S. epidermidis TYH1 WT and ΔhdcA mutant strains were examined for the presence of genes coding pathogenicity factors, including classical enterotoxin genes sea, seb, sec, sed, see, enterotoxin-like toxin Q gene (selq), and TSST-1 gene (tst1) (12 (link)), coagulase (13 (link)), and nuclease (14 (link)). Table 1 shows the PCR primer pairs. PCR amplifications were performed as described by Rahmdel et al. (15 (link)). For selq, tst1, coa and nuc detection, the uniplex PCR assay using each primer pair was applied. The reaction mixture (25 μL) contained 12.5 μL of Taq DNA Polymerase 2.0× Master Mix RED (1.5mM MgCl2; Ampliqon, Copenhagen, Denmark), 0.4 μM of each primer, and 50–100 ng DNA template. Superantigenic toxin genes, (SEs), were co-amplified by multiplex PCR according to Omoe et al. (16 (link)). The positive control strains used in this study were S. aureus DSM 19040 (sec, see), and S. aureus DSM 19041 (sea, seb, and sed).
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Genetic Profiling of S. epidermidis Pathogenicity
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Other organizations : Jahrom University, Shiraz University of Medical Sciences, Yasuj University of Medical Sciences, University of California, San Diego
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Variable analysis
independent variables
- Presence or absence of the hdcA gene in S. epidermidis TYH1 strain (WT vs. ΔhdcA mutant)
- Presence or absence of genes coding pathogenicity factors, including classical enterotoxin genes (sea, seb, sec, sed, see), enterotoxin-like toxin Q gene (selq), and TSST-1 gene (tst1)
- Presence or absence of coagulase (coa) gene
- Presence or absence of nuclease (nuc) gene
- PCR primer pairs (Table 1)
- PCR amplification conditions as described by Rahmdel et al. (15)
- Positive control strains: S. aureus DSM 19040 (sec, see), and S. aureus DSM 19041 (sea, seb, sed)
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