Food Safety Issues



*       Facts about E.coil O157:H7:

*       About Campylobacter

*       About Ciguatera Fish Poisoning

*       About Cyclosporiasis

*       About Hepatitis A

*       About Salmonella

*       About Vibrio

*       Historical Overview of Key Issues in Food Safety

*       About the Costs of Food Borne Illness in The USA



FACTS ABOUT E.coli O157:H7: Toxin-producing Escherichia coli


Several strains of the bacterium E.coil cause a variety of diseases in humans and animals.  E.coli O157:H7 is a type associated with a particularly severe form of human disease.  E.coli O157:H7 is one of the most virulent (highly infectious) pathogens known to enter the world food supply.  It causes diarrhoea, abdominal pain, and in some cases, intestinal bleeding and kidney failure.


The initial symptoms of E.coli O157:H7 illness generally occur within two days after eating contaminated food, though periods of three to five days have been reported.  Symptoms increase in intensity during the next 24-48 hours, lasting from four to 10 days.  Less than ten E.coli O157:H7 cells may be enough to cause illness in humans.  A low infectious dose of two to 2,000 cells has been associated with outbreaks in food borne illness. E-coli O157:H7 can survive in acidic environments that are lethal to other pathogens, such as in fermented foods like sausage and apple cider.  Though potentially deadly to humans, E.coli O157:H7 is not pathogenic to cattle.  A  single cow, or a number of cattle within the same herd, may contain more than one strain of E.coli O157:H7.  Some strains are thought to have greater acid tolerance than others.


The source of E.coli O157:H7 contamination on carcasses is likely due to faecal contamination during animal production and slaughter operations.  Carcasses may become contaminated during hide removal or by cross-contamination with equipment and workers’ hands.  HACCP (food safety control) systems in processing plants cannot eliminate E.coli O157:H7 from foods unless a treatment is added that will kill the pathogen, such as heat pasteurisation or irradiation.  Current research shows that competitive exclusion has the potential to eliminate E.coli O157:H7 from cattle before slaughtering.  Competitive exclusion involves the use of non-pathogenic micro-organisms to outgrow pathogens in the gastrointestinal tracts of animals.


If swallowed, faecal contaminated water in freshwater swimming areas may cause E.coli O157:H7 infection in both cattle and humans.  Fresh manure used to fertilise garden fruits and vegetables may contaminate them with  E.coli O157:H7.  The largest reported E.coli O157:H7 outbreak, which caused thousands of illnesses, occurred in Japan in 1996.  Radish sprouts were implicated as the source of infection.


Though ground beef has been most often associated with E.coli O157:H7 outbreaks in the United States, other implicated foods include raw milk, apple cider, dry-cured salami, lettuce, produce from manure-fertilised gardens, potatoes, radish and alfalfa sprouts, yoghurt, sandwiches and water.


E.coli O157:H7 causes hemorrhagic colitis, which begins with watery diarrhoea and severe abdominal pain and rapidly progresses to passage of bloody stools.  It has been associated with HUS,  a life-threatening complication of hemorrhagic colitis characterised by acute kidney failure that is particularly serious in young children. E-coli O157:H7 is found in cattle, but there may be other reservoirs; the dynamics of E.coli O157:H7 in food-producing animals are not well understood.  Approximately 25,000 cases of food borne illness can be attributed to E.coli O157:H7 every year, with as many as 100 deaths resulting.  E.coli O157:H7 outbreaks have recently been associated with ground beef, raw milk, lettuce and minimally processed and fresh fruit juices.  An outbreak in the fall of 1996 in three western states and British Columbia was associated with unpasteurised apple juice and sickened 66 people, causing the death of one child.





Estimations are that in the United States, between two and eight million people become sick and 200 to 800 die because of campylobacter every year.  The infection has also been linked to Guillain-Barr syndrome, which causes severe nerve damage.  Studies indicate that 20 to 40 percent of the 5,000 annual cases of Guillain-Barre follow a bout with campylobacter.


More than 70 per cent of chickens and up to 100 per cent of turkeys are infected with it.  Campylobacter also infects cattle, hogs and sheep. 


Heat kills campylobacter even more readily than salmonella, so temperatures used to control salmonella will also be effective against campylobacter.





Ciguatera fish poisoning in humans is most commonly caused by eating carnivorous fish contaminated by a toxin produced by a toxin dinoflagellate Gambierdiscus toxicus.  The toxin bio-accumulates through the food chain, and carnivorous fish such as barracuda, red snapper, grouper, sturgeon and amberjack are usually the most commonly involved.


In Canada, most cases of ciguatera poisoning reported in the past have involved Canadian who ate fish in the Caribbean while on holiday.  These cashes have implicated grouper in the Dominican Republic, kingfish in Jamaica, and barracuda in Haiti.  A fish casserole caused the illness in 57 people during a trip to Cuba. Ciguatera poisonings have also been reported as a result of importing certain fish.  Dried barracuda brought back from Jamaica in 1983 and imported red snapper bought in an Ontario market were identified sources.





On September 29, 1997 at the 37th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) in Toronto, Canada, Dr. David Relman presented a review and update of current knowledge of cyclosporiasis as an emerging infectious disease.  He reminded listeners that, variably acid-fast organisms with an approximate diameter of 8-10 microns resembling large forms of Cryptosporidium have been identified in faecal samples from patients exhibiting episodes of watery diarrhoea since the 1980s.  It was in 1993 that Ortega and Sterling published a report identifying the organism as Cyclospora sp.  in the New England Journal of Medicine.  Relman himself has generated data for the sequence of ribosomal RNA genes for this organism, and confirmed its identity as Cyclospora sp.


Dr Relman described a typical clinical course for infected patients as intermittent watery diarrhoea after a 7 day incubation period.  Untreated disease can lead to anorexia, fatigue and weight loss lasting for weeks in immunocompetent hosts, and even longer in immunocompromised hosts.  The infection can be successfully treated with trimethoprim/sulfamethoxazole.  Relapses are not uncommon in treated patients.  No suitable alternative therapy has been identified for sulpha-allergic persons.  There are no data for the efficacy of trimethoprim alone.


Dr Relman offered additional insight into the epidemiology of cyclosporiasis.  Infection or colonisation of asymoptomatic persons is common (endemic) in Asia (especially in Nepal), Peru and Haiti, but uncommon in Tanzania (the latter based on comments offered during the question and answer session).  In the US approximately 0.5% of fecal samples from symptomatic persons will contain Cyclospora.  This low incidence suggests that there are many naïve hosts in North America, and Relman suggests that this may in part explain the relatively recent emergence of this disease in North America.  Last year’s documented outbreaks involved Guatemalan raspberries, while in 1997, mesclun lettuce and basil from other sources as well as Guatemalan raspberries have been implicated.  Between 1,600 and 1,700 cases have been reported in the US and Canada this year.





Hepatitis A (HAV) is a virus that infects the liver and causes hepatitis A, an illness with an abrupt onset that can include fever, malaise, nausea, abdominal discomfort, dark urine and jaundice after a prolonged incubation period (for example, more than two months).  In children less than six years old, most infections (70 percent) are asymptomatic, but in older children and adults, infection is usually symptomatic, with jaundice occurring in more than 70 percent of patients.  Signs and symptoms of Hepatitis A usually last more than two months, but there are no chronic consequences.  About 130,000 infections with HAV and 100 deaths occur every year in the U.S..  The primary mode of transmission for HAV is person-to-person by the faecal-oral route.  (Preparing food with unwashed hands after using the toilet or changing diapers, is a typical faecal-oral route).  Recognised food borne Hepatitis A outbreaks account for only 2 to 5 percent of Hepatitis A cases reported in the U.S. every year, most of which are caused by an infected food handler.  Outbreaks caused by foods contaminated before preparation have been associated with widely distributed products such as shellfish, lettuce, frozen raspberries and frozen strawberries.  Hepatitis A can be prevented by good personal hygiene and safe food-handling practices.





Salmonella bacteria cause diarrhoea and systemic infections, which can be fatal particularly in susceptible persons, such as the immunocompromised, the very young and the elderly.  Animals used for food production are common carriers of Salmonella, which can subsequently contaminate foods such as meat, dairy products and eggs.  Foods often implicated in outbreaks include poultry and poultry products, meat and meat products, dairy products, egg products, seafood and fresh produce.  An estimated 800,000 to four million infections occur every year in the U.S.  Between 128,000 and 640,000 of those infections are associated with Salmonella enteritidis in eggs.  Over the past decade, more than 500 outbreaks have been attributed to Salmonella enteritidis, resulting in more than 70 deaths.  In 1994 an estimated 224,000 people became ill from consuming ice cream in one outbreak alone.





Vibrio bacteria are most commonly associated with foods containing seafood.  Vibrio parahaemolyticus is the species most commonly reported as a cause of food borne disease; it generally causes watery diarrhoea and abdominal pain lasting one to seven days and commonly follows consumption of improperly handled cold seafood salads.  Vibrio vulnificus is one of the more serious food borne pathogens, with a case fatality rate that exceeds 50 percent of infected people. Most cases of food borne Vibrio vulnificus infections occur in persons with underlying illness (particularly liver disorders) who eat raw molluscs.





E.M. Foster

Madison, Wisconsin, USA


Food borne transmission of pathogenic and toxigenic micro-organisms has been a recognized hazard for decades.  Even half a century ago we knew about the dangers of botulism from underprocessed canned foods; staphylococcal poisoning from unrefrigerated cream-filled pastries, sliced ham, meat and poultry salads; and salmonellosis from infected animal products.  Despite new protective measures, changes in preservation techniques and failure to follow recognised procedures have created new dangers.  Moreover, we now recognize new organisms that can cause food borne illness.  Listeria monocytogenes, Escherichia coli O157:H7, Campylobacter jejuni, Vibrio parahaemolyticus, Yersinia enterocolitica and others.  Controlling these organisms will require widespread education and possibly new regulatory initiatives.


When I was growing up on my parent’s farm in East Texas, we never thought about food poisoning or unsafe food.  The only foods we bought were sugar, salt, flour and oatmeal; everything else we produced and preserved on the farm.  My mother spent all summer canning fruits and vegetables for winter.  We had no refrigeration; we cured our own meat and drank raw milk.  But I never heard of botulism, staph poisoning, or salmonellosis or perfringens poisoning until I studied bacteriology in college.  Only then did I wonder how we survived with no refrigeration in a hot climate.  Finally, the answer came to me.  We just did not give the bacteria time enough to develop so they could hurt us.  Leftovers from breakfast – hot biscuits, eggs, ham, bacon or sausage, oatmeal, coffee or milk – went right out to the chickens.  Lunch leftovers – biscuits, cornbread, vegetables, or fried chicken – were saved for a cold supper 4 or 5 hours later.  Any food left went to the pigs.  The bacteria had only a maximum of 3 or 4 hours to grow, and that usually is not enough.  I survived and went on to study food microbiology, which included what was known then about food poisoning.  The guru of food poisoning in those days was Professor Gail M. Dack at the University of Chicago.  Dr. Dack was a protégé of Professor E.O. Jordan, who in 1917 published a 107 page book entitled Food Poisoning.  Dr. Dack took over the book and published his first version of Food Poisoning in 1943.  In 1949 and 1956, subsequent editions appeared in which certain truisms became apparent.  Botulism was considered a problem of canners, both home and commercial.  Thus, adequate heat processing would seem to solve the problem.  Perhaps it did for the canner, but now we know that heating will not eliminate all botulism.  Many foods, including salmon eggs, smoked fish, garlic in oil, vacuum packaged lotus roots, and baked potatoes can support growth and Botulinum toxin formation if the storage temperature is suitable.  Similarly, we thought staphylococcal poisoning was limited to cream-filled pastries and cured ham.  In recent years, outbreaks of staphylococcal poisoning have been traced to cheese, whipped butter, ham salad, fermented sausages and canned corned beef.


We now know how to prevent staphylococcal poisoning, but not all food handlers understand and fully comply with the appropriate control measures.

Salmonellosis was once thought a problem with meat from infected animals.  Now we know that a variety of food products can serve as vehicles of this disease.  As early as World War II, we found that dried eggs from the United States could transmit this disease to our British allies.  Thousands of causes of human salmonellosis in the United States and other industrialised countries have been transmitted by ice cream, chocolate, potato salad, cheddar cheese, raw milk, black pepper, pate, aspic, ham, pasteurised milk and drinking water.


Clostridium perfringens, known since the 1940s, causes a problem only when there is gross temperature abuse of cooked food.  Clostridium botulinum, Staphylococcus aureus, C.perfringens and the salmonellae were well known in Dr. Dack’s day, although the food vehicles might have changed.  Not so well known were many of the organisms that preoccupy us today.


We used to think of Escherichia coli as merely an indicator organism that suggested insanitary handling.  Now we know forms of E.coli can kill.  Thirty years ago, Listeria monocytogenes, Campylobacter jejuni, Aeromonas hydrophila, Plesiomonas shigelloides, Vibrio parahaemolyticus, and Yersinia entercolitica were not known; now these are well-established food borne pathogens that we must control. We thought that fresh, uncracked eggs were essentially sterile and safe to eat.  We did not recognise the ability of Salmonella Enteritidis to invade the laying hen and thereby the yolk of an egg.  An outbreak of S. Enteritidis at a Chicago hotel taught us not to rely on the safety of eggs merely because the shell was intact.  S. Enteritidis in shell eggs is still a serious health problem and a growing concern to egg and poultry producers.  Of equal, if not greater, concern is Salmonella Typhimurium strain DT 104.  Widely distributed in cattle herds of England, Scotland and Wales this organism is resistant to several antibiotics, including ampicillin, chloramphenicol, streptomycin, sulfonamides, and tetracycline.  Between 1990 and 1995, the number of S. Typhimurium DT 104 isolated from humans in Britain increased from 259 to 3,837 per year a 15-fold increase.  Moreover, the percentage of drug-resistant isolates increased from 39% in 1990 to 97% in 1995.  S. Typhimurium DDDT 104 has been isolated in the United States from sheep, pigs, horses, goats, emus, cats, dogs, elk, mice, coyotes, ground squirrels, raccoons, chipmunks and birds.  American egg and poultry producers are concerned about its entry into U.S. poultry flocks.  S. Typhimurium DT 104 infection in humans has been associated with the consumption of chicken, sausage, and meat paste as well as with the handling of sick animals.  More than one-third of the patients have required hospitalisation, and 3% have died; these figures are very unusual for ordinary Salmonella infections and indicate serious problems ahead.





Most Americans only worried about becoming sick from eating contaminated food when they travelled to distant lands. After all, it was almost indisputable that the U.S. food supply was the safest in the world.  But a chain of recent events has raised doubts in the minds of many.  These days, it seems that all food is suspect.  Ground meat may be contaminated with dangerous new strains of Eschericihia coli and poultry is rife with another recently publicised bacterium call campylobacter.  The faithful staple, the egg, is a carrier of salmonella; the vegetable bin and fruit bowl may harbour protozoans with names like Toxoplasma and Cryptosporidium.  Outbreaks of Hepatitis A have been traced to strawberries.  It may seem like a good idea to post a table of food borne pathogens on the refrigerator door.  The threat, however, is frighteningly real.


The Council for Agricultural Science and Technology, a private non-profit organisation, estimated that as many as 9,000 deaths and 6.5 to 33 million illnesses in the United States each year are food related.  The Department of Agriculture estimates that medical costs and productivity losses for seven specific pathogens in food, range from $6.5 billion to $34.9 billion annually. And, if the growing list of food recalls is any indication, the situation seems to be getting worse.  The current message from the Food and Drug Administration is “Treat all foods as if they are potentially contaminated”.



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