JCVI: An Enterotoxin-bearing Pathogenicity Island In Staphylococcus epidermidis
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Madhusoodanan, J., Seo, K. S., Remortel, B., Park, J. Y., Hwang, S. Y., Fox, L. K., Park, Y. H., Deobald, C. F., Wang, D., Liu, S., Daugherty, S. C., Gill, A. L., Bohach, G. A., Gill, S. R.

An Enterotoxin-bearing Pathogenicity Island In Staphylococcus epidermidis

J Bacteriol. 2011 Feb 11;

PubMed Citation


Co-colonization of human mucosal surfaces causes frequent encounters between various staphylococcal species, creating opportunities for the horizontal acquisition of mobile genetic elements. The majority of Staphylococcus aureus toxins and virulence factors are encoded on S. aureus pathogenicity islands (SaPIs). Horizontal movement of SaPIs between S. aureus strains plays a role in the evolution of virulent clinical isolates. Although there have been reports of TSST-1, enterotoxin, and other superantigen production by coagulase-negative staphylococci, no associated pathogenicity islands have been found in the genome of Staphylococcus epidermidis, a generally less virulent relative of S. aureus. We show here the first evidence of a composite S. epidermidis pathogenicity island (SePI), the product of multiple insertions in the genome of a clinical isolate. Taxonomic placement of strain S. epidermidis FRI909 was confirmed by a number of biochemical tests and multi-locus sequence typing. The genome sequence of this strain was analyzed for other unique gene clusters and their location. This pathogenicity island encodes and expresses staphylococcal enterotoxin (SE) C3 (SEC3) and SE-like (SEl) L (SElL), as confirmed by semi-quantitative real-time RT-PCR and immunoblots. We present here an initial characterization of this novel pathogenicity island, establish that it is stable, expresses enterotoxins and is not obviously transmissible by phage transduction. We also describe the genome sequence, excision, replication and packaging of a novel bacteriophage in S. epidermidis FRI909, and attempts to mobilize the SePI element by this phage.