Does β-toxin Production Contribute to the Cytotoxicity of Hypervirulent Staphylococcus aureus?
Journal of Infectious Diseases March 1, 2015 211 (5) P.846-847
Céline Dupieux, Caroline Camus, Gérard Lina, François Vandenesch, Frédéric Laurent, and Jean-Philippe Rasigade
TO THE EDITOR—The recent article by Salgado-Pabón et al, which reported that excision of the staphylococcal β-toxin–converting bacteriophage φSa3 is common in φSa3-positive strains, was interesting .
By demonstrating that β-toxin production is selected for by in vivo infection and enhances virulence in rabbit models of pneumonia and infective endocarditis, Salgado-Pabón et al identified a previously unsuspected role for β-toxin in φSa3-positive Staphylococcus aureus.
Regarding infective endocarditis, they insightfully predicted that the increase in vegetation size associated with β-toxin production could be linked to its nucleoprotein ligase activity.
However, other mechanisms by which β-toxin could contribute to pathogenesis in these models were not discussed. Interestingly, β-toxin has been shown to participate in the intracellular virulence of S. aureus . β-toxin production, along with production of phenol-soluble modulins, is reportedly required for the disruption of phagosomal membranes by S. aureus after internalization and for the bacterium to gain access to the cytoplasm of the infected cell, eventually triggering cell death.
Interestingly, hypervirulent strains such as S. aureus USA300 escape phagosomes and are highly cytotoxic despite harboring φSa3 . Facing this apparent contradiction, some authors hypothesized that intraphagosomal oxidative stress induces φSa3 excision and restores β-toxin production ….