Macrolide-inducible resistance to clindamycin and the D-test.

Clindamycin has been used to treat serious infections caused by susceptible Staphylococcus aureus strains in children for more than 30 years. It remains effective for many infections caused by community-acquired methicillin-resistant S. aureus (CAMRSA). Clindamycin also is useful for selected infections caused by pneumococci, group A streptococci, and a number of other microbes. Absorption after oral administration is nearly complete, yielding serum concentrations that approximate those from intravenous (IV) administration. This permits early transition to outpatient management of susceptible infections without the complications of continued IV access. Clindamycin resistance is common among health care-associated MRSA strains. Most CA-MRSA remain susceptible to date, but resistance rates vary by region. Pneumococcal resistance to clindamycin may exceed 30% in some areas of the US, while about 4% of group A streptococcal isolates are resistant. Macrolide-inducible resistance to clindamycin was first recognized in the laboratory in the early 1960s. Clinical isolates resistant to clindamycin were first recognized in 1968. Relapse of S. aureus infection in a rabbit model of endocarditis during clindamycin therapy was observed in the early 1970s. Clinical and bacteriologic relapse in a patient with S. aureus endocarditis during the fourth week of clindamycin therapy after initial improvement was reported in 1976. The initial isolate was susceptible to erythromycin and clindamycin while that from the relapse was resistant to both. This led to abandonment of clindamycin for treatment of endocarditis. The mechanism by which resistance to clindamycin can emerge during therapy, the D-test used to detect it, and the clinical implications are discussed in this review.