With recent estimates attributing the ongoing German E. coli outbreak to 3,406 illnesses and 39 deaths, it has become the deadliest — and second largest — E. coli outbreak in history. And while already singular in its impact, the outbreak sets itself farther apart in that its infections have resulted not from the infamous E. coli strain O157:H7, but O104:H4, a rare strain never before linked to a large foodborne illness outbreak.
In the weeks following the outbreak’s onset in Germany, an unprecedented collaboration of scientists worldwide have taken to studying O104, analyzing its genes to compare it to other strains and better understand its underlying characteristics. Jorge Girón, Ph.D., E. coli researcher and associate professor of microbiology at the University of Florida’s Emerging Pathogens Institute, believes this outbreak could lead to significant adjustments in how both agriculture producers and healthcare providers deal with E. coli.
What most predominantly differentiates O104 from O157 is its adoption of numerous traits not typically found congregated in one strain: Not only does it produce the noxious Shiga toxin of the virulent enterohemorrhagic strains, it also possesses defensive enteroaggregative traits –a combined mouthful of properties much more difficult to tolerate physically than verbally.
The term “enteroaggregative” refers to sticky strains of the bacteria that group together –aggregate — into a “stacked-brick pattern” and cling to intestinal tracts. Once there, they induce heavy mucus production in their host’s intestines, which they then use for both protection and sustenance.
Enteroaggregative E. coli are known to cause persistent diarrhea, but are historically unrelated to hemorrhaging and hemolytic-uremic syndrome (HUS), the acute kidney disease caused by Shiga toxin-producing enterohemorrhagic E. coli.
O157 is enterohemorrhagic, but not enteroaggregative. The bacteria do not aggregate together, but they possess cell structures that help them adhere to intestines, where they produce the Shiga toxin known for inflicting HUS and making E. coli a household name among pathogens.
By comparison, O104 clumps together and spurs mucus production for protection while also releasing Shiga toxin into the bloodstream, an adaptation that has resulted in at least 826 cases of HUS in this outbreak.
As Ross Anderson reported for Food Safety News two weeks ago, this outbreak’s ratio of HUS cases — now roughly one in four — is alarmingly high, at least for the time being. HUS cases among O157 infections generally average closer to one in 10.
Though Girón cautioned it is too early to tell if O104 is truly more virulent than O157, he said O104’s nasty combination of traits likely gives it the edge.
“The mucus production explains why these bacteria are so persistent,” he said. “It’s very hard for the immune system to get rid of them while they’re embedded in the host material, and it could be that the bacteria are releasing the toxins without even being attacked.”
O104 is not the first known strain with this particular résumé of traits — a similar strain known as O111:H2 caused a small outbreak in France in 1992 — but it has by far caused the greatest impact, and it distinguishes itself even further in the victims it affects.
Girón voiced special concern in the fact that O104 has predominantly caused HUS in adults, when children and the elderly are historically the main victims of Shiga toxin-producing E. coli. On Tuesday, a 2-year-old boy became the first child to die from the outbreak, which has killed 37 adults — mainly women.
Thus far, no clear explanation for this discrepancy has surfaced, though it might be partially related to eating habits, with children less likely to eat the sprouts that have been implicated as the source of the outbreak.
Numerous other commentators, including “Superbug” author and blogger Maryn McKenna, have brought up O104’s extensive list of antibiotic resistances, citing it as an enormous –though tangential — public health concern. Physicians know not to prescribe antibiotics for O157 infections because the sudden killing of the bacteria can release HUS-inducing and potentially deadly amounts of Shiga toxin.
As Girón pointed out, that fact could have created one major problem in the early development of the outbreak: It is likely that German hospitals were only screening the first enterohemorrhagic E. coli symptoms for O157 and not O104, which no one would have suspected before news of the outbreak spread.
“When people come into a hospital with bloody diarrhea, they would normally assume it’s O157 and not give antibiotics to the patients,” he said. “In this case, because it wasn’t O157, the physicians might have thought it was okay to give antibiotics, not knowing that O104 would produce the Shiga toxin.”
This potential misunderstanding over antibiotics might at least partially explain the high rate of HUS among the ill. Girón said this outbreak may necessitate new screening procedures at hospitals to account for O104 alongside O157, ensuring patients don’t receive antibiotics that could exacerbate their illness or kill them.
In regard to its environmental origins, O104 takes after the more-prevalent enteroaggregative E. coli in that only humans are its host, not cattle or other ruminants. It can spread through contact with objects in the environment, water, food, or human fecal matter.
As a final caution, Girón warned that only sufficient cooking can eliminate E. coli from vegetables. Just weeks ago, he and several colleagues published a study showing that E. coli can infiltrate and survive in the inner tissues of spinach after industrial washing techniques and thorough washing in kitchens.
“If vegetables are contaminated with E. coli, the only way to absolutely make sure they’re safe is to boil or cook the plant. That’s something we’re just now starting to understand,” he said. “All of this is going to change how produce is treated at the industrial setting.”