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. 2011 Nov;225(3):161-9.
doi: 10.1620/tjem.225.161.

Superantigenic toxin genes coexist with specific staphylococcal cassette chromosome mec genes in methicillin-resistant Staphylococcus aureus

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Superantigenic toxin genes coexist with specific staphylococcal cassette chromosome mec genes in methicillin-resistant Staphylococcus aureus

Dong-Liang Hu et al. Tohoku J Exp Med. 2011 Nov.
Free article

Abstract

Staphylococcus aureus is a leading cause of human disease in the hospital setting and the community. Superantigenic toxin-producing methicillin-resistant Staphylococcus aureus (MRSA) is currently important for nosocomial infections and food-borne diseases worldwide because of its global spreading and difficulty in therapy. Superantigenic toxins can bypass normal antigen presentation and have strong T cell mitogenic activity, leading to massive release of proinflammatory cytokines and contributing to the severity of S. aureus sepsis. In this study, a total of 131 MRSA isolates from patients in the University Hospital were searched for staphylococcal cassette chromosome mec (SCCmec) genes and the staphylococcal superantigenic toxin genes by multiplex polymerase chain reactions. The MRSA isolates were classified into SCCmec type II (74.8%), type I (13.0%), type IV (3.8%), type V (2.3%), and type I and type II (3.8%). MRSA isolates (102/131) also carried a number of superantigenic toxin genes including staphylococcal enterotoxin (se) and toxic shock syndrome toxin-1 (tst-1) genes. The most frequent superantigen gene profile (55/131, 42.0%) of the MRSA isolates includes staphylococcal enterotoxin C (sec), seg, sei, staphylococcal enterotoxin-like L (sell), selm, seln, selo, and tst-1. Furthermore, SCCmec type I or type II MRSA isolates more frequently harbor sec, seg, sei, sell, selm, seln, selo, and tst-1 genes, compared to other types of MRSA. These results indicate that the selected superantigenic toxin genes are linked to SCCmec type I and type II. The coexistence of these toxins and the SCCmec genes in S. aureus may contribute to the biological fitness and pathogenicity of MRSA.

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