What type of antibiotic is clindamycin?

Clindamycin Classification

Clindamycin is a lincosamide antibiotic that inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit of susceptible bacteria. 1, 2

Mechanism and Classification

• Clindamycin is a semisynthetic lincosamide antibiotic produced by 7(S)-chloro-substitution of the 7(R)-hydroxyl group of the parent compound lincomycin 2, 3

• The drug binds specifically to the 23S RNA of the 50S ribosomal subunit, thereby inhibiting bacterial protein synthesis 2

• Clindamycin is primarily bacteriostatic, though it can be bactericidal against autolytic species such as pneumococci at higher concentrations achievable in vivo 1

Spectrum of Activity

• Primary activity against:

  • Aerobic gram-positive cocci (staphylococci, streptococci) 1
  • Anaerobic bacteria (both gram-positive and most gram-negative anaerobes) 1
  • Specific anaerobes including Clostridium perfringens, Fusobacterium necrophorum, Fusobacterium nucleatum, Peptostreptococcus anaerobius, and Prevotella melaninogenica 2

• No activity against:

  • Haemophilus influenzae 1
  • Moraxella catarrhalis 1
  • Enterococci 4
  • Limited activity against aerobic gram-negative bacilli such as Enterobacter cloacae 1

Pharmacologic Properties

• Clindamycin is predominantly metabolized by Cytochrome P450 3A4 (CYP3A4), with minor contribution from CYP3A5, to form clindamycin sulfoxide and N-desmethylclindamycin 2, 5

• The drug has excellent tissue penetration, particularly in bone and abscesses, but limited penetration into cerebrospinal fluid 1

• After oral administration, clindamycin is almost completely absorbed, with mean peak serum levels reached in 45 to 60 minutes 6

• The average biological half-life is 2.4 hours, allowing dosing at six-hour intervals 2, 6

Unique Clinical Properties

• Clindamycin suppresses bacterial toxin production, making it particularly valuable for treating infections caused by toxin-producing anaerobes and group A streptococci 1, 7

• Due to its bacteriostatic nature, clindamycin is not recommended for endovascular infections such as infective endocarditis or septic thrombophlebitis 1

Resistance Considerations

• Resistance is most often caused by modification of specific bases of the 23S ribosomal RNA 2

• Cross-resistance exists between clindamycin and lincomycin (complete), and sometimes among lincosamides, macrolides, and streptogramin B due to overlapping binding sites 2

• Macrolide-resistant isolates of staphylococci and beta-hemolytic streptococci should be screened for induction of clindamycin resistance using the D-zone test 1, 2

• Susceptibility rates to clindamycin are higher among community-acquired MRSA than healthcare-associated MRSA, with significant geographic variation 1