Expression of staphylococcal superantigens during nasal colonization is not sufficient to induce a systemic neutralizing antibody response in humans.

Staphylococcus aureus carriers have high-titer serum antibodies against non-enterotoxin gene cluster (egc) superantigens, whereas they lack anti-egc antibodies, suggesting different superantigen expression profiles in vivo. We measured the superantigen transcripts in S. aureus directly isolated from the nose of persistent carriers and correlated them with the superantigen-neutralizing antibody response. While neutralizing serum antibodies against the staphylococcal enterotoxins A and C (SEA and SEC) were found in carriers, antibodies against the egc-encoded staphylococcal enterotoxin-like toxin O (SElO) were rare. Surprisingly, the transcription of selo was comparable to sea and sec during nasal colonization. Thus, egc superantigens are transcribed during nasal colonization, but this is not sufficient to induce a serum antibody response.

Clonal distribution of superantigen genes in clinical Staphylococcus aureus isolates.

Staphylococcus aureus is both a successful human commensal and a major pathogen. The elucidation of the molecular determinants of virulence, in particular assessment of the contributions of the genetic background versus those of mobile genetic elements (MGEs), has proved difficult in this variable species. To address this, we simultaneously determined the genetic backgrounds (spa typing) and the distributions of all 19 known superantigens and the exfoliative toxins A and D (multiplex PCR) as markers for MGEs. Methicillin- sensitive S. aureus strains from Pomerania, 107 nasal and 88 blood culture isolates, were investigated. All superantigen-encoding MGEs were linked more or less tightly to the genetic background. Thus, each S. aureus clonal complex was characterized by a typical repertoire of superantigen and exfoliative toxin genes. However, within each S. aureus clonal complex and even within the same spa type, virulence gene profiles varied remarkably. Therefore, virulence genes of nasal and blood culture isolates were separately compared in each clonal complex. The results indicated a role in infection for the MGE harboring the exfoliative toxin D gene. In contrast, there was no association of superantigen genes with bloodstream invasion. In summary, we show here that the simultaneous assessment of virulence gene profiles and the genetic background increases the discriminatory power of genetic investigations into the mechanisms of S. aureus pathogenesis.