Enlarge (credit: Zechariah Judy)
In the early 2000s, a deadly gut infection began to surge. After decades of lurking in intestines and hospitals—more opportunistic nuisance than lethal threat—the bacterium Clostridium difficile abruptly exploded, spreading rapidly and causing more severe diarrheal disease than ever before. By 2011, the Centers for Disease Control and Prevention estimated that C. diff infected nearly half a million people in the US that year, killing approximately 29,000.
Two strains led the deadly reign: RT027 and RT078 (named based on the genetic code of their ribosomes, or “ribotype”). But scientists could only speculate as to why this duo was suddenly so menacing. At least one of them turned up with resistance to a class of antibiotics called fluoroquinolones, which contains ciprofloxacin among other common antibiotics. This fact led some researchers to suggest that the bacteria’s rise may have been linked to development of that drug resistance.
But scientists had identified fluoroquinolone resistance in C. diff back in mid-80s. Why would it suddenly matter? There was another, cryptic factor at play, it seemed.
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