HINXTON, UK—In May 2004, a 64-year-old woman with a hemodialysis catheter entered a community hospital in Indiana with traces of the bacterium Enterococcus faecalis in her blood. Testing revealed the strain to be ampicillin susceptible but vancomycin resistant. Because of the woman's history of penicillin allergy, she was treated with another antibiotic, linezolid, to clear the infection. Not long afterward, her platelet count dropped dangerously low, so doctors switched her to yet another antibiotic—oral ciprofloxacin—and discharged her. A few days later, she returned to the hospital with a fever and was put on daptomycin, a last line of defense for the management of drug resistant Gram-positive bacterial infections, and again sent home. Just two weeks later, she came back with signs of daptomycin-resistant bacteria, and she died soon thereafter (Clin. Infect. Dis. 41, 565–566, 2005).
What happened? To help put together the pieces, a team led by Cesar Arias, an infectious diseases physician at the University of Texas Medical School in Houston, turned to faster 'next generation' genetic sequencing. Reporting at the Infectious Diseases Genomics and Global Health meeting here last month, Arias's team found that the microbe that had ultimately killed the woman had acquired a handful of mutations that rendered it immune to daptomycin—the first time that an E. faecalis infection gained spontaneous daptomycin resistance while a patient was receiving therapy. (In 2004, less than a year after daptomycin first became available in the US, clinicians also observed the emergence of daptomycin resistance in patients with Enterococcus faecium and those with methicillin-resistant Staphylococcus aureus.)
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