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Antimicrobial Agents and Chemotherapy, August 2007, p. 2674-2678, Vol. 51, No. 8
0066-4804/07/$08.00+0     doi:10.1128/AAC.01582-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Effect of Fluoroquinolone Treatment on Growth of and Toxin Production by Epidemic and Nonepidemic Clostridium difficile Strains in the Cecal Contents of Mice{triangledown}

Daniel A. Adams, Michelle M. Riggs, and Curtis J. Donskey*

Research Service, Louis Stokes Cleveland Veterans Affairs Medical Center, Case Western Reserve University, Cleveland, Ohio 44106

Received 19 December 2006/ Returned for modification 26 February 2007/ Accepted 29 May 2007

Several recent outbreaks of Clostridium difficile-associated disease (CDAD) have been attributed to the emergence of an epidemic strain with increased resistance to fluoroquinolone antibiotics. Some clinical studies have suggested that fluoroquinolones with enhanced antianaerobic activity (i.e., gatifloxacin and moxifloxacin) may have a greater propensity to induce CDAD than ciprofloxacin and levofloxacin do. We examined the effects of subcutaneous fluoroquinolone treatment on in vitro growth of and toxin production by epidemic and nonepidemic C. difficile isolates in cecal contents of mice and evaluated the potential for these agents to inhibit fluoroquinolone-susceptible isolates during treatment. When C. difficile isolates were inoculated into cecal contents collected 2 days after the final antibiotic dose, gatifloxacin and moxifloxacin promoted significantly more growth and toxin production than ciprofloxacin and levofloxacin did. During treatment, gatifloxacin and moxifloxacin inhibited growth of fluoroquinolone-susceptible but not fluoroquinolone-resistant isolates. Ciprofloxacin and levofloxacin promoted growth of C. difficile when administered at higher doses (i.e., 20 times the human dose in mg/kg of body weight), and levofloxacin inhibited growth of fluoroquinolone-susceptible, but not fluoroquinolone-resistant, C. difficile isolates when administered in combination with ceftriaxone. Thus, fluoroquinolones with enhanced antianaerobic activity (i.e., gatifloxacin and moxifloxacin) promoted C. difficile growth to a greater extent than did ciprofloxacin and levofloxacin in this model. However, our findings suggest that fluoroquinolones may exert selective pressure favoring the emergence of epidemic fluoroquinolone-resistant C. difficile strains by inhibiting fluoroquinolone-susceptible but not fluoroquinolone-resistant isolates during treatment and that agents such as levofloxacin or ciprofloxacin can exert such selective pressure when administered in combination with antibiotics that disrupt the anaerobic microflora.

* Corresponding author. Mailing address: Louis Stokes Cleveland Veterans Affairs Medical Center, Infectious Diseases Section, 10701 East Blvd., Cleveland, OH 44106. Phone: (216) 791-3800, ext. 5103. Fax: (216) 229-8509. E-mail: curtisd123{at}yahoo.com

{triangledown} Published ahead of print on 11 June 2007.

Antimicrobial Agents and Chemotherapy, August 2007, p. 2674-2678, Vol. 51, No. 8
0066-4804/07/$08.00+0     doi:10.1128/AAC.01582-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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