Toxic shock syndrome and clindamycin

American Academy of Pediatrics. Group A Streptococcal Infections. In: Kimberlin DW, Brady MT, Jackson MA, Long SS, eds. Red Book®: 2015 REPORT OF THE COMMITTEE ON INFECTIOUS DISEASES. American Academy of Pediatrics; 2015; 732-744.

TOXIC SHOCK SYNDROME: “As outlined in Tables 3.70 and 3.71 (p 740), most aspects of management are the same for toxic shock syndrome caused by group A streptococci or by S aureus. Paramount are immediate aggressive fluid replacement management of respiratory and cardiac failure, if present, and aggressive surgical débridement of any deep-seated infection. Because S pyogenes and S aureus toxic shock syndrome are difficult to distinguish clinically, initial antimicrobial therapy should include an antistaphylococcal agent and a protein synthesis-inhibiting antimicrobial agent, such as clindamycin. The addition of clindamycin to penicillin is recommended for serious GAS infections, because the antimicrobial activity of clindamycin is not affected by inoculum size (does not have the Eagle effect that can be observed with the beta-lactam antibiotics), has a long postantimicrobial effect, and acts on bacteria by inhibiting protein synthesis. Inhibition of protein synthesis results in suppression of synthesis of the S pyogenes antiphagocytic M-protein and bacterial toxins. Clindamycin should not be used alone as initial antimicrobial therapy in life-threatening situations, because in the United States, 1% to 2% of GAS strains are resistant to clindamycin. Higher resistance rates have been reported for strains associated with invasive infection and may be as high as 10%.

Once GAS infection has been confirmed, antimicrobial therapy should be tailored to penicillin and clindamycin. Intravenous therapy should be continued until the patient is afebrile and stable hemodynamically and blood is sterile as evidenced by negative culture results. The total duration of therapy is based on duration established for the primary site of infection.”


Parks T, Barrett L, Jones N. Invasive streptococcal disease: a review for clinicians. Br Med Bull. 2015 Sep;115(1):77-89.

“The early use of clindamycin is generally recommended as an adjunct because of a number of potential benefits, including a direct effect on toxin production. [28] A handful of small retrospective clinical studies have investigated the use of clindamycin, [5] including two recently published observational reports from Sweden [29] and Australia [30] that both found that the drug was associated with improved survival.”

Full-text for Emory users.


Chuang YY, et al. Toxic shock syndrome in children: epidemiology, pathogenesis, and management. Paediatr Drugs. 2005;7(1):11-25.

“Despite the susceptibility of GAS to penicillin, the outcome among individuals who have streptococcal TSS remains poor. In a mouse model of streptococcal myositis, penicillin was ineffective when treatment was delayed; the clindamycin-treated group had significantly better survival rates even if treatment was delayed.  [107] The failure of penicillin to eradicate the organisms may be due to the slow replication rate of the organisms when a large inoculum is present, or due to the inoculum effect. The large inocula may reach stationary growth phase rapidly and diminish the expression of penicillin-binding proteins, the target sites for penicillin activity. Clindamycin is more effective because:

  • the antimicrobial activity is not affected by the inoculum size;
  • it acts by inhibiting protein synthesis, is not dependent on penicillin-binding proteins, and thus also inhibits the synthesis of antiphagocytic M protein and bacterial toxins (SPEs), subsequently reducing the superantigenicity of SPEs;
  • it has a longer postantibiotic effect than β-lactams such as penicillin. [102,107,108]

Thus, clindamycin (25–40 mg/kg/day in three or four divided doses administered intravenously is recommended in addition to penicillin as therapy for severe, invasive GAS infections.  Clindamycin should not be used alone as initial empiric because 1–2% of S. pyogenes are resistant to clindamycin. [102]” (From pg. 21)

Full-text for Children’s and Emory users.


More PubMed results on TSS and clindamycin.

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