There are presently two recognized mechanisms of resistance to macrolide antibiotics in species of the genus Streptococcus: target modification and efflux. Target modification occurs in the ribosomes through the production of a ribosomal methylase codified for the erm genes and it is phenotypically known as MLSB resistance. Expression of MLSB resistance can be inducible or constitutive. Active efflux has been recently described in S. pyogenes and S. pneumoniae, and its expression is known as M phenotype. We studied the susceptibility, by determining the MIC using agar dilution, to penicillin, erythromycin and clindamycin, of 295 strains of the genus Streptococcus clinically isolated from 1993 to 1996 (70 S. pyogenes, 81 S. pneumoniae, 37 viridans group, and 107 S. milleri). We also studied the phenotype pattern of erythromycin-clindamycin resistance in the strains resistant to erythromycin by using the double-disc test. We found a 17.2% resistance to erythromycin and a 12.5% resistance to clindamycin. The M phenotype, initially described in S. pyogenes, was also observed in 6.6% of our S. pneumoniae strains, 25% of S. viridans spp., and 4.8% in the S. milleri group.