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See Inside January 2007

Meet Resistance Head-On

DRUG-RESISTANT



KARI LOUNATMAA Photo Researchers, Inc.
Finding traces of pollution in a supposedly pristine mountain brook is sadly no longer surprising. But when the contaminants are genes for antibiotic resistance, the implications should still raise concern. With resistance to antibiotics growing at an alarming pace among pathogenic bacteria, humans must become more aggressive. In keeping with the "ounce of prevention" principle, early intervention in the processes that foster resistance would be a very good start.

A news story beginning on page 22 describes work by Colorado scientists who make a case for monitoring and mitigating the dangerous DNA as one would any other environmental pollutant. The researchers sampled the variety and concentrations of resistance DNA in and near Colorado's Cache la Poudre River. They found the genes inside living microbes and even as free-floating DNA. Predictably, the intensity of the problem increased nearer to human and agricultural waste sources, peaking in the bovine cesspools known as dairy lagoons.

One need only return to last summer's contaminated spinach scare to understand how we are literally breeding the bugs that come back to bite us. The Escherichia coli strain involved in that deadly outbreak, O157:h7, gained its virulence in the antibiotic-saturated world of large-scale cattle processing. Inside the cows and their effluent, the surviving bacteria engage in a frenetic swap meet, trading genes for both pathogenicity and drug resistance. Then they make their way into hamburger patties, foul the water supply or dirty the spinach crop of a nearby farm.

In January 2006 Europe forbade all nontherapeutic use of antibiotics in animals to stanch this flow of superbugs from farms to people. A total ban on agricultural use of avoparcin, a derivative of the antibiotic vancomycin--currently the last-hope treatment for deadly, resilient pathogens such as methicillin-resistant Staphylococcus aureus (MRSA)--was already in place. Liberal use of avoparcin to promote animal growth had been conclusively linked to increasing vancomycin resistance in human gut pathogens and from there to resistant staph strains ravaging hospital patients.

Parts of Europe are also pioneering ways to fight MRSA in hospitals. In the Netherlands and Denmark, rather than waiting for staph symptoms to appear, hospitals preemptively isolate all incoming high-risk patients (such as those who have been on catheters or who have lived in nursing homes) until tests show them to be MRSA-free. This step prevents carriers of MRSA from passing the infection to other patients and hospital workers. As a result, less than 1 percent of staph infections in Dutch hospitals are MRSA; the comparable U.S. figure is 64 percent.

In the U.S., where MRSA kills 13,000 annually, hospitals are reluctant to adopt this search-and-destroy strategy in part because of its cost. That may be a false economy: an MRSA infection can add tens of thousands of dollars to a patient's hospital bill. The Centers for Disease Control and Prevention did not back search-and-destroy methods in its most recent guidelines to hospitals but rather preached traditional hygiene-based prevention. To be sure, doctors and nurses are still woefully noncompliant with recommendations that they wash their hands more often between patients, and that simple measure can dramatically lower infection rates. Nevertheless, the ongoing rise in antibiotic-resistant infections suggests that the old standbys are not enough.

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