Clindamycin: An overview
- Melissa Johnson, PharmD
Melissa Johnson, PharmD
- Clinical Pharmacist
- Duke University Medical Center
Clindamycin is a lincosamide antibiotic that has been approved by the US Food and Drug Administration (FDA) for the treatment of anaerobic, streptococcal, and staphylococcal infections. Its major disadvantage is its propensity to cause antibiotic-associated diarrhea, including Clostridium difficile colitis. (See "Clostridium difficile in adults: Epidemiology, microbiology, and pathophysiology".)
There has been increased interest in the use of clindamycin because it achieves high intracellular levels in phagocytic cells, high levels in bone, and appears to be able to reduce toxin production in toxin-elaborating strains of streptococci and staphylococci. (See "Epidemiology, clinical manifestations, and diagnosis of streptococcal toxic shock syndrome".)
The spectrum of activity, pharmacology, and adverse effects of clindamycin will be reviewed here. The clinical use of clindamycin is discussed separately in the appropriate topic reviews on specific infections. (See "Anaerobic bacterial infections" and "Complications, diagnosis, and treatment of odontogenic infections" and "Deep neck space infections" and "Submandibular space infections (Ludwig's angina)" and "Peritonsillar cellulitis and abscess" and "Lung abscess" and "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of skin and soft tissue infections" and "Methicillin-resistant Staphylococcus aureus in children: Treatment of invasive infections".)
MECHANISM OF ACTION
Clindamycin works primarily by binding to the 50s ribosomal subunit of bacteria. This agent disrupts protein synthesis by interfering with the transpeptidation reaction, which thereby inhibits early chain elongation. Chloramphenicol and macrolides such as erythromycin, clarithromycin, and azithromycin also act at the 50s ribosomal subunit and may compete for binding at this site. Clindamycin and the related drug lincomycin are often discussed along with the macrolides but are not chemically related. (See "Azithromycin, clarithromycin, and telithromycin".)
Clindamycin may potentiate the opsonization and phagocytosis of bacteria even at subinhibitory concentrations [1,2]. By disrupting bacterial protein synthesis, clindamycin causes changes in the cell wall surface, which decreases adherence of bacteria to host cells and increases intracellular killing of organisms. The drug also exerts an extended postantibiotic effect against some strains of bacteria, which may be attributed to persistence of the drug at the ribosomal binding site.
- Veringa EM, Lambe DW Jr, Ferguson DA Jr, Verhoef J. Enhancement of opsonophagocytosis of Bacteroides spp. by clindamycin in subinhibitory concentrations. J Antimicrob Chemother 1989; 23:577.
- Veringa EM, Verhoef J. Influence of subinhibitory concentrations of clindamycin on opsonophagocytosis of Staphylococcus aureus, a protein-A-dependent process. Antimicrob Agents Chemother 1986; 30:796.
- Nastro LJ, Finegold SM. Bactericidal activity of five antimicrobial agents against Bacteroides fragilis. J Infect Dis 1972; 126:104.
- Sande MA, Johnson ML. Antimicrobial therapy of experimental endocarditis caused by Staphylococcus aureus. J Infect Dis 1975; 131:367.
- Schlievert PM, Kelly JA. Clindamycin-induced suppression of toxic-shock syndrome--associated exotoxin production. J Infect Dis 1984; 149:471.
- Ohlsen K, Ziebuhr W, Koller KP, et al. Effects of subinhibitory concentrations of antibiotics on alpha-toxin (hla) gene expression of methicillin-sensitive and methicillin-resistant Staphylococcus aureus isolates. Antimicrob Agents Chemother 1998; 42:2817.
- Kremsner PG, Radloff P, Metzger W, et al. Quinine plus clindamycin improves chemotherapy of severe malaria in children. Antimicrob Agents Chemother 1995; 39:1603.
- Leclercq R, Courvalin P. Bacterial resistance to macrolide, lincosamide, and streptogramin antibiotics by target modification. Antimicrob Agents Chemother 1991; 35:1267.
- Brisson-Noël A, Delrieu P, Samain D, Courvalin P. Inactivation of lincosaminide antibiotics in Staphylococcus. Identification of lincosaminide O-nucleotidyltransferases and comparison of the corresponding resistance genes. J Biol Chem 1988; 263:15880.
- Leclercq R, Courvalin P. Intrinsic and unusual resistance to macrolide, lincosamide, and streptogramin antibiotics in bacteria. Antimicrob Agents Chemother 1991; 35:1273.
- Castor ML, Whitney CG, Como-Sabetti K, et al. Antibiotic resistance patterns in invasive group B streptococcal isolates. Infect Dis Obstet Gynecol 2008; 2008:727505.
- DiPersio LP, DiPersio JR. High rates of erythromycin and clindamycin resistance among OBGYN isolates of group B Streptococcus. Diagn Microbiol Infect Dis 2006; 54:79.
- Phares CR, Lynfield R, Farley MM, et al. Epidemiology of invasive group B streptococcal disease in the United States, 1999-2005. JAMA 2008; 299:2056.
- Back EE, O'Grady EJ, Back JD. High rates of perinatal group B Streptococcus clindamycin and erythromycin resistance in an upstate New York hospital. Antimicrob Agents Chemother 2012; 56:739.
- Capraro GA, Rambin ED, Vanchiere JA, et al. High rates of inducible clindamycin resistance among prenatal group B streptococcal isolates in one northwest Louisiana academic medical center. J Clin Microbiol 2013; 51:2469.
- Malbruny B, Werno AM, Anderson TP, et al. A new phenotype of resistance to lincosamide and streptogramin A-type antibiotics in Streptococcus agalactiae in New Zealand. J Antimicrob Chemother 2004; 54:1040.
- Snydman DR, Jacobus NV, McDermott LA, et al. National survey on the susceptibility of Bacteroides fragilis group: report and analysis of trends in the United States from 1997 to 2004. Antimicrob Agents Chemother 2007; 51:1649.
- Snydman DR, Jacobus NV, McDermott LA, et al. National survey on the susceptibility of Bacteroides Fragilis Group: report and analysis of trends for 1997-2000. Clin Infect Dis 2002; 35:S126.
- Hecht DW. Prevalence of antibiotic resistance in anaerobic bacteria: worrisome developments. Clin Infect Dis 2004; 39:92.
- NCCLS. Methods for antimicrobial susceptibility testing of anaerobic bacteria; approved standard- fourth edition. NCCLS document M11-A4. NCCLS, 940 West Valley Road, Suite 1400, Wayne, Pennsylvania 19087-1898 USA, 1997.
- Gurwith MJ, Rabin HR, Love K. Diarrhea associated with clindamycin and ampicillin therapy: preliminary results of a cooperative study. J Infect Dis 1977; 135 Suppl:S104.
- Tedesco FJ, Barton RW, Alpers DH. Clindamycin-associated colitis. A prospective study. Ann Intern Med 1974; 81:429.
- Parry MF, Rha CK. Pseudomembranous colitis caused by topical clindamycin phosphate. Arch Dermatol 1986; 122:583.
- Meadowcroft AM, Diaz PR, Latham GS. Clostridium difficile toxin-induced colitis after use of clindamycin phosphate vaginal cream. Ann Pharmacother 1998; 32:309.
- Tian D, Mohan RJ, Stallings G. Drug rash with eosinophilia and systemic symptoms syndrome associated with clindamycin. Am J Med 2010; 123:e7.
- Pharmacia & Upjohn Company Cleocin Phosphate (Clindamycin Phosphate) package insert. Kalamazoo, MI; April 1997.
- Muller AE, Mouton JW, Oostvogel PM, et al. Pharmacokinetics of clindamycin in pregnant women in the peripartum period. Antimicrob Agents Chemother 2010; 54:2175.
- Ugwumadu A, Manyonda I, Reid F, Hay P. Effect of early oral clindamycin on late miscarriage and preterm delivery in asymptomatic women with abnormal vaginal flora and bacterial vaginosis: a randomised controlled trial. Lancet 2003; 361:983.
- MECHANISM OF ACTION
- SPECTRUM OF ACTIVITY
- Allergic reactions
- Local reactions
- DRUG INTERACTIONS
- DOSING AND ADMINISTRATION
- - Children
- - Adults
- SPECIAL POPULATIONS
- Renal and hepatic dysfunction
- MONITORING DURING THERAPY