Confronting Clostridium difficile in Inpatient Health Care Facilities

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Abstract
There are now a number of reports of increasing rates and outbreaks of severe Clostridium difficile–associated disease (CDAD) [1,2,3–4]. Much of this changing epidemiology is thought to be because of the emergence of a hypervirulent, epidemic strain that is known variously as North American PFGE type 1, restriction enzyme analysis type BI, and PCR ribotype 027 (NAP1/BI/027) [1, 2]. The exact cause of hypervirulence in the NAP1/BI/027 strain is not known; however, the strain does produce greater levels of toxins A and B in vitro and produces an extra toxin known as binary toxin [1, 5]. This strain was uncommon as a cause of human disease prior to 2001 but has become widespread coincident with its development of high levels of fluoroquinolone resistance, affording the disease increased fitness in the present era of widespread fluoroquinolone use. Although this strain first garnered international attention by causing CDAD outbreaks in a number of hospitals in Quebec from late 2003 through 2004 [2], it had, by that time, already infiltrated the University of Pittsburgh Medical Center–Presbyterian (UPMC; Pittsburgh, PA), where, in 2000, there was a nearly 4-fold increase in the rate of C. difficile infection, and dozens of patients either died or underwent colectomy for toxic megacolon [6, 7].

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