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Clindamycin is a lincosamide antibiotic (see Lincosamides, Oxazolidinones, and Streptogramins ) that is primarily bacteriostatic. It binds to the 50S subunit of the ribosome, thus inhibiting bacterial protein synthesis.
The spectrum of activity for clindamycin is similar to that of the macrolide erythromycin (see Table: Some Clinical Uses of Macrolides) except that clindamycin is
Effective for infections due to anaerobes (particularly Bacteroidessp, including B. fragilis), community-acquired methicillin-resistant Staphylococcus aureus, and macrolide-resistant, clindamycin-susceptible Streptococcus pneumoniae
Not reliably active against mycoplasmas, chlamydiae, Chlamydophila sp, and legionellae
Aerobic gram-negative bacilli and enterococci are resistant.
Clindamycin is usually used for anaerobic infections; however, clindamycin resistance has emerged among these organisms in some regions. Because these infections often also involve aerobic gram-negative bacilli, additional antibiotics are also used. Clindamycin is part of combination therapy for the following:
Clindamycin can be used for infections (eg, skin and soft-tissue infections) in communities where community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is common; whether clindamycin is useful depends on local resistance patterns.
Clindamycin can be used for infections due to clindamycin- and erythromycin-susceptible strains. However, some CA-MRSA strains are clindamycin-susceptible and erythromycin-resistant; erythromycin resistance in these strains may be due to an active efflux mechanism or to erythromycin-inducible modification of the ribosomal target. If the infecting strain of clindamycin-susceptible CA-MRSA is resistant to erythromycin because of the efflux mechanism, patients can be expected to respond to clindamycin. However, if the strain is erythromycin-resistant because of erythromycin-inducible ribosomal target modification, patients may not respond clinically to clindamycin because certain mutants can emerge during clindamycin therapy; these mutants are resistant to clindamycin and erythromycin because of constitutive modification of the ribosomal target. (Constitutive means that resistance is always present regardless of whether an inducer, such as erythromycin, is present.)
Erythromycin resistance due to efflux can be differentiated from that due to inducible ribosomal target modification with a commonly used double disk diffusion assay (D test). A clindamycin disk is placed at a standard distance from an erythromycin disk on an agar plate streaked with a standard inoculum of the CA-MRSA strain in question. Zone of growth inhibition (shaped like the letter “D”) around the clindamycin disk, with a flattened zone nearest the erythromycin disk indicates inducible ribosomal resistance. Patients who have moderate to severe infection with an inducible ribosomal-resistant CA-MRSA strain and a positive D test should not be treated with clindamycin.
Clindamycin cannot be used for CNS infections (other than cerebral toxoplasmosis) because penetration into the brain and CSF is poor.
Topical clindamycin is used for acne.
The main adverse effect is
Clostridium difficile–associated diarrhea (pseudomembranous colitis—see Clostridium difficile –Induced Diarrhea )
Clindamycin, penicillins, cephalosporins, and, most recently, fluoroquinolones have been associated with C. difficile–associated diarrhea. Clindamycin has been associated with C. difficile–associated diarrhea in up to 10% of patients regardless of route, including topical.
Hypersensitivity reactions may occur. If not swallowed with water, clindamycin may cause esophagitis.
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