Why give Clindamycin for a Group A Strep infection that is already adequately covered by a Beta-lactam?

Proposed rationale: Clindamycin blocks 50s ribosomal subunit and therefore inhibits bacterial protein synthesis. It is thought that this will reduce endo/exotoxin production which is how Streptococcus pyogenes elicits its pathogenic effect. (It also increases opsonization and phagocytosis by inhibiting M-protein synthesis). Hence, it will act synergistically with the Beta-lactam (which is destroying the cell wall) to reduce the amount of toxin that is subsequently released into the blood. Clindamycin has a longer postantibiotic effect than penicillin.

The exotoxins of group A streptococci include the erythrogenic toxins (pyrogenic exotoxins) and the cytolytic toxins (streptolysins S and O)

References

1. Stevens DL. Streptococcal Toxic-Shock Syndrome: Spectrum of Disease, Pathogenesis, and New Concepts in Treatment. Emerg Infect Dis. 1995, Sept. Available from http://wwwnc.cdc.gov/eid/article/1/3/95-0301

 2. Marek, S. Current indications for the use of clindamycin: A critical review. Can J Infect Dis. 1998 Jan-Feb; 9(1): 22–28. 

3. Kalyan S, Chow AW. Staphylococcal toxic shock syndrome toxin-1 induces the translocation and secretion of high mobility group-1 protein from both activated T cells and monocytes. Mediators Inflamm. 2008. 2008:512196.

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