In early summer 2008 Timothy Walsh of Cardiff University in Wales got an e-mail from Christian Giske, an acquaintance who is a physician on the faculty of Sweden’s Karolinska Institute. Giske had been treating a 59-year-old man hospitalized that past January in Örebro, a small city about 100 miles from Stockholm. The man had lived with diabetes for many years, suffered several strokes and had lately developed deep bedsores. But those were not the subject of Giske’s message. Instead he was worried about a bacterium that a routine culture had unexpectedly revealed in the man’s urine. Would Walsh, who runs a lab that unravels the genetics of antibacterial resistance, be willing to take a look at the bug?
Walsh agreed and put the isolate through more than a dozen assays. It was Klebsiella pneumoniae, a bacterium that in hospitalized patients is one of the most frequent causes of pneumonia and bloodstream infection. This strain, though, contained something new, a gene that Walsh had never seen before. It rendered the Klebsiella, which was already resistant to many antibiotics used in critical care medicine, insensitive to the only remaining group that worked reliably and safely—the carbapenems, the so-called drugs of last resort. The one medication the investigators found that had any effect on the resistant strain was colistin, a drug that had been out of general use for years because of its toxic effects on the kidneys. Walsh named the enzyme that this gene produced New Delhi metallo-beta-lactamase, or NDM-1, for the city where the man acquired the infection just before he returned home to Sweden.