Playing Chicken With Our Antibiotics

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s the sort of thing any good poultry farmer notices right away: a few of the birds in a so-called grow-out building have started snickering--the chicken equivalent of coughing. A respiratory infection, if that's what they have, could spread to the 20,000 other birds in the chicken house in a matter of days. The vet recommends the antibiotic enrofloxacin--the animal version of Cipro. Since it's not practical to treat the birds individually, the farmer pours a 5-gal. jug of the drug into the flock's drinking water. Five days later the birds are doing fine. Disaster has been averted.

Or has it? While enrofloxacin kills the type of bacteria that sickened the chickens, it doesn't quite eliminate a different strain, called Campylobacter, that lives in the intestine. The surviving germs, which don't cause any poultry diseases, quickly multiply and spread the genes that helped them fend off the antibiotic. Six weeks later, when the broilers are carved up at the slaughterhouse, resistant bacteria spill out everywhere. Even with the best sanitary controls, some campylobacter is shrink-wrapped along with the thighs, breasts and drumsticks that are delivered to your kitchen counter.

That's where the real trouble begins. Campylobacter is a major cause of food poisoning in humans. Less than diligent hand washing or improperly cooked meat could park you on the toilet for the next few days. And if you're sick enough to need medical treatment, you might be out of luck. Chicken Cipro is so closely related to human Cipro that any germ that has become resistant to the animal drug can shrug off the human one just as easily. Before 1996, when enrofloxacin was approved in the U.S. for use in poultry, the number of Campylobacter infections in people that were resistant to Cipro and its chemical cousins was negligible. By 1999, it had jumped to 18%--a clear sign, many researchers argue, that at least part of the increase is directly tied to the use of antibiotics on poultry farms.

Welcome to the harrowing world of antibiotic resistance, where drugs that once conquered everything from pneumonia to tuberculosis are rapidly losing their punch. Chicken Cipro is only the latest example of how humans are burning their pharmacological bridges. Feed-lot operators are dosing their livestock with antibiotics to keep them healthy under stressful growing conditions. Parents are demanding the most powerful broad-spectrum agents--often by brand name--for their children's upper-respiratory infections. Consumers are snapping up cutting boards, dishwashing soap and baby toys laced with antibacterial compounds, hoping to make their homes perfectly sterile and safe.

Doctors have long understood that the indiscriminate use of antibiotics usually backfires, selecting for germs that are tough to kill. But no one was prepared for how easily resistance could spread even when the drugs were used in what was thought of as appropriate treatment.

The problem is that bacteria share genetic information much more readily than anyone thought. Individual cells--often from different species--routinely exchange tiny loops of DNA called plasmids. They will even pick up snippets of DNA from dead bacteria or viruses. Once a strain of bacteria survives destruction by antibiotics, chances are it will eventually pass on the genes for resistance to other germs. "It's a numbers game," says Dr. Stuart Levy, a Tufts researcher and author of The Antibiotic Paradox. And because they live everywhere and reproduce quickly, bacteria have the upper hand.

It doesn't help matters that many Americans have come to think of antibiotics as tools for prevention. Patients will often ask for the drugs to keep their colds from turning into sinus infections, even though antibiotics have no effect on the viruses that cause colds in the first place.

What's harder to evaluate is the treatment of something like a middle-ear infection, which is indeed caused by several different types of bacteria, including Pneumococcus. Left alone, a handful of these infections could lead to permanent hearing loss. And yet their treatment has, in just the past 10 years in the U.S., boosted the prevalence of penicillin-resistant pneumococci to more than 20%.

No one yet advocates allowing all bacterial infections to run their course. But don't be surprised if your doctor takes more of a wait-and-see approach with your next case of flu (which, like a cold, is caused by viruses). Hospitals are also learning how to vary the drugs they give their patients to diminish the chances of selecting for ever more resistant germs.

Relief may soon be on the way. Thanks to advances in the new science of genomics, researchers have started to scour bacterial DNA for new and possibly better targets for drug development. The goal is to produce a compound that works so differently from today's antibiotics that germs won't know how to start developing resistance. Other research has produced drugs that help restore penicillin's ability to clobber resistant germs, provided the compounds are given in combination.