Clindamycin

Clindamycin (rINN) is a lincosamide antibiotic used in the treatment of infections caused by susceptible microorganisms. Clindamycin is a semisynthetic antibiotic derived from lincomycin by 7(S)-chloro-substitution of the 7(R)-hydroxyl group of the lincomycin. Clindamycin is marketed under various trade names including Dalacin (Pfizer), Cleocin (Pfizer) and Evoclin (Connetics) - in a foam delivery system.

Indications

Clindamycin is used primarily to treat infections caused by susceptible anaerobic bacteria. Such infections might include respiratory infections, septicemia and peritonitis. In patients with hypersensitivity to penicillins, clindamycin may be used to treat susceptible aerobic infections as well. It is also used to treat bone-infections caused by Staphylococcus aureus. Topical application of clindamycin phosphate can be used to treat severe acne.

It is most effective against infections involving the following types of organisms:

  • Aerobic gram-positive cocci, including some members of the Staphylococcus and Streptococcus (eg. pneumococcus) genera.
  • Anaerobic gram-negative bacilli, including some members of the Bacteroides and Fusobacterium genera.

    • Available forms

    Clindamycin preparations for oral administration include capsules (containing clindamycin hydrochloride) and oral suspensions (containing clindamycin palmitate hydrochloride). It is also available for intravenous injection as clindamycin phosphate. Topical preparations contain either clindamycin hydrochloride or clindamycin phosphate.

    Mechanism of action

    Clindamycin has a bacteriostatic effect. Clindamycin interferes with bacterial protein synthesis, in a similar way as erythromycin and chloramphenicol, by binding to the 50S subunit of the bacterial ribosome. This causes antagonism if administered simultaneously and possible cross-resistance.

    Pharmacokinetics

    Approximately 90% of an oral dose of clindamycin is absorbed from the gastrointestinal tract and it is widely distributed throughout the body, excluding the central nervous system. Adequate therapeutic concentrations can be achieved in bone. There is also active uptake into leucocytes.

    Clindamycin is extensively metabolised in the liver, with some of its metabolites being active, such as N-dimethyl clindamycin and clindamycin sulfoxide. The elimination half-life is 1.5–5 hours. Both clindamycin and its metabolites are excreted primarily in the urine (Klasco, 2006).

    Adverse effects

    Common adverse drug reactions (ADRs) (≥1% of patients) associated with clindamycin therapy include: diarrhoea, pseudomembranous colitis, nausea, vomiting, abdominal pain/cramps, rash, and/or itch. High intravenous doses may cause a metallic taste, and topical application may cause contact dermatitis (Rossi, 2006).

    Pseudomembranous colitis is a potentially-lethal condition commonly associated with clindamycin and lincomycin therapy, but also occurs with other antibiotics. It may affect up to 2–10% of patients treated with clindamycin. Overgrowth of Clostridium difficile, which is inherently resistant to clindamycin, results in the production of a toxin that causes a range of adverse effects ranging from diarrhoea to colitis and toxic megacolon (Rossi, 2006).

    Rarely (<0.1% of patients), clindamycin therapy has been associated with anaphylaxis, blood dyscrasias, polyarthritis, jaundice, raised liver enzymes and/or hepatotoxicity (Rossi, 2006).

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