Staphylococcal infections cause a variety of cutaneous and systemic
infections, including
impetigo, furuncle, subcutaneous
abscess,
staphylococcal scalded skin syndrome (SSSS),
toxic shock syndrome (TSS) and neonatal
toxic shock syndrome-like exanthematous disease (NTED), in association with microbial
virulence factors. The
virulence factors produced by Staphylococcus aureus have a wide array of
biological properties, including disruption of the epithelial barrier, inhibition of opsonization by antibody and
complement, interference with neutrophil chemotaxis, cytolysis of neutrophils, and inactivation of
antimicrobial peptides.
Exfoliative toxins (ETs) induce the 'acantholytic'
infection of S. aureus due to the disruption of cell-to-cell cohesion, which allows the pathogenic organisms to spread within the epithelium. Furthermore, S. aureus expresses
exotoxins with
biological properties of
superantigens that induce T-cell activation with subsequent anergy and immunosuppression. Of the S. aureus leukotoxins,
Panton-Valentine leukocidin (PVL) is involved in the development of multiple
furuncles with more intense
erythema, particularly in healthy young adults. TSS is an acute life-threatening illness caused by TSS toxin-1 (TSST-1) and is usually classified into two categories; menstrual TSS, originally described in association with tampon use, and nonmenstrual TSS with a variety of clinical settings. NTED is a
neonatal disease induced by
TSST-1 although clinical symptoms are much milder than those of TSS. In TSS and NTED, the expansion of TSST-1-reactive Vbeta2-positive T cells is observed. The production of pathogenic S. aureus
exotoxins and biofilm formation is regulated by the accessory gene regulator (agr) locus in the quorum-sensing signaling pathway. There is no doubt that targeting the quorum-sensing signaling pathway or anti-toxin
therapy is a promising therapeutic approach supportive of primary
antibiotic therapy.