Every illness is a story, and Annie Page’s began with the kinds of small, unexceptional details that mean nothing until seen in hindsight. Like the fact that, when she was a baby, her father sometimes called her Little Potato Chip, because her skin tasted salty when he kissed her. Or that Annie’s mother noticed that her breathing was sometimes a little wheezy, though the pediatrician heard nothing through his stethoscope.

The detail that finally mattered was Annie’s size. For a while, Annie’s fine-boned petiteness seemed to be just a family trait. Her sister, Lauryn, four years older, had always been at the bottom end of the pediatrician’s growth chart for girls her age. By the time Annie was three years old, however, she had fallen off the chart. She stood an acceptable thirty-four inches tall but weighed only twenty-three pounds—less than ninety-eight per cent of girls her age. She did not look malnourished, but she didn’t look quite healthy, either.

“Failure to thrive” is what it’s called, and there can be scores of explanations: pituitary disorders, hypothyroidism, genetic defects in metabolism, inflammatorybowel disease, lead poisoning, H.I.V., tapeworm infection. In textbooks, the complete list is at least a page long. Annie’s doctor did a thorough workup. Then, at four o’clock on July 27, 1997—“I’ll never forget that day,” her mother, Honor, says—the pediatrician called the Pages at home with the results of a sweat test.

It’s a strange little test. The skin on the inside surface of a child’s forearm is cleaned and dried. Two small gauze pads are applied—one soaked with pilocarpine, a medicine that makes skin sweat, and the other with a salt solution. Electrodes are hooked up. Then a mild electric current is turned on for five minutes, driving the pilocarpine into the skin. A reddened, sweaty area about an inch in diameter appears on the skin, and a collection pad of dry filter paper is taped over it to absorb the sweat for half an hour. A technician then measures the concentration of chloride in the pad.

Over the phone, the doctor told Honor that her daughter’s chloride level was far higher than normal. Honor is a hospital pharmacist, and she had come across children with abnormal results like this. “All I knew was that it meant she was going to die,” she said quietly when I visited the Pages’ home, in the Cincinnati suburb of Loveland. The test showed that Annie had cystic fibrosis.

Cystic fibrosis is a genetic disease. Only a thousand American children per year are diagnosed as having it. Some ten million people in the United States carry the defective gene, but the disorder is recessive: a child will develop the condition only if both parents are carriers and both pass on a copy. The gene—which was discovered, in 1989, sitting out on the long arm of chromosome No. 7—produces a mutant protein that interferes with cells’ ability to manage chloride. This is what makes sweat from people with CF so salty. (Salt is sodium chloride, after all.) The chloride defect thickens secretions throughout the body, turning them dry and gluey. In the ducts of the pancreas, the flow of digestive enzymes becomes blocked, making a child less and less able to absorb food. This was why Annie had all but stopped growing. The effects on the lungs, however, are what make the disease lethal. Thickened mucus slowly fills the small airways and hardens, shrinking lung capacity. Over time, the disease leaves a child with the equivalent of just one functioning lung. Then half a lung. Then none at all.

The one overwhelming thought in the minds of Honor and Don Page was: We need to get to Children’s. Cincinnati Children’s Hospital is among the most respected pediatric hospitals in the country. It was where Albert Sabin invented the oral polio vaccine. The chapter on cystic fibrosis in the “Nelson Textbook of Pediatrics”—the bible of the specialty—was written by one of the hospital’s pediatricians. The Pages called and were given an appointment for the next morning.

“We were there for hours, meeting with all the different members of the team,” Honor recalled. “They took Annie’s blood pressure, measured her oxygen saturation, did some other tests. Then they put us in a room, and the pediatrician sat down with us. He was very kind, but frank, too. He said, ‘Do you understand it’s a genetic disease? That it’s nothing you did, nothing you can catch?’ He told us the median survival for patients was thirty years. In Annie’s lifetime, he said, we could see that go to forty. For him, he was sharing a great accomplishment in CF care. And the news was better than our worst fears. But only forty! That’s not what we wanted to hear.”

The team members reviewed the treatments. The Pages were told that they would have to give Annie pancreatic-enzyme pills with the first bite of every meal. They would have to give her supplemental vitamins. They also had to add calories wherever they could—putting tablespoons of butter on everything, giving her ice cream whenever she wanted, and then putting chocolate sauce on it.

A respiratory therapist explained that they would need to do manual chest therapy at least twice a day, half-hour sessions in which they would strike—“percuss”—their daughter’s torso with a cupped hand at each of fourteen specific locations on the front, back, and sides in order to loosen the thick secretions and help her to cough them up. They were given prescriptions for inhaled medicines. The doctor told them that Annie would need to come back once every three months for extended checkups. And then they went home to start their new life. They had been told almost everything they needed to know in order to give Annie her best chance to live as long as possible.

The one thing that the clinicians failed to tell them, however, was that Cincinnati Children’s was not, as the Pages supposed, among the country’s best centers for children with cystic fibrosis. According to data from that year, it was, at best, an average program. This was no small matter. In 1997, patients at an average center were living to be just over thirty years old; patients at the top center typically lived to be forty-six. By some measures, Cincinnati was well below average. The best predictor of a CF patient’s life expectancy is his or her lung function. At Cincinnati, lung function for patients under the age of twelve—children like Annie—was in the bottom twenty-five per cent of the country’s CF patients. And the doctors there knew it.

It used to be assumed that differences among hospitals or doctors in a particular specialty were generally insignificant. If you plotted a graph showing the results of all the centers treating cystic fibrosis—or any other disease, for that matter—people expected that the curve would look something like a shark fin, with most places clustered around the very best outcomes. But the evidence has begun to indicate otherwise. What you tend to find is a bell curve: a handful of teams with disturbingly poor outcomes for their patients, a handful with remarkably good results, and a great undistinguished middle.

In ordinary hernia operations, the chances of recurrence are one in ten for surgeons at the unhappy end of the spectrum, one in twenty for those in the middle majority, and under one in five hundred for a handful. A Scottish study of patients with treatable colon cancer found that the ten-year survival rate ranged from a high of sixty-three per cent to a low of twenty per cent, depending on the surgeon. For heartbypass patients, even at hospitals with a good volume of experience, risk-adjusted death rates in New York vary from five per cent to under one per cent—and only a very few hospitals are down near the one-per-cent mortality rate.