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Penetration of clindamycin into experimental Staphylococcus aureus infections
Abstract:
Inactivation of clindamycin at the site of experimental infection with Staphylococcus aureus was studied using rabbits with plastic capsules implanted in the peritoneal cavity. The mean percentage penetration of bioactive clindamycin (concentration in capsule divided by simultaneous concentration in serum times 100) into infected and noninfected capsules was 30.4 per cent and 13.0 per cent, respectively. In contrast, the mean penetration of radiolabeled clindamycin into infected capsules was 38.4 per cent. These findings indicate that the observed loss of bioactivity in infected capsules is due to intracapsular inactivation of clindamycin and not to an alteration in capsular permeability. Biologic inactivation of clindamycin was not evident after in vitro incubation of the drug with Staphylococcus aureus. These results suggest that the observed loss of bioactivity may be due to chemical modification by enzymes in the inflammatory exudate or to binding of the antibiotic to tissue components.
Insights
Clindamycin bioactivity is lost at infection sites due to inactivation within the capsule, not altered permeability. This suggests chemical modification by inflammatory enzymes or tissue binding, not bacterial action.
Area of Science:
- Pharmacology
- Infectious Diseases
- Microbiology
Background:
- Clindamycin is an antibiotic used to treat Staphylococcus aureus infections.
- Understanding drug behavior at infection sites is crucial for effective treatment.
Purpose of the Study:
- To investigate the inactivation of clindamycin at experimental infection sites.
- To determine if altered capsule permeability or drug inactivation causes reduced bioactivity.
Main Methods:
- Rabbits with implanted peritoneal capsules were infected with Staphylococcus aureus.
- Penetration of bioactive and radiolabeled clindamycin into infected and noninfected capsules was measured.
- In vitro incubation of clindamycin with Staphylococcus aureus was performed.
Main Results:
- Bioactive clindamycin penetration was lower in infected capsules (30.4%) compared to noninfected (13.0%).
- Radiolabeled clindamycin penetration was higher (38.4%) in infected capsules, indicating no altered permeability.
- No biologic inactivation of clindamycin was observed in vitro with Staphylococcus aureus.
Conclusions:
- Loss of clindamycin bioactivity at infection sites is due to intracapsular inactivation.
- Inactivation likely results from chemical modification by inflammatory exudate enzymes or binding to tissue components.
- Bacterial metabolism is not the cause of clindamycin inactivation in this model.