On May 18, a team working at the Walter Reed Army Institute of Research here had its first look at a sample of the bacterium Escherichia coli, taken from a 49-year-old woman in Pennsylvania. Her sample was one of six from across the country delivered to the lab of microbiologist Patrick McGann. Within hours, a preliminary analysis deepened concern at the lab. Over the next several days, more sophisticated genetic sleuthing confirmed McGann's worst fears. There, in the bacterium's DNA, was a gene [that] made the pathogen impervious to the venerable antibiotic colistin. More ominously, the gene's presence ... suggested that it could readily jump to other E. coli bacteria, or to entirely different forms of disease-causing organisms. That would make them impervious to colistin as well. It was a milestone public health officials have been anticipating for years. In a steady march, disease-causing microbes have evolved ways to evade the bulwark of medications used to treat bacterial infections. For a variety of those illnesses, only colistin continued to work every time. Now this last line of defense had been breached as well. Almost as soon as they were given to patients, scientists began finding evidence that disease-causing bacteria were developing resistance to these new wonder drugs. Humans have accelerated this natural process by indiscriminately prescribing antibiotics and by routinely feeding the drugs to livestock.
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