An Epidemic, Toxin Gene-Variant Strain of Clostridium difficile

doi:10.1056/NEJMoa051590

Volume 353:2433-2441		December 8, 2005		Number 23

An Epidemic, Toxin Gene–Variant Strain of Clostridium difficile

L. Clifford McDonald, M.D., George E. Killgore, Dr.P.H., Angela Thompson, M.M.Sc., Robert C. Owens, Jr., Pharm.D., Sophia V. Kazakova, M.D., M.P.H., Ph.D., Susan P. Sambol, M.T., Stuart Johnson, M.D., and Dale N. Gerding, M.D.

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by Bartlett, J. G.

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ABSTRACT

Background Recent reports suggest that the rate and severityof Clostridium difficile–associated disease in the UnitedStates are increasing and that the increase may be associatedwith the emergence of a new strain of C. difficile with increasedvirulence, resistance, or both.

Methods A total of 187 C. difficile isolates were collectedfrom eight health care facilities in six states (Georgia, Illinois,Maine, New Jersey, Oregon, and Pennsylvania) in which outbreaksof C. difficile–associated disease had occurred between2000 and 2003. The isolates were characterized by restriction-endonucleaseanalysis (REA), pulsed-field gel electrophoresis (PFGE), andtoxinotyping, and the results were compared with those froma database of more than 6000 isolates obtained before 2001.The polymerase chain reaction was used to detect the recentlydescribed binary toxin CDT and a deletion in the pathogenicitylocus gene, tcdC, that might result in increased productionof toxins A and B.

Results Isolates that belonged to one REA group (BI) and hadthe same PFGE type (NAP1) were identified in specimens collectedfrom patients at all eight facilities and accounted for at leasthalf of the isolates from five facilities. REA group BI, whichwas first identified in 1984, was uncommon among isolates fromthe historic database (14 cases). Both historic and current(obtained since 2001) BI/NAP1 isolates were of toxinotype III,were positive for the binary toxin CDT, and contained an 18-bptcdC deletion. Resistance to gatifloxacin and moxifloxacin wasmore common in current BI/NAP1 isolates than in non-BI/NAP1isolates (100 percent vs. 42 percent, P<0.001), whereas therate of resistance to clindamycin was the same in the two groups(79 percent). All of the current but none of the historic BI/NAP1isolates were resistant to gatifloxacin and moxifloxacin (P<0.001).

Conclusions A previously uncommon strain of C. difficile withvariations in toxin genes has become more resistant to fluoroquinolonesand has emerged as a cause of geographically dispersed outbreaksof C. difficile–associated disease.

Source Information

From the Epidemiology and Laboratory Branch, Division of Healthcare Quality Promotion, Centers for Disease Control and Prevention, Atlanta (L.C.M., G.E.K., A.T., S.V.K.); the Departments of Pharmacy and Infectious Diseases, Maine Medical Center, Portland (R.C.O.); the College of Medicine, University of Vermont, Burlington (R.C.O.); and the Infectious Disease Section and Research Service, Department of Medicine, Hines Veterans Affairs Hospital and Loyola University Stritch School of Medicine, Hines, Ill. (S.P.S., S.J., D.N.G.).

Address reprint requests to Dr. McDonald at 1600 Clifton Rd., MS A35, Atlanta, GA 30333, or at cmcdonald1{at}cdc.gov.

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N Engl J Med 2006; 354:1199-1203, Mar 16, 2006. Correspondence

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