Streptococcal toxic shock syndrome

Background

• A toxic shock syndrome caused by Streptococcus pyogenes infection

Case Definition

• Source: CDC case definition 2010

Clinical Description

• Streptococcal toxic shock syndrome (STSS) is a severe illness associated with invasive or noninvasive group A streptococcal (Streptococcus pyogenes) infection. STSS may occur with infection at any site but most often occurs in association with infection of a cutaneous lesion. Signs of toxicity and a rapidly progressive clinical course are characteristic, and the case fatality rate may exceed 50%.

Clinical Criteria

• An illness with the following clinical manifestations*:
  • Hypotension defined by a systolic blood pressure less than or equal to 90 mm Hg for adults or less than the fifth percentile by age for children aged less than 16 years.
  • Multi-organ involvement characterized by two or more of the following:
    • Renal impairment: Creatinine greater than or equal to 2 mg/dL (greater than or equal to 177 µmol/L) for adults or greater than or equal to twice the upper limit of normal for age. In patients with preexisting renal disease, a greater than twofold elevation over the baseline level.
    • Coagulopathy: Platelets less than or equal to 100,000/mm3 (less than or equal to 100 x 106/L) or disseminated intravascular coagulation, defined by prolonged clotting times, low fibrinogen level, and the presence of fibrin degradation products.
    • Liver involvement: Alanine aminotransferase, aspartate aminotransferase, or total bilirubin levels greater than or equal to twice the upper limit of normal for the patient's age. In patients with preexisting liver disease, a greater than twofold increase over the baseline level.
    • Acute respiratory distress syndrome: defined by acute onset of diffuse pulmonary infiltrates and hypoxemia in the absence of cardiac failure or by evidence of diffuse capillary leak manifested by acute onset of generalized edema, or pleural or peritoneal effusions with hypoalbuminemia.
    • A generalized erythematous macular rash that may desquamate.
    • Soft-tissue necrosis, including necrotizing fasciitis or myositis, or gangrene.
• Clinical manifestations do not need to be detected within the first 48 hours of hospitalization or illness, as specified in the 1996 case definition. The specification of the 48 hour time constraint was for purposes of assessing whether the case was considered nosocomial, not whether it was a case or not.

Laboratory Criteria for Diagnosis

• Isolation of group A Streptococcus.

Case Classification

• Probable: A case that meets the clinical case definition in the absence of another identified etiology for the illness and with isolation of group A Streptococcus from a non-sterile site.
• Confirmed: A case that meets the clinical case definition and with isolation of group A Streptococcus from a normally sterile site (e.g., blood or cerebrospinal fluid or, less commonly, joint, pleural, or pericardial fluid).

Management

• Penicillin or other antistreptococcal beta-lactam
  • All GAS is susceptible to penicillin, so we need that or equivalent
• Plus adjunctive clindamycin for 72 hours and improving clinically
  • Clindamycin/erythromycin may be more active in animal models of necrotizing fasciitis and myonecrosis
    • Erythromycin resistance is still rare, but increasing
  • PBPs are not expressed during stationary-phase growth, so penicillin is less helpful when there is a large burden of bacteria (Eagle phenomenon)
  • Clindamycin blocks protein production (exotoxin and M protein)
  • Clindamycin has a longer half-life than penicillin
  • The two antibiotics are not antagonistic in vitro, so combination shouldn't cause problems
  • Clindamycin and azithromycin suppress cytokine production
• Alternative to clindamycin would be linezolid
• Consider daily IVIg
  • 0.5 mg/kg x1 followed by 25 g daily x2
  • 1 mg/kg x1 followed by 0.5 mg/kg daily x2