Introduction: Treatment failure of clindamycin therapy has been reported due to multiple mechanisms that confer resistance to macrolide, lincosamide and streptogramin antibiotics..Moreover in vitro routine tests may fail to detect inducible clindamycin resistance due to erm genes. So detection of inducible clindamycin resistance among clinical isolates of staphylococcus aureus is of utmost clinical significance. Materials and Methods: The detection of Staph. aureus and MRSA was done using standard guidelines &inducible clindamycin resistance was performed by D–test using erythromycin and clindamycin discs as per CDC guidelines. .P value was calculated by SPSS v.18 software . Results: Among 184 Staph aureus, 54 ( 29.35% ) were MRSAand 130 ( 70.65 %) were MSSA ; 76 (41.30 %) were male and 108     (58.70 %) were female ;78 (42.40%) were resistant to Erythromycin and106 (57.60%)  were Sensitive to Erythromycin; Out of 106 Erythromycin sensitive Staph. aureus all were Clindamycin sensitive and  31 (16.84%) were MRSA and 75 ( 40.76 %) were MSSA.Among 78  Erythromycinresistantstrain, 23 ( 12.5%) were MRSA and  55 ( 29.89%)   were MSSA;MRSA showed 10(5.43 %)cMLS_{B ,}  1 (0.54 %)iMLS_B&12 ( 6.52 %)MS Phenotype whereasMSSA showed  14 (7.61 %)cMLS_B, 16 ( 8.69 %)iMLS_B&25(13.58 %)MS Phenotype. Conclusion:Although several data available from developed countries, data from the developing countries are lacking.The study contributes to distinguish different resistance phenotypes in erythromycin–resistant S. aureus which helps to guide clinicians to formulate empiric therapy when culture reports are pending.