Background:Community acquired methicillin resistant staphylococcus aureus (CA-MRSA) is emerging in hospitals, worldwide. Method: In Suez Canal University Hospitals(SCUH), we documented causing hospital acquired- (HA-) sepsis, by polymerase chain reaction (PCR) amplification of major virulence determinant genes, namely: Panton-Valentine leukocidin pvl, accessory regulator I and III, and staphylococcal cassette chromosome mec genes IV and V. Antibiograms were determined by disk diffusion and minimum inhibitory concentration (MIC). Results: Methicillin resistant staphylococcus aureus was detected in 90 hospital acquired infections (HAIs), including bacteremia, pneumonia, osteomyelitis, soft tissue infections, and meningitis. Pvl gene, characterizing CA-MRSA, was detected in 24/90 MRSA strains (26.7%). Pvl+ve strains were subtyped into SCCmec gene type II (8.3%), type IV (75%), type V (8.3%), and 8.3% were non-typeable. They showed only agr group I (62.5%), and III (37.5%). Co-trimoxazole resistance was detected in 41.6% of CA-MRSA. Only 12.5% of strains were susceptible to all non-beta-lactam drugs. There was no statistical correlation between SCCmec or agr groups, and co-trimoxazole resistance in CA-MRSA; nor between SCCmec types and agr groups. Conclusion: Community aquired-MRSA is emerging in all wards of SCU hospitals, causing HAI, mostly soft tissue infections. The classical antibiogram of is no longer prevailing. Diagnosis of should rely upon detection of pvl gene, rather that clinical and antibiogram-profiles. The name CA-MRSA is no longer satisfactory to describe such strains in hospital settings; instead, Pvl +ve MRSA is more accurate and reliable term to use.