Consumers who like their veggies raw may find themselves more and more in the position of “making faith-based purchases when it comes to produce,” says Kevin Allen, a UBC food safety expert who studies E. coli and other pathogens.
In May, several U.S. states had issued massive recalls for romaine lettuce contaminated by E. coli. Days later, the Canadian Food Inspection Agency also issued a recall of romaine lettuce.
Upon hearing the news, Allen purged his fridge of salad mixes containing romaine. With children ages two and six, he wasn’t taking any chances. He explains that bacteria known as Shiga toxin-producing E. coli (STEC) can cause severe illnesses, among them hemolytic uremic syndrome (HUS).
“Children are more likely to develop HUS which may result in kidney damage, potentially leading to death,” says Allen, assistant professor in the Food, Nutrition and Health program of the Faculty of Land and Food Systems.
The HUS mortality rate is three per cent for children five years and younger. In persons who are 60 years and older, that mortality rate climbs.
Currently, government and beef and produce industries have procedures in place to monitor and test for E. coli O157:H7 bacterium. However, there are not yet any detection methods available to show up a strain such as E. coli O145 which was associated with the romaine outbreak in May.
That killer pathogens are found at all on products such as lettuce represents a tremendous shift in the epidemiology of foodborne diseases over the past decade, says Allen.
Traditionally, foodborne illnesses have been associated with meat, poultry and eggs. With these products, consumers could rely on the fact that thorough cooking would kill pathogenic organisms.
“But if your salad leaves are contaminated by a pathogen, there is no remedy.”
Processing plants that prepare pre-washed salads or other produce use a dilute water and chlorine solution which may fail to eliminate E. coli or salmonella. In the home, repeated washings may also fail to rid produce of bacteria, particularly if the organisms have been internalized by the plant.
While it is important that consumers continue to include fresh fruit and vegetables in their diet, notes Allen, they also need to understand that our produce is not risk free. “Certain commodities such as alfalfa sprouts and certain leafy greens are frequently associated with foodborne disease.”
An important facet of Allen’s work is looking at how and why E. coli is so successful at finding its way into, and surviving in, our food chain.
Currently, E. coli strains enter the human food supply through various means, the main source being large-scale cattle operations. The organism is cycled into the environment through fecal matter. E. coli O157:H7 and other toxigenic strains frequently infect and subsequently colonize cattle and possibly other animals that come into contact with cattle such as deer or mice.
“One of the most significant reasons why we have E. coli O157 in cattle is that their feed is often contaminated by the organism,” says Allen.
Run-off water from cattle operations can contaminate irrigation ponds and rivers, and may serve as infection points for wild game. Fecal contamination of hides and carcasses during slaughter is the primary cause of contaminated beef.
Indirect fecal contamination of produce by contaminated manure, fertilizer or irrigation water is thought to be responsible for the increase in foodborne disease attributed to produce.
Allen stresses, “We need to better understand how to minimize its presence in cattle, and design more effective intervention strategies that successfully eliminate it in foods, particularly produce.”
Prior to joining UBC in January, Allen worked within industry, researching a vaccine to minimize E. coli O157 prevalence in cattle. He continues this task at UBC.
Allen is also comparing various strains of E. coli O157 to devise better food safety policies and intervention strategies. This fall, he will collect physiological data on how different stressors such as heat or chemicals affect the bacteria.
“What we’re going to do is look at stress response and virulence gene expression and compare three lineages to see if there are differences explaining why these lineages are linked differentially to human disease.”