This study evaluated the antimicrobial activity of clindamycin, a newly developed chlorinated derivative of lincomycin, against over 500 bacterial isolates. Clindamycin was tested using quantitative minimum inhibitory concentration (MIC) methods and compared with lincomycin, erythromycin, benzylpenicillin, and oxacillin. The antibiotic demonstrated high activity against most Gram-positive cocci, including coagulase-positive and coagulase-negative staphylococci, Streptococcus pneumoniae, β-hemolytic streptococci, and viridans streptococci, with most strains inhibited at concentrations of 0.025-0.05 μg/ml. Clindamycin was 4 to 16 times more active than lincomycin against staphylococci on a weight-for-weight basis. The drug showed moderate activity against Haemophilus influenzae but was inactive against Gram-negative enteric bacteria and relatively inactive against Streptococcus faecalis. Resistance was uncommon among staphylococci, with only 2 of 300 coagulase-positive strains showing high resistance and 7 showing low-level resistance. The inoculum effect was small compared to benzylpenicillin. The enhanced potency suggests clindamycin could be used at lower doses than lincomycin, potentially reducing gastrointestinal side effects.

Key findings

• Clindamycin demonstrated 4-16 times greater activity than lincomycin against staphylococci and was highly effective against most Gram-positive cocci at low concentrations (0.025-0.05 μg/ml)
• Only 9 of 300 coagulase-positive staphylococcal strains showed resistance to clindamycin, with resistance being uncommon compared to lincomycin and erythromycin
• Clindamycin was inactive against Gram-negative enteric bacteria and relatively ineffective against Streptococcus faecalis, unlike its activity against other streptococci
• The small inoculum effect with clindamycin (median MIC ratio rarely exceeding 4-fold across a 4-log inoculum range) suggests reliable in vitro predictability
• Clindamycin showed moderate activity against Haemophilus influenzae, with all 10 strains tested inhibited at 1.6 μg/ml