The E. coli strain sickens more than 60,000 North Americans every year, and sometimes kills. Seven died and 23,000 became ill in Canada’s worst incident when O157 contaminated the water supply in Walkerton, ON in 2000. While there were no fatalities linked to contaminated beef at XL Foods’ Alberta plant in 2012, it made national headlines and prompted a massive recall of beef products.
“E. coli O157 wasn’t really linked with foods until the 1990s when the term ‘hamburger disease’ was coined following the incident at the (American burger chain) Jack in the Box and a few other outbreaks,” notes Darren Korber, a professor of food and bioproduct sciences and an expert on the pathogen.
“Since then, there have been thousands and thousands of laboratory-confirmed cases. That’s partly because the symptoms are so drastic and we’ve become very good at detecting it, but it really has spread.”
Korber is a strong advocate of food-safety measures, but says they must extend from “farm to fork,” and O157 outbreaks show this is a challenging concept for many consumers.
“There’s really no reason for anybody to get sick from E. coli O157 from raw meat products,” says Korber. “It bugs me when I see food thrown into the dump because E. coli O157 was detected in hamburger, as was the case with XL Foods. You cannot get sick from beef as long as it is handled and cooked properly.”
It’s also a misconception that this pathogen can be entirely eliminated from the food system, and Korber’s extensive research into O157 shows why. Take, for example, his work on its ability to survive in soil.
“The general thinking used to be that these organisms don’t survive very long out of the gastrointestinal tract,” he says. “But in sterile soils, you could detect them more than a year later and they even increased in number if you added water. These were organic soils with a bit of material for them to grow on. And you would see the numbers increase from, say, one million to 100 million cells per gram of soil in only a few weeks.”
In another study, Korber found upwards of 60 per cent of feedlot cattle were infected with O157. It lives (harmlessly) in the cow’s rumen and is constantly being excreted, not only contaminating the soil in the pen but clinging to the legs and bellies of cattle.
So it’s inevitable it will show up at slaughter plants, and that presents a huge challenge. While these facilities use a variety of cleaning procedures, O157 is a determined foe. In a recent paper with colleague Sinisa Vidovic, Korber notes the genetic make-up of this variety of E. coli has given it “survival capabilities to endure a wide spectrum of stressors found within the human food chain.”
Expose it to cold or heat, and O157 becomes better able to withstand extreme temperatures, and the same thing happens if you expose it to low pH. That’s not good if your approach to cleaning is limited to using hot water with an acidic disinfectant in it.
And the pathogen’s adaptive ability doesn’t stop there.
“We often see something called cross-protection,” says Korber. “If you expose them to low pH, for example, they become more resistant to high temperature or oxidative stress, and more difficult to kill.”
Research has found O157 can even acquire resistance while in what’s called the “stationary” phase when it’s not actively growing, he notes.
“It’s a bit like an onion — you keep pulling back layers and finding new ones below them,” says Korber. “We’re finding these organisms have multiple stress-response mechanisms and have evolved and developed very complex regimes to survive all of these things that we call ‘insults’ — UV irradiation, oxidation, pH, temperature, and other stresses. Their repertoire is really quite amazing.”
The cattle industry would love to have a vaccine to eliminate O157, and one is licensed for Canada. But it’s not a silver bullet — it only reduces “shedding” of the pathogen in infected cattle. Even if you could develop one that was 100 per cent effective and lasted for a cow’s entire life, it likely wouldn’t be enough. O157 is not the only type of E. coli that produces the shiga-toxin that causes hemorrhagic diarrhea and, in severe cases, kidney failure, notes Korber.
“It would be nice to have a vaccine that was effective for O157 so we could get rid of it,” he says. “But the truth is that it isn’t the only one and, with time, another one would come along and replace it. In fact, we now test for various hemorrhagic non-O157 strains that include what is called the Big 6, which together cause more illnesses than O157.
“So I’m not harbouring any illusions that we can eradicate these organisms any time soon. We may learn something about it that could have general applicability to a whole range of pathogens that rely on similar infective mechanisms. But that’s probably the best-case scenario.”
However, that would be a big step forward in developing new defences against pathogens, and that is why Korber and others keep peeling back the onion layers, looking at things such as extracytoplasmic stress response and rpoE sigma factor (a regulator of stress response).
“We hope by understanding the molecular response, we will learn ways to interrupt the way these pathogens utilize these stress response pathways. That sounds pretty nebulous for the general public, but that’s essentially what we’re trying to do.”
But the key message is plain: This is a battle centred around building multiple lines of defence, and not by eliminating the enemy.
“When we talk about food safety barriers against pathogens, we typically are referring to what we call ‘hurdle technology,’” he says. “We want to set up as many barriers as we can against the pathogenic organism growing, surviving, or occurring in food.”
Reducing rates of infection in cattle, whether through vaccines or better management practices, is one part of that, as are all the prevention and control procedures in slaughter plants and food-processing facilities. An extensive monitoring and testing system has also been created to detect hazards and to sound a quick alert when something goes awry.
“You identify where the hazard may occur and you control that hazard,” says Korber.
And that’s the approach consumers must also take, he adds.
“People are getting sick and dying from some of these outbreaks, but science can’t make E. coli O157 disappear,” he says. “That’s why consumer education is critical.”