particular sprout seeds with the outbreaks. But a link is not proof.
Not surprisingly, the Egyptians have objected to their seeds being blamed for the outbreak. I have some sympathy with them - as far as I am aware, O104:H4 has not been isolated from any seed samples. If these seeds are the source, then we have another problem on our hands.
If the seeds were imported to Germany and France, and perhaps other countries, the implication is that any E. coli O104:H4 present in the seeds survived for between two and three years before the sprouting process allowed them to multiply and cause the outbreak. This raises a number of questions: is this strain of E. coli particularly hardy, so that it can survive for years in dry seeds? Were all the infected seeds exported from Egypt? If not, were there any O104:H4 cases in Egypt between 2009 and the present? If there were cases, why have we not heard about it?
I don't believe that we have heard the last of this by a long chalk.
Friday, July 8, 2011
Mud hoppers
This post is not directly about food, but it is about eating stuff.
Over the last weekend, an annual event was run (well actually, quite a bit of it was crawled) over a 6km course in Auckland. Nothing unusual about cross country running in New Zealand, but this one involved obstacles to crawl under or climb over and a very large amount of mud. Two TV news presenters took part, so there was plenty of footage to analyse.
I am all for active sports, but I wonder how many of the competitors will regret the weekend's activities, and not just for sore muscles. At one point, the competitors crawled, sploshed or "swam" though a trench full of thick mud. At least one competitor dived headfirst into the mud as if he were diving into the surf. None of the participants could have avoided getting some of the mud in their mouths.
Soil is interesting stuff - it's the goto place for microbiologists if they need to isolate a microorganism that has a particular characteristic; it's one of the best sources of bacteria. If animals have been grazed on the paddock, or water in the mud has drained from a farm, it is likely that the mud will contain many faecal organisms. In 2008, there was a significant outbreak of campylobacteriosis after a mountain bike race, in which competitors got very muddy. None of the support crews became ill.
I'm sure that mud running allows us to relive our childhood without being scolded for getting dirty and it's certainly a good spectator sport, but competitors should be aware of the risks associated with eating the stuff.
Over the last weekend, an annual event was run (well actually, quite a bit of it was crawled) over a 6km course in Auckland. Nothing unusual about cross country running in New Zealand, but this one involved obstacles to crawl under or climb over and a very large amount of mud. Two TV news presenters took part, so there was plenty of footage to analyse.
I am all for active sports, but I wonder how many of the competitors will regret the weekend's activities, and not just for sore muscles. At one point, the competitors crawled, sploshed or "swam" though a trench full of thick mud. At least one competitor dived headfirst into the mud as if he were diving into the surf. None of the participants could have avoided getting some of the mud in their mouths.
Soil is interesting stuff - it's the goto place for microbiologists if they need to isolate a microorganism that has a particular characteristic; it's one of the best sources of bacteria. If animals have been grazed on the paddock, or water in the mud has drained from a farm, it is likely that the mud will contain many faecal organisms. In 2008, there was a significant outbreak of campylobacteriosis after a mountain bike race, in which competitors got very muddy. None of the support crews became ill.
I'm sure that mud running allows us to relive our childhood without being scolded for getting dirty and it's certainly a good spectator sport, but competitors should be aware of the risks associated with eating the stuff.
Saturday, July 2, 2011
Can we control toxigenic E. coli?
Last week at the New Zealand Institute of Food Science and Technology annual conference, I presented a paper on non-O157:H7 shigatoxigenic E. coli. That's a bit of a mouthful, if you'll pardon the unfortunate pun. These bacteria have gained the ability to produce a toxin that can destroy intestinal epithelial cells and also damage the kidney. E. coli O157:H7 is probably the best known of the Enterohaemorrhagic E. coli (EHEC) types. The strain causing the outbreak in Germany and other parts of Europe is a non-O157 type and indeed appears to be from a different group - the Entero-Aggregtive EC.
During the session, two other papers were presented, one on Cronobacter sakazakii - the neonate nasty, and one on Salmonella. All three presenters talked about control of these food borne disease-causing organisms.
During the discussions, it became apparent that there was some difference of opinion on the effectiveness of control measures during production and processing of foods.
For example, the poultry industry in New Zealand has been remarkably successful in controlling Salmonella in poultry flocks by strict management of biosecurity, and thus eggs and chicken meat are essentially free of Salmonella. Unfortunately, these controls have not worked for Campylobacter and there is still a significant rate of C. jejuni illness that can be traced to poultry, though this rate has fallen over the past two years.
Similarly, when I suggested that control of Salmonella would likely also control E. coli, a friend and colleague stood up and said that these two organisms are significantly different and controls would need to be tailored to each. I invited him to come outside and we'd sort it out by fisticuffs! However, it became obvious that we were talking at cross purposes and we were both right.
Salmonella, Cronobacter and E. coli are all vegetative bacteria. That is, they do not form spores and are not particularly heat or chemical resistant. Thus, during food processing or in the hands of the consumer, control is easy - heating to about 75-80C for a few seconds will kill them all. If we prevent cross contamination, then the finished food will be safe to eat.
It is much more difficult to set conditions during primary production that will control these bacteria. Vegetables are usually grown in soil. They therefore become contaminated with soil organisms. Even hydroponic growing systems may become colonised by bacterial biofilms and thus contaminate the products. Animals and birds all carry populations of bacteria in their guts or on hides, hair, feathers and feet. It is impossible to eradicate these bacteria, so they must be controlled during processing.
But what do we do with vegetable sprouts? These products must be regarded as hazardous - they are grown in conditions of high humidity and at temperatures that support the rapid growth of bacteria. If pathogens, such as E. coli O104:H4 are present in the seeds, in the water or the equipment, they can grow rapidly. Stir-frying will probably kill the bacteria, provided the temperature gets high enough. Sprouts are also eaten raw, so there is no controlled lethal process step and the consumer ingests the bacteria, sometimes with fatal results. If people are to continue to eat raw sprouts, we need to develop some means of decontaminating them, such as a rinse in a bactericidal chemical solution. Nothing is perfect, but control of production, processing and distribution, together with consumer education, should decrease the likelihood of a similar outbreak to that currently occurring in Germany.
During the session, two other papers were presented, one on Cronobacter sakazakii - the neonate nasty, and one on Salmonella. All three presenters talked about control of these food borne disease-causing organisms.
During the discussions, it became apparent that there was some difference of opinion on the effectiveness of control measures during production and processing of foods.
For example, the poultry industry in New Zealand has been remarkably successful in controlling Salmonella in poultry flocks by strict management of biosecurity, and thus eggs and chicken meat are essentially free of Salmonella. Unfortunately, these controls have not worked for Campylobacter and there is still a significant rate of C. jejuni illness that can be traced to poultry, though this rate has fallen over the past two years.
Similarly, when I suggested that control of Salmonella would likely also control E. coli, a friend and colleague stood up and said that these two organisms are significantly different and controls would need to be tailored to each. I invited him to come outside and we'd sort it out by fisticuffs! However, it became obvious that we were talking at cross purposes and we were both right.
Salmonella, Cronobacter and E. coli are all vegetative bacteria. That is, they do not form spores and are not particularly heat or chemical resistant. Thus, during food processing or in the hands of the consumer, control is easy - heating to about 75-80C for a few seconds will kill them all. If we prevent cross contamination, then the finished food will be safe to eat.
It is much more difficult to set conditions during primary production that will control these bacteria. Vegetables are usually grown in soil. They therefore become contaminated with soil organisms. Even hydroponic growing systems may become colonised by bacterial biofilms and thus contaminate the products. Animals and birds all carry populations of bacteria in their guts or on hides, hair, feathers and feet. It is impossible to eradicate these bacteria, so they must be controlled during processing.
But what do we do with vegetable sprouts? These products must be regarded as hazardous - they are grown in conditions of high humidity and at temperatures that support the rapid growth of bacteria. If pathogens, such as E. coli O104:H4 are present in the seeds, in the water or the equipment, they can grow rapidly. Stir-frying will probably kill the bacteria, provided the temperature gets high enough. Sprouts are also eaten raw, so there is no controlled lethal process step and the consumer ingests the bacteria, sometimes with fatal results. If people are to continue to eat raw sprouts, we need to develop some means of decontaminating them, such as a rinse in a bactericidal chemical solution. Nothing is perfect, but control of production, processing and distribution, together with consumer education, should decrease the likelihood of a similar outbreak to that currently occurring in Germany.
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