Microcosm_ E. Coli and the New Science of Life - Carl Zimmer [32]
I go with my wife and two daughters to a few fairs each summer, and each time we go, I lose my sense of time. I feel as if I’m back in an age when a typical ten-year-old would know how to shear a sheep. But just when I’ve almost completely lost my moorings in a tent full of livestock, I notice a wooden post staked in the ground by the entrance, holding a box of soap. It snaps me back to the twenty-first century, and when we leave the tent I make very sure my daughters scrub their hands.
These tents are home to some exquisitely vicious bacteria. The microbes live in the animals winning the ribbons at the fairs, and they fall with the droppings into the hay, float off on motes of dust, hitchhike on the bristles of flies. They spread through the tents, sticking to floors and fences and wool and feathers. It takes a tiny dose of them—just a dozen entering the mouth—to make a person hideously ill. The intestines bleed; kidneys fail. Antibiotics only make the attack worse. All doctors can do is hook their patients to an intravenous line of saline solution and hope for the best. Most people do eventually recover, but some will suffer for the rest of their lives. A few will die.
When pathologists test the fatal bacteria, they meet up with a familiar friend: E. coli.
E. coli comes in many strains. All of them share the same underlying biology, but they range enormously in how they make a living. Most are harmless, but outside laboratories, E. coli also comes in forms that can sicken or kill. To know E. coli, to know what it means for it to be alive, it’s not enough to study a tame strain such as K-12. The deadly strains are members of the species as well.
Scientists did not appreciate how dangerous E. coli could be for decades after Theodor Escherich discovered the bacteria. The first clear evidence that not all strains of E. coli were harmless bystanders came in 1945. John Bray, a British pathologist, had been searching for the cause of “summer diarrhea,” a deadly childhood disease that swept across Britain and many other industrialized countries every year. Bray hunted for bacteria that were common in sick children and missing from healthy ones.
Bray searched for the bacteria with antibodies, the best tools of his day. Antibodies are made by our immune cells when they encounter proteins from a pathogen. The antibodies can then attack the pathogen by recognizing its protein. Because antibodies are so exquisitely specific to their targets, they will ignore just about any other protein they encounter. Bray created antibodies to pathogens such as Salmonella by injecting the bacteria into a rabbit. Once the rabbit’s immune system had mounted an attack, Bray extracted the antibodies from its blood. He then added the antibodies to cultures of bacteria he reared from the diarrhea of sick children. He wanted to see if they would reveal any pathogens. They did not.
As Bray puzzled over what kind of antibodies to make next, a pediatrician mentioned to him that children sick with summer diarrhea give off a semen-like smell. Bray knew that was also the smell of certain strains of E. coli. So he made antibodies to E. coli and added them to his cultures. They immediately found their targets. Bray found that 95 percent of the sick children responded to his antibody test. Only 4 percent of the healthy children did.
Bray had identified only a single strain of disease-causing E. coli, but in later years scientists would identify many others. Some had long been known to medicine, but under different names. In 1897, Kiyoshi Shiga, a Japanese bacteriologist, discovered the cause of a form of bloody diarrhea called bacillary dysentery. It had E. coli’s basic rod-shaped anatomy, but Shiga did not call it E. coli. After all, many other species were rod shaped as well. And Shiga’s microbe produced a cell-killing toxin that no one had ever observed E. coli make. In addition, E. coli could digest lactose, the sugar in milk, but Shiga’s bacteria could