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Clindamycin-Resistant Clostridium difficile

Dale N. Gerding, Stuart Johnson

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Abstract

In light of subsequent data regarding clindamycin use as a risk factor for disease caused by clindamycin-resistant strains of Clostridium difficile, it is also tempting to speculate that an outbreak was caused by clindamycin-resistant C. difficile. Overall, 21% of the 308 C. difficile isolates were resistant to clindamycin, yet by serogrouping, the researchers were able to show that clindamycin resistance was concentrated in specific groups of strains of C. difficile. Studies from the United States, Canada, and Europe confirm the widespread presence of clindamycin resistance among C. difficile isolates during the first 10 years following the discovery that the organism was the cause of pseudomembranous colitis (PMC). The accepted breakpoint for clindamycin resistance based on drug concentrations in serum is an MIC of >4 μg/ml. The current best explanation of this is that the disruption of normal intestinal flora is likely the determining antibiotic event that makes patients susceptible to infection with C. difficile. The Belgium study was important in showing not only the relationship of clindamycin use and clindamycin resistance but also the possible clonal nature of clindamycin-resistant strains. Although the researchers did not correlate risk of infection with the strain with the use of clindamycin, they did place clindamycin use under restriction and observed in retrospect an associated decline in C. difficile-associated diarrhea (CDAD) rates, suggesting that clindamycin resistance and clindamycin use were important risk factors in the outbreak.

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What this paper is about

In light of subsequent data regarding clindamycin use as a risk factor for disease caused by clindamycin-resistant strains of Clostridium difficile, it is also tempting to speculate that an outbreak was caused by clindamycin-resistant C. difficile. Overall, 21% of the 308 C. difficile isolates were resistant to clindamycin, yet by serogrouping, the researchers were able to show that clindamycin resistance was concentrated in specific groups of strains of C. difficile. Studies from the United States, Canada, and Europe confirm the widespread presence of clindamycin resistance among C. difficile isolates during the first 10 years following the discovery that the organism was the cause of pseudomembranous colitis (PMC). The accepted breakpoint for clindamycin resistance based on drug concentrations in serum is an MIC of >4 μg/ml. The current best explanation of this is that the disruption of normal intestinal flora is likely the determining antibiotic event that makes patients susceptible to infection with C. difficile. The Belgium study was important in showing not only the relationship of clindamycin use and clindamycin resistance but also the possible clonal nature of clindamycin-resistant strains. Although the researchers did not correlate risk of infection with the strain with the use of clindamycin, they did place clindamycin use under restriction and observed in retrospect an associated decline in C. difficile-associated diarrhea (CDAD) rates, suggesting that clindamycin resistance and clindamycin use were important risk factors in the outbreak.

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Available abstract

In light of subsequent data regarding clindamycin use as a risk factor for disease caused by clindamycin-resistant strains of Clostridium difficile, it is also tempting to speculate that an outbreak was caused by clindamycin-resistant C. difficile. Overall, 21% of the 308 C. difficile isolates were resistant to clindamycin, yet by serogrouping, the researchers were able to show that clindamycin resistance was concentrated in specific groups of strains of C. difficile. Studies from the United States, Canada, and Europe confirm the widespread presence of clindamycin resistance among C. difficile isolates during the first 10 years following the discovery that the organism was the cause of pseudomembranous colitis (PMC). The accepted breakpoint for clindamycin resistance based on drug concentrations in serum is an MIC of >4 μg/ml. The current best explanation of this is that the disruption of normal intestinal flora is likely the determining antibiotic event that makes patients susceptible to infection with C. difficile. The Belgium study was important in showing not only the relationship of clindamycin use and clindamycin resistance but also the possible clonal nature of clindamycin-resistant strains. Although the researchers did not correlate risk of infection with the strain with the use of clindamycin, they did place clindamycin use under restriction and observed in retrospect an associated decline in C. difficile-associated diarrhea (CDAD) rates, suggesting that clindamycin resistance and clindamycin use were important risk factors in the outbreak.

Key concepts: Clindamycin, Clostridium difficile, Microbiology, Pseudomembranous colitis, Antibiotics, Medicine, Antibiotic resistance, Outbreak

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