ArticleAntimicrobial agents and chemotherapy2015
Ambush of Clostridium difficile spores by ramoplanin: activity in an in vitro model.
Article in Antimicrobial agents and chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Updated sequence of ramoplanin biosynthetic gene cluster from Actinoplanes ramoplaninifer ATCC 33,076.Journal of applied genetics · 2026Article
- Unravelling three-way interactions betweenJournal of medical microbiology · 2025Review
- Review
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- RelQ-mediated alarmone signaling regulates growth, sporulation, and stress-induced biofilm formation inbioRxiv : the preprint server for biology · 2024Article
- Opportunities for Nanomedicine inAntibiotics (Basel, Switzerland) · 2021Review
- Emerging peptide antibiotics with therapeutic potential.Medicine in drug discovery · 2021Review
- Investigational Treatment Agents for RecurrentJournal of experimental pharmacology · 2020Review
- Novel therapies and preventative strategies for primary and recurrent Clostridium difficile infections.Annals of the New York Academy of Sciences · 2019Review
- Novel Antimicrobials for the Treatment ofFrontiers in medicine · 2018Review
- A Review of Experimental and Off-Label Therapies for Clostridium difficile Infection.Infectious diseases and therapy · 2017Review
- Article
- The Synergistic Effect of High Pressure COFrontiers in microbiology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium difficile infection (CDI) is a gastrointestinal disease caused by C. difficile, a spore-forming bacterium that in its spore form is tolerant to standard antimicrobials. Ramoplanin is a glycolipodepsipeptide antibiotic that is active against C. difficile with MICs ranging from 0.25 to 0.50 μg/ml. The activity of ramoplanin against the spores of C. difficile has not been well characterized; such activity, however, may hold promise, since posttreatment residual intraluminal spores are likely elements of disease relapse, which can impact more than 20% of patients who are successfully treated. C. difficile spores were found to be stable in deionized water for 6 days. In vitro spore counts were consistently below the level of detection for 28 days after even brief (30-min) exposure to ramoplanin at concentrations found in feces (300 μg/ml). In contrast, suppression of spore counts was not observed for metronidazole or vancomycin at human fecal concentrations during treatment (10 μg/ml and 500 μg/ml, respectively). Removal of the C. difficile exosporium resulted in an increase in spore counts after exposure to 300 μg/ml of ramoplanin. Therefore, we propose that rather than being directly sporicidal, ramoplanin adheres to the exosporium for a prolonged period, during which time it is available to attack germinating cells. This action, in conjunction with its already established bactericidal activity against vegetative C. difficile forms, supports further evaluation of ramoplanin for the prevention of relapse after C. difficile infection in patients.
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