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In 2000, Muto and associates noted a spike in fluoroquinolone use in a Pittsburgh hospital that predated the increase of severe CDAD cases by 9 months. This strain produces a binary toxin of unknown significance and has an 18 bp deletion in a gene that regulates toxin production. This mutation allows for increased production of toxins A and B in vitro, which may explain why it appears to cause more severe disease. The strain has since acquired resistance to gatifloxacin and moxifloxacin.