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Intracellular penetration and antimicrobial activity of antibiotics.

Abstract
Delayed response or recurrence of clinical infections may, in part, be due to the inability of certain antibiotics to penetrate human polymorphonuclear leukocytes (PMN) and exert intracellular antibacterial activity. We determined the penetration of PMN by certain hydrophilic and certain lipophilic antibiotics, and assessed their activity against intracellular Haemophilus influenzae, type b or Staphylococcus aureus. We found that penicillin G was excluded from human PMN while chloramphenicol was concentrated within these cells; chloramphenicol killed significantly more intracellular H. influenzae than did penicillin or ampicillin. Clindamycin and trimethoprim penetrated into normal and chronic granulomatous disease (CGD) PMN equally and were at least transiently concentrated in the cells. Clindamycin and the combinations trimethoprim/sulphamethoxazole and trimethoprim/rifampicin were most effective in killing intracellular Staph. aureus in vitro; these antibiotics reduced the bacterial density in CGD PMN to values comparable to those in normal PMN. The mechanism by which clindamycin and rifampicin killed intracellular Staph. aureus appeared to be due to direct antimicrobial activity. Antibiotics that penetrate into phagocytes may be more effective in infections due to pathogens capable of intracellular survival.
AuthorsR F Jacobs, C B Wilson
JournalThe Journal of antimicrobial chemotherapy (J Antimicrob Chemother) Vol. 12 Suppl C Pg. 13-20 (Oct 1983) ISSN: 0305-7453 [Print] England
PMID6605963 (Publication Type: Journal Article)
Chemical References
  • Anti-Bacterial Agents
Topics
  • Anti-Bacterial Agents (metabolism, pharmacology)
  • Bacteria (drug effects)
  • Granulomatous Disease, Chronic (blood)
  • Haemophilus influenzae (drug effects)
  • Humans
  • In Vitro Techniques
  • Microbial Sensitivity Tests
  • Neutrophils (metabolism, microbiology)
  • Staphylococcus aureus (drug effects)
  • Time Factors

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