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Competing interests The authors declare that they have no competing interests. Authors’ contributions JR propagated and purified the phage, sequenced the genome, cloned the lysis gene, analyzed the genome and wrote the paper. KT supervised the work, analyzed the genome sequence and wrote the paper. Both authors read and approved the final manuscript.”
“Background Staphylococcus MK-8931 cost aureus is an important human pathogen, causing learn more a wide range of diseases from skin and soft tissue infections to life threatening sepsis [1]. Methicillin-resistant S. aureus (MRSA), which causes infections in hospitals and in the community, has become a major
public health problem worldwide. MRSA strains can be classified into different clonal groups and subgroups according to their genotypic characteristics. Epidemiologic data have indicated that certain strains are more commonly associated with invasive infections than others [2]. Experimental studies using human neutrophils and a mouse model suggested that community-associated MRSA (CA-MRSA) strains are more virulent than hospital-associated Resminostat MRSA (HA-MRSA) strains [3]. For CA-MRSA strains, USA300 showed higher virulence than USA400 in a rat pneumonia model [4]. These findings suggest that the virulence of S. aureus strains in the animal models may correlate with the clinical outcomes. However, to date, there are 17 major clonal complexes and many more subgroups identified from the S. aureus isolates collected worldwide, including MSSA and MRSA strains, and more are expected to be identified [5]. Given this complexity it is difficult to compare the virulence of these strains using mammalian models. We previously utilized the nematode, C. elegans, as a host model to analyze the virulence of major local clinical MRSA isolates, including those belonging to USA300, USA400, and Canadian epidemic strains MRSA 2 (CMRSA2) and CMRSA6. Our results demonstrated that CA-MRSA strains are more virulent than HA-MRSA strains [6]. Moreover, the virulence of MRSA in the C.