Abstract
In recent years, the incidence and severity of Clostridium difficile-associated disease (CDAD) have increased dramatically. Beginning in 2000, widespread regional outbreaks associated with a previously uncommon hypervirulent strain of C. difficile have occurred in North America and Europe. Most likely because of increased toxin production as well as other virulence factors, this epidemic strain has caused more severe and refractory disease leading to complications, including intensive care unit admission, colectomies, and death. Worldwide increasing use of fluoroquinolones and cephalosporins has likely contributed to the proliferation of this epidemic strain, which is highly resistant to both. The elderly have been disproportionately affected by CDAD, but C. difficile has also recently emerged in populations previously considered to be at low risk, including healthy outpatients and peripartum women, although it is unknown if these cases are related to the epidemic strain. Nevertheless, transmission within hospitals is the major source of C. difficile acquisition, and previous or concurrent antimicrobial use is almost universal among cases. Applying current evidence-based strategies for management and prevention is critically important, and clinicians should maintain an awareness of the changing epidemiology of CDAD and take measures to reduce the risk of disease in patients.
Highlights
Since the discovery of Clostridium difficile-associated disease (CDAD) approximately 30 years ago [1,2], much progress has been made in our understanding of the pathogenesis and management of this infection
Toxin-producing strains of C. difficile, an anaerobic sporeforming bacillus, cause illnesses ranging from mild diarrhea to fulminant colitis and toxic megacolon leading to sepsis and even death
Since resistance of the BI/North American Pulsed-Field Type 1 (NAP1)/027 strain to fluoroquinolones is a class effect resulting in higher minimum inhibitory concentrations (MICs) to all fluoroquinolones [4], the incidence of disease caused by such resistant strains is not likely to be reduced without controlling fluoroquinolone use in general
Summary
Since the discovery of Clostridium difficile-associated disease (CDAD) approximately 30 years ago [1,2], much progress has been made in our understanding of the pathogenesis and management of this infection. Further studies are needed to determine whether the vaccine responses confer protective immunity against CDAD and whether adequate immune responses are achieved in the elderly or in patients with recurrent C. difficile Another immune therapy approach, the use of human antitoxin A and B monoclonal antibodies, reduced mortality in a hamster model of CDAD [78]. Formulary substitutions of 8-methoxyfluoroquinolones for levofloxacin have been proposed to control CDAD outbreaks caused by the BI/NAP1/027 strain While this appeared to be effective in one study [90], it was ineffective in another, most likely because the overall use of fluoroquinolones in the hospital was not controlled [91]. Since resistance of the BI/NAP1/027 strain to fluoroquinolones is a class effect resulting in higher minimum inhibitory concentrations (MICs) to all fluoroquinolones [4], the incidence of disease caused by such resistant strains is not likely to be reduced without controlling fluoroquinolone use in general
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