Fidaxomicin disrupts Clostridium difficile biofilms

Reuters Health Information: Fidaxomicin disrupts Clostridium difficile biofilms

Fidaxomicin disrupts Clostridium difficile biofilms

Last Updated: 2017-10-17

By Will Boggs MD

NEW YORK (Reuters Health) - Fidaxomicin, a narrow-spectrum macrocyclic antibiotic, disrupts Clostridium difficile biofilms and kills vegetative cells and spores in vitro, researchers report.

"These findings emphasize the potential role of biofilms in the pathogenesis of the disease," Dr. Laurent Chesnel from Merck and Company, Inc., Kenilworth, New Jersey, told Reuters Health by email. "If biofilms were a reservoir for relapse and/or environmental contamination, then accessing biofilms may be clinically important."

Many clinically important strains of C. difficile form biofilms that protect them against antibiotic penetration and provide a potential reservoir for spore persistence.

Dr. Chesnel and colleagues assessed the ability of fidaxomicin, the cyclic lipopeptide antibiotic surotomycin, vancomycin, and metronidazole to penetrate and disrupt C. difficile biofilm structure in vitro. The findings were published online October 6 in the Journal of Antimicrobial Chemotherapy.

All four antibiotics were effective against C. difficile grown on agar. However, after C. difficile biofilms were allowed to grow for 24 or 48 hours, antibiotic concentrations 50 times the minimum inhibitory concentrations (MICs) of fidaxomicin, surotomycin, and metronidazole were required in order to achieve similar count deductions - and concentrations of vancomycin 100 times its MIC resulted in only 1.1 to 2.7 log reductions.

When biofilms were allowed to grow for 72 hours before antibiotic treatment, mean log reductions in vegetative cells were significantly greater with fidaxomicin than with vancomycin or metronidazole, and mean log reductions in spore counts were significantly greater with fidaxomicin than with metronidazole - and nominally greater with fidaxomicin than with vancomycin.

Fidaxomicin penetrated biofilms faster than surotomycin, but both antibiotics (unlike metronidazole) caused significant disruption of the biofilm structure.

"The clinical implication is unknown and remains to be investigated," Dr. Chesnel said. "The ability of a drug targeting C. difficile to penetrate biofilms and reduce both vegetative and spore burden could have an implication in decreasing relapse and/or environmental contamination."

"Additional studies are needed to further characterize the relevance of C. difficile biofilms in the disease process," he concluded.

Merck and Company, Inc., funded the research, employed Dr. Chesnel, and contracted with the other five authors to conduct portions of this work.

SOURCE: http://bit.ly/2wQRpoq

J Antimicrob Chemother 2017.

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