Resistance mechanisms to macrolide antibiotics involving lincosamide and streptogramin type B antibiotics were described in bacteria. Phenotype in the resistant microorganism is generally observed as one of two characteristics, i.e., decrease of intracellular macrolide-accumulation and inactivation of the drugs. The former phenotypic resistance results from one of three mechanisms: (1) mono- or di- methylation of a specific adenine residue in 23 S ribosomal RNA and (2) impaired uptake and (3) enhanced efflux of the antibiotics. The latter is caused by one of two mechanisms: (1) degradation of the drugs by a hydrolytic enzyme such as an esterase and (2) drug modification by one of enzymes such as nucleotidyl- and phospho- transferases.