Abstract
Many bacteria secrete toxic agents, which influence their hit rate and replication within the host. The relative amounts of such toxins in the microenvironment during any given infection are crucial to host defences. Staphylococci can secrete up to 40 molecular species during the course of an infection, usually causing the host to produce a massive neutrophil response, leading to pus formation. However, there are exceptions to this pattern, for example, in cases of staphylococcal toxic-shock syndrome, in which staphylococci on a small burn or mucosal lesion cause severe or lethal illness with little or no visible pus or inflammation. Vojtov et al. [ 1. Vojtov N. et al. Global repression of exotoxin synthesis by staphylococcal superantigens. Proc. Natl. Acad. Sci. U. S. A. 2002; 99: 10102-10107 Crossref PubMed Scopus (82) Google Scholar ] have recently proposed an explanation for this following in vitro studies exploring toxin production by Staphylococcus aureus. They showed that strains of bacteria producing toxic-shock-syndrome toxin-1 (TSST-1) were distinctive in that they did not produce large amounts of other toxins. Those producing staphylococcal enterotoxin B showed behaved similarly. Further investigation revealed that these superantigens downregulate the genetic expression of other commonly secreted molecules, although the exact mechanism of this is unclear. Inhibition of this kind occurs in most staphylococcal toxic-shock-syndrome or toxic-food-poisoning cases, and might account for the lack of a pustular response.
Published Version
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