Escherichia coli is back. Every year an attack of food vs. people grips us, makes us think twice about crunching into that fresh cucumber or apple or celery stick, and reminds us of how deep in excrement we all are.
This year’s E. coli outbreak in Germany is by all accounts a real doozy. In the past two weeks, 2,000 people across Europe and at least four in the United States have been affected. About 500 have developed hemolytic uremic syndrome—an otherwise rare complication that damages kidneys and destroys red blood cells—and 22 have died. Indeed, this outbreak appears to have stricken ill a record number of people for E. coli, though it falls far short of the legendary salmonella outbreak in 1994 that hit 224,000 people who ate contaminated American ice cream.
The severity of this E. colihas led some talking heads to hint that this might be the big one—a super-toxic, super-drug-resistant, super-sticky, never-before-seen, Armageddon sort of thing. To add to the drama, irate Spanish farmers are dumping vegetables at the local German Embassy, haggard public health officials are advising simultaneous calm with extra-heightened awareness (read: paranoia), and clumsy medical experts are grinning on TV like they just won the lottery. It’s the typical circus that accompanies most public-health calamities, which begs the question: Should we be significantly more frightened of the German strain than of other E. coli?
My strong sense is no— the facts simply don’t support a doomsday scenario. While any new strain carries the potential for a new wrinkle, this one seems to have only the usual bag of E. coli tricks. The German E. coli is categorized scientifically as strain O104 (that’s oh-104, not zero-104) based on various characteristics of its cellular composition. Yet it causes a disease identical to that caused by the famous O157 strain, previously the dominant perpetrator of severe E. coli- related intestinal disease.
Beyond its lack of novelty, the most important clue that this is not the big one is the lack of secondary cases; the disease has spread to few if any people living with or caring for the sick. In contrast, outbreaks of diseases like cholera are fueled by secondary (and tertiary, etc.) cases, such that a single person can sicken an entire town. With the German O104, ingestion of bean sprouts (or perhaps another food to be blamed later) is the cause, not your neighbor’s lousy hygiene.
Yet here we are in the midst of extreme hype around the situation. Why all the fuss? There are at least two distinct reasons for the mismatch. First is the always-present, always-perverse financial incentive for news organizations to goose up any outbreak or fan any panic: For them, bigger and badder sells more papers, drives more clicks, and attracts more eyeballs.
The larger reason, however, is this: People become ill from E. coliby eating shit. Simple, right? Little attention is given to the likeliest reason so many people have been affected by the German strain—they probably ingested unusually large amounts of the bacteria. Whatever (bean sprouts or cucumbers or whatever) was contaminated was really contaminated. But try getting Anderson Cooper to explain that your illness is due to the fact that too much bacteria from an animal’s colon have ended up in your stomach.
Consider this: Recent U.S. outbreaks (mostly O157) have come from across the edible spectrum—luncheon meat, hazelnuts, cheese, romaine lettuce, and beef. What do all of these things have in common, other than being comestibles? Almost nothing, except that all those foods are awash with shit. Excrement is marvelous fertilizer—cheap and plentiful and always nearby. So it ends up on tomatoes and cucumbers and berries (and bean sprouts) and pretty much everything else that grows close to the ground. It also seeps into water tables, contaminating what we drink and what we wash our fruits and vegetables with.
Cows and pigs and the other animals we eat are full of shit as well. Not surprisingly, given the brutality of how we kill them, a slaughtered animal’s intestinal contents can end up on their prized carcass … and then in that hamburger you just ate. Mes amis, despite its French name, an abattoir lacks a certain Parisian refinement. The crap flies.
So rather than give us the straight stuff, the CDC and Anderson Cooper and all the experts tiptoe around the inconvenient truth by medicalizing and scientific-izing the topic, perhaps trying to induce a high school science class type stupor. We hear of “horizontal transmission of genetic elements” and “virulence factors” and see photos showing 100X images of E. coli on an agar plate as if they were mug shots. They’re like parents too nervous to tell their curious child how babies are made; they fall into recitations about meiosis and reproductive glands and ova and how Mommy and Daddy love each other and succeed only in conveying (and amplifying) anxiety while failing to impart useful information.
As things finally settle in Hamburg, it’s worth recalling the first E.coli outbreaks that occurred at restaurants like McDonalds and Jack in the Box in the 1980s. These and others stemmed from undercooked hamburgers and introduced the world to E. coli O157. The behavior of this bacterium, once elucidated, proved to be truly chilling. Unlike previously known E. coli, O157 borrowed a gene from a completely different bacterium (Shigella flexneri) that produces the shiga toxin, which causes dysentery. This Yankee swap of genetic bits across species is what gives scientists nightmares. E. coli demonstrated evolution in action, right under our noses and at Warp 7 speed. Creationists take notice: This is the real deal.
The current German O104 situation is surely awful and tragic, but it has introduced no novel threat. It has grimly served to remind us of the frailty of life and the wonders of good plumbing. More than anything else, the science behind E. coliemphatically points out something far more horrifying than any one outbreak: Naturedoesn’t like us. It doesn’t hate us, but it doesn’t like us. Rather, it is perfectly and eternally disinterested.