IT HAPPENED ON THE MOST ordinary of plays. Sixteen-year-old Boone Baker, playing wide receiver on the Austin High Maroons junior varsity last October 7, sprinted a quick five yards before turning and snagging a short pass from his quarterback sometime in the second half of a Friday night game against archrival Westlake High. Immediately after Boone caught the pass, he was tackled, hard, with his left shoulder crashing into the artificial turf of Chaparral Stadium. He remembers feeling a burning abrasion on his shoulder when he got up, but he shrugged it off and returned to the huddle.

As football games go, it was a mundane moment, with nothing to presage the medical nightmare that three months later would almost cost Boone his life and temporarily rob him of his mobility and his eyesight in one eye. On that seemingly insignificant play, this strapping, 176-pound, six-foot-two-inch teenager unknowingly joined the swelling ranks of athletes—from the National Football League to high school wrestlers—plagued by a new killer “superbug,” a pernicious staph infection that mimics the flu, races through the body with lightning-quick speed, and resists normal penicillin-based antibiotics. Known as MRSA (methicillin-resistant Staphylococcus aureus), this bacterial infection first emerged in hospitals five years ago, attacking vulnerable postoperative patients with compromised immune systems. But in the past two years, MRSA has made its deadly presence known in the community at large, with athletes being a prime target, since the bacteria thrives in steamy settings like locker rooms and enters the body through nicks, abrasions, and cuts.

But it’s not just athletes who are affected; a Fort Worth woman died in February from an infection suspected to be MRSA, which she contracted during a routine pedicure. But athletes constitute a high-risk category in which MRSA continues to show up in clusters, with disastrous consequences. In 2003 MRSA claimed the life of Ricky Lannetti, who played football for Lycoming College, in Pennsylvania, and sidelined ten football players at a Connecticut college, hospitalizing two. That same year, the infection attacked five members of the St. Louis Rams. In Texas serious outbreaks have been reported among football teams in Denton County, Pasadena, and South Texas, where an alarming 81 cases were reported in 2004.

Health care professionals—from the National Athletic Trainers’ Association to the Texas Department of State Health Services—have begun campaigns to educate the public, and especially coaches and athletes, about how to prevent and detect the infection. “I almost don’t go to a meeting anymore that it is not a topic on the agenda,” says Allen Hardin, the co-director of sports medicine at the University of Texas, where the football team has gone to single-use disposable towels in its war to combat transmission of the infection. At the University Interscholastic League, which oversees public high school athletics, a medical advisory committee is developing a poster to place in locker rooms across the state, featuring pictures of an early-stage infection, which can look as harmless as a mosquito bite, and recommending tips for locker room cleanliness.

Neither the Centers for Disease Control and Prevention nor the state health department keeps statistics on how many cases have occurred in Texas or around the country, but one CDC study suggests that MRSA may occur in as many as 25 out of every 100,000 people. Anecdotal evidence is frightening: One Austin pediatric surgeon in a four-physician practice reported to me that she and her partners averaged ten surgeries per week to drain MRSA abscesses. Officials at Texas Children’s Hospital, in Houston, say that the incidences of MRSA have more than doubled since 2003, and the new bacteria now accounts for 77 percent of otherwise healthy patients with staph infections there. Since 2002, the hospital has lost six patients to MRSA, some of them infants. “This is not an athlete problem—it’s a people problem,” says Dr. Sheldon L. Kaplan, the chief of the hospital’s infectious-disease clinic.

As Boone Baker’s case illustrates, MRSA often starts out by disguising itself as an innocuous skin wound resembling a pimple or an ingrown hair. Immediately after the Westlake game, Boone showered and applied an antibiotic ointment to his shoulder burn and continued to do so all weekend. But after practice the following Monday, Boone noticed that the burn had become a purplish boil and showed it to a trainer, who directed him to see a doctor. The next day, his doctors lanced and drained the wound, cut out the pustule, took a culture, and identified the infection as MRSA. That called for a specific type of antibiotic, Septra, which, unlike penicillin-family drugs, can still knock out MRSA. Ten days later, Boone was cleared to return to football.

“I thought it was completely behind us,” says Missy Baker, Boone’s mom. When Boone fell ill with the flu this January, as did many other students at Austin High, the thought of a recurrence of MRSA, attacking his flu-weakened immune system, never entered her mind. Suffering nausea and a high fever, Boone lay on a couch for several days while Missy consulted his pediatrician’s nurse by phone. Certain that Boone’s lethargy was brought on by dehydration, Missy plied her son with Gatorades, but nothing about his condition made her panic.

Until Thursday, January 19. Early in the day, Boone complained of excruciating back pain.  He rebounded, but soon the pain returned with scarier symptoms: fast and shallow breathing, neck pain, and a sudden inability to move his legs. Fearful that Boone had meningitis, Missy and her husband, Coalter, raced their son to an emergency room.

Life-threatening infections like Boone’s could be avoided with some basic health precautions. Yet a CDC study released in February about the Rams’ experience indicates that, even at the professional level, trainers have been slow to appreciate the risk of MRSA. On an average week, Rams players reported two to three “turf burns,” severe abrasions where the skin is rubbed raw by high-velocity contact with artificial turf. Most of the burns were left uncovered during subsequent play. Trainers who treated the wounds on the sidelines did not have ready access to hand-washing or sanitizing materials. Players shared soap, towels, whirlpools, and workout equipment. The CDC study also determined that the infected players had a history of unusually high use of antibiotics, which could have made them more susceptible to the methicillin-resistant strain of staph. In fact, researchers believe that overuse of antibiotics in the community at large has enabled the new strain of bacteria to emerge. The CDC is advising schools that the best way to prevent MRSA is to disinfect common areas, like whirlpools and showers; stop the practice of sharing towels and soap; and encourage frequent hand washing. Players should see trainers about every abrasion, which should be cleaned and covered immediately.

If the prevention of MRSA is relatively simple, the treatment is anything but. When Boone arrived at Brackenridge Hospital, he was immediately placed in the intensive-care unit. For the first night, he was given fluids intravenously while awaiting the results of blood tests to determine whether he had MRSA. By the time the infection was confirmed as MRSA, two days later, the bacteria had erupted in pustules all over his body. Doctors ordered massive doses of antibiotics and waited for his system to respond. But it didn’t. Something was blocking the antibiotics from taking effect. Boone’s heart was racing at a rate that doctors compared to running a marathon at top speed. His midsection became bloated as his kidneys and liver began to fail. “He was dying, effectively,” his dad recalls.

By this time, whole teams of doctors were standing at Boone’s bedside. A decision was made to conduct a full-body MRI. After a torturous five-hour session (the MRI was halted several times when Boone’s temperature spiked and sent him into uncontrollable chills), doctors found the source of his paralysis: two baseball-size abscesses around the base of his spine. On Monday, Boone underwent back surgery to drain and remove the abscesses and received another round of intensive antibiotics. He remained in the ICU, and doctors immediately began to see progress.

But Wednesday brought another scare: Upon removal of the breathing tube that had been placed down his throat during surgery, Boone said, “Mom, I can’t see out of my right eye.” Yet another specialist was called in, who confirmed that the MRSA was indeed attacking his eye. For the next couple days, Boone would need to be awakened every hour so a nurse could administer three types of antibiotic eyedrops.

On Super Bowl Sunday, seventeen days after he had arrived at the hospital, Boone was allowed to have visitors. A physical therapist helped him take his first painful steps with the aid of a walker. But Boone experienced another setback when it was discovered that he had some blood clots and that a small pustule on his lung had not responded to the antibiotics. More surgery would be needed.

While Boone had fought for his life in the hospital, his illness had become a statistic in one of the ongoing issues involving MRSA: whether artificial turf can cause the infection. This is a question that affects sports at all levels and can have a major economic impact on companies that produce artificial turf. The CDC, however, is not inclined to blame turf. In its study of the St. Louis Rams outbreak, testing of the turf did not turn up evidence of contamination. “We didn’t really feel it was the main mechanism for transmission,” says Jeff Hageman, an epidemiologist for the CDC. Rather, Hageman said, researchers found a high incidence of infection among players with the most skin-to-skin contact.

But that has not stopped the MRSA scare from fueling the prolonged dispute between natural-turf and artificial-turf advocates. Brad Fresenburg, a University of Missouri turf grass expert, recently conducted studies of the temperature of his school’s synthetic field and found an astonishing 173-degree temperature on a 98-degree day, a temperature disparity he believes contributes to bacterial proliferation. “Natural grass has a microbial system. It’s self-cleaning,” Fresenburg wrote. “These synthetic fields don’t have that.” He suggests that synthetic turf be sprayed with a disinfectant when an infection is suspected.

Advocates for synthetic fields disagree, noting that the new generation of turf contains ground automobile tires, which include sulfur and zinc, agents that kill bacteria. “There’s no evidence to support the theory that synthetic turf breeds bacteria,” says Andrew McNitt, an assistant professor of soil science at Penn State University. “The majority of the data shows that the fact that there are more abrasions means the athletes have more entry points for the bacteria to get in their bodies.”

Yet the industry itself is concerned about the possibility of bacterial contamination. In November Astro Corporation unveiled a new product containing an antibacterial agent that it says will protect the turf from corrosion. Several companies have developed products to fight MRSA, including Cleveland-based Pioneer Manufacturing, which, in addition to making paint used to mark athletic fields, now sells an artificial-turf disinfectant called Titan Turf Gard. But the CDC’s Hageman believes that the best way to prevent MRSA from spreading is for trainers to immediately treat and cover wounds like Boone’s.

Boone’s doctors don’t know where the MRSA originated, though they believe it entered his body through the turf burn. Westlake trainer Brad Hawkins says he knows of no MRSA cases at the school, leading him to conclude that the school’s artificial turf is not contaminated. But Westlake athletic director and head football coach Derek Long acknowledges that the school once scrubbed down its field following a staph outbreak (not of the MRSA variety), in 2003. The Bakers aren’t interested in assigning blame but want parents, kids, and trainers to know what to watch for and how to avoid infections. Coalter is haunted by a doctor’s comment that Boone would have died if he and Missy had waited another day to get him to the emergency room.

Shortly before Boone left the hospital, I took my son, Michael, who is a friend of Boone’s, for a brief visit. Missy had prepared us to expect him to look like a prisoner of war. She wasn’t exaggerating: He had lost 41 pounds. Finally, on February 14, more than three weeks after he had been rushed to the emergency room, Boone was cleared to go home, where he remained for a couple months, staying current on his schoolwork and taking his antibiotics intravenously. His vision has returned, but he can’t return to playing sports until he finishes all his medicine—July at the earliest—and an orthopedic specialist determines that no bones have been compromised.

I dropped in to see him a few days after he got home, and though he had put on a few pounds, he still looked gaunt. He was sitting in a chair with an IV in his arm. We chatted for a few minutes, and then I asked him: “Will you play football again?” His answer was immediate. “Oh, sure,” he said, as if nothing had ever happened.