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Aspirin plus ticlopidine prevented experimental endocarditis due to Enterococcus faecalis and Streptococcus
Tiago Rafael Veloso1, Frank Oechslin1, Yok-Ai Que2
1Department of Fundamental Microbiology, University of Lausanne, CH-1015 Lausanne, Switzerland.
Insights
Aspirin and ticlopidine significantly reduced infective endocarditis (IE) in rats caused by Enterococcus faecalis and Streptococcus gallolyticus. This combination therapy shows promise for preventing IE in high-risk individuals.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Pharmacology
Background:
- Infective endocarditis (IE) is a serious bloodstream infection often caused by bacteria like Enterococcus faecalis and Streptococcus gallolyticus.
- Antibiotic prophylaxis is ineffective for preventing IE originating from low-level bacterial translocation.
- Previous studies showed aspirin plus ticlopidine protected against IE caused by other bacteria.
Purpose of the Study:
- To evaluate the efficacy of aspirin plus ticlopidine in preventing IE caused by Enterococcus faecalis and Streptococcus gallolyticus.
- To determine if this combination therapy can reduce vegetation weight and mortality in a rat model.
Main Methods:
- A rat model of infective endocarditis was used.
- Rats were treated with aspirin plus ticlopidine.
- Vegetation weight and survival rates were measured to assess treatment efficacy.
Main Results:
- Aspirin plus ticlopidine significantly reduced vegetation weight in rats with IE.
- The treatment protected 73% of rats from Enterococcus faecalis IE.
- The treatment protected 64% of rats from Streptococcus gallolyticus IE.
Conclusions:
- Aspirin plus ticlopidine demonstrates significant protective effects against IE caused by Enterococcus faecalis and Streptococcus gallolyticus.
- These findings support the potential use of aspirin plus ticlopidine for the global prevention of IE in high-risk patient populations.
Abstract:
Enterococcus faecalis and Streptococcus gallolyticus cause infective endocarditis (IE), which can originate from the continuous release or translocation of low bacterial numbers into the bloodstream. In this context, IE cannot be prevented with antibiotics. We previously demonstrated that aspirin plus ticlopidine protected rats from IE due to S. gordonii and Staphylococcus aureus. Here we showed that aspirin plus ticlopidine significantly reduced vegetation weight and protected 73 and 64% rats (P < 0.005) from IE due to E. faecalis and S. gallolyticus, respectively. These results further support the potential use of aspirin plus ticlopidine for a global prevention of IE in high-risk patients.
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