Abstract
Clindamycin is a protein synthesis inhibitory agent that has the ability to suppress the expression of virulence factors in Staphylococcus aureus. Recent guidelines recommend the use of clindamycin for the treatment of toxin-mediated infections. Clindamycin modulates virulence expression at sub-inhibitory concentrations (sub-MICs) in clindamycin-susceptible S. aureus strains but previous report shown that this effect was supressed for constitutive clindamycin resistant strains. However, no data are currently available on the impact of clindamycin at sub-MICs on the virulence of inducible clindamycin-resistant S. aureus strains. Here, we show that sub-MICs of clindamycin decrease Panton–Valentine leucocidin, toxic-shock-staphylococcal toxin (TSST-1) and alpha-haemolysin (Hla) expression in six inducible clindamycin-resistant isolates cultivated in vitro in CCY medium. These results suggest that the clindamycin anti-toxin effect is retained for inducible clindamycin-resistant S. aureus isolates; therefore, its usage should be considered within the treatment regimen of toxin related infections for inducible clindamycin-resistant S. aureus.
Highlights
Clindamycin is a protein synthesis inhibitory agent that has the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations
Several studies have reported the ability of clindamycin at sub-minimal inhibitory concentrations (MIC) to decrease the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla) [1,2,3,4,5,6]
Staphylococcus aureus produces many virulence factors that play an important role in the pathogenesis of infection, such as Hla [12], PVL [13, 14] and TSST-1 [15]
Summary
Clindamycin is a protein synthesis inhibitory agent that has the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Recent guidelines recommend the use of clindamycin for the treatment of toxin-mediated infections (e.g., toxic shock syndrome and necrotizing pneumonia) [7]. This modulation of virulence expression by clindamycin occurs in clindamycin-susceptible S. aureus strains but is abolished in constitutive clindamycin-resistant strains [5]. Contrary to constitutive clindamycinresistant strains, no data are currently available on the impact of clindamycin at sub-MICs on the virulence of inducible clindamycin-resistant S. aureus strains. We have shown in a selection of inducible clindamycinresistant S. aureus strains that clindamycin maintains its anti-toxin effect at sub-inhibitory concentrations
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