It started with something that looked like a spider bite.
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Mollie Logan barely noticed it. She was focused on 15-day-old Isabella, the baby she and her husband had longed and tried for since their marriage four years earlier. The new mom was too happy, and far too sleep-deprived, to pay much attention to the small, hard red bump on her inner thigh.
The bump hurt, and it itched; Logan, then 24, absently scratched it. And it grew: In three days, the dime-sized pimple spread into a hot red band that encircled her leg. She headed to her primary care doctor, who drained the swelling and gave her an antibiotic mild enough to let her keep breast-feeding. Relieved the episode was over, she hurried home to Isabella.
That evening, while the baby was nursing, Logan felt an unfamiliar warmth. She rolled Isabella gently outward and froze: The baby’s right chest was as flushed and swollen as her mother’s thigh. Logan and her husband, Brian, rushed the feverish, limp infant to a pediatric emergency room in their section of Omaha, Nebraska, where doctors hooked Isabella to an IV of fluids to keep her hydrated.
It took 48 hours to find the right mix of drugs that could force down the baby’s 103.5-degree fever, while the Logans and their extended family fretted sleeplessly in hospital chairs. And it was another day before tests pinpointed the source of the problem. Isabella and her mother were both infected with an organism no one in their family had ever heard of, a bacterium known as community-associated methicillin-resistant Staphylococcus aureus—CA-MRSA for short.
The doctors explained that the bug was an aggressive staph infection with an ugly twist: Only a few drugs worked against it. Mother and baby needed much stronger antibiotics. Logan would have to stop breast-feeding, because her milk could pass even more drugs to Isabella, throwing off the baby’s treatment. Worse, 3-week-old Isabella required immediate surgery to clean out the angry abscess that was spreading across her chest. Two years later, Logan still weeps when she talks about it. “They told me, ‘We have only one chance to get this right,’” she says. “It was the toughest thing ever, to hand her over.”
Just the beginning
Isabella sailed through the surgery; the swelling quickly subsided, and her color and energy improved. After 10 days in the hospital, Logan brought her home. She had lost much of the first month of her daughter’s life but assumed the crisis was over.
She had no idea that this was only the beginning of her odyssey to the limits of medicine.
Bacteria and the drugs we deploy to kill them have been locked in an arms race since penicillin, the first mass-produced antibiotic, was first given to a patient in 1941. The first penicillin-resistant organism was found only one year later. Now a broad array of scientists and health authorities worry that the bacteria are gaining an edge in the race: Germs with built-in protection against antibiotics, such as the one that attacked the Logans, become more common every year.
“Every known bacteria capable of infecting humans has developed resistance to some antimicrobials,” says Robert C. Moellering Jr., M.D., professor of medicine and medical research at Harvard Medical School in Boston who has studied the issue of antibiotic resistance for more than 35 years. The overuse of antibiotics exacerbates the problem, Dr. Moellering says, because the more we expose germs to the drugs, the better they become at building resistance. Researchers suspect that the use of antibiotics in animal feed plays a role; drug-resistant bacteria may develop in animals such as cows, chicken and salmon and then infect humans who eat them.
For the past few decades, the perpetual struggle between bugs and drugs took place mostly in hospitals, among the most medically fragile patients. Almost 2 million people contract infections in U.S. hospitals every year, and about 90,000 of them die, according to the Centers for Disease Control and Prevention in Atlanta. Now the problem has begun to appear outside hospital walls, with resistant organisms causing a wide variety of infections in otherwise healthy people.
In 2001, for example, one in four children in day care centers studied in Michigan had a resistant form of a bacterium that causes ear infections, a scourge of toddlers. The same year, a study in The New England Journal of Medicine found that 22 percent of women treated for urinary tract infections at two college health centers in California and Minnesota had a drug-resistant form of E. coli. And in March of last year, the CDC reported finding a strain of the almost-vanished disease tuberculosis that is immune to at least five drugs, making it virtually impossible to treat except with the 19th-century method of cutting out pieces of lung.
The drug-defying bug that attacked Mollie and Isabella Logan unnerves researchers perhaps more than any other. In less than 10 years, CA-MRSA has soared from a barely noticeable blip on disease charts to a major cause of widespread, devastating and sometimes fatal infections. A strain of it has been linked to rare illnesses that were almost never caused by old-fashioned, nonresistant staph: severe infections of the bloodstream that cause multiorgan failure, for instance, and pneumonia that kills by destroying the tissue of the lungs. It has even triggered necrotizing fasciitis, the “flesh-eating” infection associated with several types of bacteria.
Some CA-MRSA victims had preexisting health problems that might have made them vulnerable to the bacterium, such as a paraplegic woman in Fort Worth, Texas, who may have been infected during a salon pedicure and who died after complications from the infection triggered a heart attack. But others were strikingly healthy: Emory University in Atlanta has been battling an outbreak in its athletic department for the past two years; four female athletes, including swimmers and volleyball players, were among those mysteriously infected.
A study published last August in The New England Journal of Medicine made clear how aggressively MRSA has proliferated in communities: Nearly 60 percent of people who came to emergency departments in 11 different cities with skin infections had it. Cases have sprung up in every area of the country, and most of them cannot be linked to a larger CA-MRSA outbreak. “This is widespread,” says Henry M. Blumberg, M.D., professor of medicine in the division of infectious diseases at Emory University School of Medicine in Atlanta. “And everybody is potentially at risk.”
Isabella’s early brush with illness deeply frightened her parents. Once she came home from the hospital, they agreed that Brian would go back to work as an auto mechanic, but Mollie, who had been working as a nanny, would become a stay-at-home mom. The origin of the family’s infection remained a mystery: Isabella had clearly contracted the bug from her mother at birth, but doctors could not identify the source of Logan’s infection. Because she had the community version of MRSA, not the type confined to hospitals, it was impossible to know for sure where she picked it up.
To her parents’ relief, Isabella thrived—she had no more signs of illness and no indications that the potent drugs had affected her. But in November 2005, 15 months after her first scare, Logan found a hard, red pimple on her own right breast. Oh no, she thought. I know what this is.
Tests confirmed her suspicions. The bacteria had lurked somewhere in or on her body and recurred. A second set of doctors, from Infectious Disease Associates of Omaha, ordered lab tests to make sure the bug was vulnerable to the kind of antibiotics that can be taken at home in pill form—the very strongest tend to be given only by IV—and put her on a 20-day course of pills. Then they recommended a grueling 30-day cleansing called decolonization, which would wipe out any staph lingering on the Logans’ bodies or in their home.
Logan changed their sheets and towels every day, laundering each batch with a cup of bleach, which kills bacteria. She bought new hairbrushes, toothbrushes and combs. All three of them washed daily with Hibiclens, a harsh antibacterial soap used in hospitals. After they showered, Mollie and Brian sprayed the bathroom with Lysol; they did the same thing after either one of them used the toilet. They regularly wiped down every surface in the house with Clorox Disinfecting Wipes. And three times a day, they painted the inside of their nostrils with Bactroban, a thick antibacterial ointment. “If this was what we had to do to make sure our daughter didn’t have to fight for her life again, we were going to do it,” Logan says.
New tests showed that Mollie and Brian were clear of infection. But baby Isabella was carrying CA-MRSA in her rectum. Neither drugs nor the decolonization ritual had knocked it out. She could reinfect herself, or them, at any time.
The bacteria known as staph were discovered in the 1880s, but researchers guess that they are one of mankind’s oldest companions because they display such skill at living with and on us. According to the CDC, about one third of the U.S. population carries staph around on the outside of the body or on mucous membranes, usually in the nostrils; most of us will go unharmed, unless the bug happens to slip through a cut or break in the skin. Because it is one of the most common causes of infections, staph was one of the first targets for antibiotics. In fact, penicillin was discovered because the mold that produced it grew on, and killed, a petri dish full of staph.
But a mere two decades after penicillin’s debut, 80 percent of staph germs had become resistant to the drug. So chemists engineered a chemical cousin, called methicillin, as a substitute. They hoped the latest formula’s protection would last for decades, but the first evidence that staph could resist it appeared within two years. Then staph demonstrated a new trick: It developed additional resistance to a huge class of drugs, called beta-lactams, that share similar chemical structures. Beta-lactam antibiotics (not only penicillin and methicillin, but amoxicillin and cephalexin as well) are the drugs that doctors prescribe routinely for things such as urinary tract infections, pneumonia, ear infections—and staph. With a simple genetic change, MRSA had taken that entire class of drugs out of the physicians’ arsenal.
Drug-resistant staph appeared mainly confined to hospitals until around 1998. “We began seeing perfectly healthy kids with no risk factors coming in from the community with serious infections,” says Robert S. Daum, M.D., professor of pediatrics and chief of pediatric infectious diseases at the University of Chicago. “So we put together a study and found that in five years, the incidence of CA-MRSA infections had increased 25-fold.” The next year, a CDC report revealed that four children in Minnesota and North Dakota had died of overwhelming infections, all of them caused by staph resistant to beta-lactams. -
Suddenly, outbreaks of community MRSA seemed to be everywhere. Disease detectives found it in a prison and in jails, and among military trainees; among Native American users of traditional saunas and gay men who frequented bathhouses; in healthy newborn infants, methamphetamine users and tattoo recipients; and among high school and college athletes and players in the National Football League.
Spreads too fast for tracking
Some of the victims shared common characteristics: They lived in settings such as correctional institutions, where hygiene was hard to maintain, or spent time in hot, wet places such as sweat lodges, where bacteria often thrive and where surfaces might transfer the bug to bare skin. The athletes were more likely to share clothes and equipment and to have contact with each other’s cuts and abrasions. The meth addicts sometimes wounded themselves by scratching their skin raw while they were high. But some had no risk factors at all. And the victims’ sheer diversity made the case that MRSA was spreading faster in the community than it could be tracked.
Studies revealed that the MRSA that was infecting people in the wider world was not the same as the strain that threatened patients inside hospitals: The hospital strain had grown resistant to almost all drugs except for two or three very strong ones, but the community variety was still susceptible to medications outside the beta-lactam class. Molecular analysis showed that the two types of MRSA were genetically different as well, having acquired their drug resistance in different ways.
The two types had an additional, crucial difference. Hospital MRSA still attacked its victims via staph’s traditional route, by slipping into wounds such as surgical incisions and cuts made to accommodate catheters. But the community-associated type had learned something new: It was breaking through skin that appeared healthy and intact. The germ may have the power to slip through tiny abrasions people haven’t noticed, or, some doctors speculate, it might be penetrating skin on its own. The first sign of trouble often looks like an insect bite. And it is often misdiagnosed that way: An outbreak of more than 900 cases in the Los Angeles County jail was discovered when inmates complained about spider bites even after the jail had been doused with insecticide.
An insect bite was Cathy Thrasher’s first thought when the teacher and mother of three from Henderson, Kentucky, spotted a quarter-sized welt on the back of her thigh in August 2005. Thrasher, then 38, had just begun teaching seventh grade, and she was reluctant to interrupt her day to go to the doctor until her school’s nurse insisted.
Thrasher’s physician, James Buckmaster, M.D., had seen CA-MRSA before. He told her there was no way to know how she had acquired it; all he could do was send off a sample to be cultured for the bacteria and start her on the right drugs. The bug demonstrated its tenaciousness: Thrasher, her husband, Jobee, and her 11-year-old son, Clint, all popped up with boils before antibiotics brought things under control.
'I was terrified'
Or so she thought. Two weeks after Thanksgiving, she woke up at midnight unable to move the left side of her face. She was alone in the house, as Jobee had taken the children to visit family. “My father had just had a stroke, and now I thought I was having one,” she says. “I was terrified.” She called her best friend, a nurse, who rushed her to the emergency room. Doctors there suspected her illness was an especially serious sinus infection, and a CAT scan revealed that about 70 percent of her sinuses were blocked. “I remember saying to the doctor, ‘I feel so bad coming in for just a cold,’” Thrasher says. “And he said, ‘Oh, sweetheart, you have so much more than a cold. You are probably the sickest person we have seen today.’”
The hospital put her on the strongest IV antibiotics and placed her in strict isolation. Her family had to don masks, gowns and gloves before entering her room. But after four days, the drugs weren’t helping. Doctors punctured and drained her sinuses in surgery, which finally revealed the cause of the blockage: a CA-MRSA abscess. After Thrasher recovered, it took four rounds of strict decolonization, including twice-daily showers with antiseptic soap and weekly baths in water laced with bleach, before the family quelled the outbreak.
Thrasher says the experience left her family with medical bills of more than $50,000—about $5,000 of it not covered by insurance—along with an awestruck respect for germs. “For our family,” she says, “it was life-altering.”
The Logan family, meanwhile, thought their ordeal was over by the spring of 2006. They had slogged through the punishing decolonization process twice, enduring itchy skin, endless laundry and the ever-present faint scent of bleach. Isabella’s body was containing her infection: Periodically her bottom would swell with angry-looking pimples, but they would subside without breaking open or making the toddler ill.
And then, last March, Logan found a boil low on her abdomen. She hoped it was an ingrown hair—but fearing for Isabella and Brian, she showed it to her primary care doctor. He lanced the swelling, ordered a culture and sent her back to Infectious Disease Associates. They delivered the bad news: It was CA-MRSA once again. The prescription was 30 more days of decolonization, along with a 30-day course of two stronger antibiotics. “We went so many months without an outbreak,” Logan says. “Now I’m wondering, What is the magic number?”
The virulence of community- associated MRSA has troubled the physicians who are aware of its advance, in part because they’ve feared that many of their fellow doctors are not. In a study coauthored by Dr. Blumberg in Atlanta, about two thirds of the patients with CA-MRSA in one hospital had initially been given one of the antibiotics that no longer work against the bug. That is not surprising, says Elizabeth Bancroft, M.D., a medical epidemiologist with the Los Angeles County Department of Public Health, who has investigated MRSA outbreaks. Diagnosing the infection correctly requires ordering a bacterial culture to find which drug will work against it, but doctors are not accustomed to routinely culturing skin infections because the standard drugs worked so well for so long. “In my mind, this is similar to what happened when HIV was first discovered,” Dr. Bancroft says. “A new bug comes to town, and people at first do not think of it when they are making diagnoses.”
Because CA-MRSA can destroy tissue so rapidly, the consequences of starting treatment with the wrong drug can be dramatic. Dee Dee Wallace, a 46-year-old mother of two in Nashotah, Wisconsin, discovered that in late 2004. She noticed a painful boil on her rear end in the midst of an 800-mile Thanksgiving car trip. When she saw her primary care doctor the following week, she was given a common penicillin-based antibiotic. The infection seemed to heal, but then recurred on her left knee around New Year’s Day. By the time it was cultured, identified as CA-MRSA and targeted with the correct drugs, it had developed into necrotizing fasciitis. To clean out the infection, surgeons had to remove more than five square inches of flesh from the inside of Wallace’s knee. Two years later, after an ICU stay, skin-graft surgery and months of recovery, she still lacks full use of her leg. “I had never heard of MRSA,” she says. “Until my husband got online and looked it up, I had no idea how serious it was.”
Drug options shrinking
Physicians lack experience with the remaining antibiotics that do work against CA-MRSA. “Are they not very effective, or are they just as good? I don’t think we know,” says Henry Chambers, M.D., chief of infectious diseases at San Francisco General Hospital. And that menu of alternate drugs may be shrinking. Several recent studies suggest that community MRSA, which originally could be distinguished from the hospital variety because it was vulnerable to more drugs than the hospital strain, is losing that vulnerability. And even as existing drugs cease to work, few new antibiotics are being developed. “The pipeline is just skimpy,” says John Bartlett, M.D., of Johns Hopkins University School of Medicine in Baltimore. “We are already starting to use drugs that we shelved because they were too toxic.”
Adding to their concern is a troubling discovery that researchers have only recently pieced together. More and more, CA-MRSA infections nationwide are caused by a single strain, known as USA 300, which emerged in 2001 and has become linked with horrific infections, including flesh-eating disease. As it spreads, USA 300 is squeezing out other MRSA strains, including the long-standing hospital variety—a sign, researchers say, that a pathogen already demonstrating a talent for survival of the fittest may have become super fit.
CA-MRSA’s emergence as a potent health problem is so new that authorities are scrambling to get the message out about it. The CDC has launched an educational campaign and convened a caucus of experts to discuss strategies for physicians to follow. Among the experts’ recommendations: Doctors should be aware of the extent of MRSA in their communities. A skin infection that staph might have caused should always be cultured to see which drugs will work against it. Complaints of spider bites should always rate a second look. “It is a change in practice,” admits Rachel Gorwitz, M.D., a CDC epidemiologist who tracks CA-MRSA. “We are asking them to do something that they may not have done before.”
Physicians with experience treating MRSA urge patients to act in their own defense. Simple precautions such as washing your hands, covering any wounds and showering immediately after contact sports can help ward off germs. If a suspicious boil does pop up, never be afraid to ask a doctor to culture it. Be especially concerned about skin problems that rise or spread rapidly or become red, swollen and painful. But doctors also concede reluctantly that the public may have to learn a hard lesson: For many infections, the time of easy, uncomplicated treatment is over.
Mollie Logan has already come to that realization. She was declared free of CA-MRSA in May 2006, after three sets of tests to prove it had been eliminated. She has had no more recurrences, and Isabella—who turned 2 years old last August—remains healthy. The family is moving on: Logan will give birth this spring to their second child. As she nears her due date in April, her obstetrician will test her again, and if she comes up positive, she will get antibiotics during labor and delivery. “But I don’t know if they really know what will happen,” she says. “It is very scary.” Meanwhile, the family continues to shower weekly with antiseptic soap, keeps a supply of prescription antibiotic ointment on hand and takes nothing for granted.
In what may eventually be the postantibiotic era, that is the only sensible attitude, says Darcy Jones, the physician’s assistant who cared for Mollie Logan at Infectious Disease Associates. “Hopefully, we have eradicated the MRSA from her, but it is not something that will last forever,” she says. “She could get this again. Any of us could.”
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