Bacteria: Virulence factors of Staph and Strep

Staphylococcus aureus and group A streptococci are both gram-positive cocci, although S. aureus strains are facultative anaerobes, whereas group A streptococci are aerotolerant anaerobes. Both organisms depend on a myriad of cell-surface and secreted virulence factors for host colonization and disease production. These cell-surface virulence factors include a variety of proteins referred to as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs). These molecules facilitate the attachment to host cells or interfere with host immune responses through antiphagocytic effects. Both organisms also produce large numbers of secreted virulence factors, including families of superantigens (SAgs) and cytolysins.

Nearly all S. aureus strains can produce one or more SAg proteins, including toxic shock syndrome toxin-1 (TSST-1), a small protein that can trigger a massive immune response that results in toxic shock syndrome (TSS). TSS is a rare but potentially life-threatening illness that is characterized by the rapid onset of symptoms, including high fever, low blood pressure, a rash resembling sunburn, and organ dysfunction.

When staphylococci come in contact with a mucosal surface, they secrete α-cytolysins, which bind to receptors on the surface of the target cell and form oligomers (clusters) that insert into the lipid bilayer, creating transmembrane pores. This allows TSST-1 to reach the deeper mucosal layers, where T cells reside. TSST-1 binds nonspecifically to T cells’ surface receptors, activating T cells to release highly inflammatory molecules, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), beginning the cascade of clinical TSS symptoms.

Treatment of TSS involves an antibiotic course, provision of fluids, and intravenous immunoglobulin (IVIg). IVIg is a purified antibody collected and pooled from multiple donors; it acts to neutralize TSST-1. In some toxin-mediated staphylococcal infections, a second antibiotic, clindamycin, is added to the treatment regimen for its anti-protein synthesis effects.