Thursday, February 12, 2009

Toxic shock syndrome & Streptococcal toxic shock syndrome(STSS)! Ahaa confused

Toxic shock syndrome (TSS), mediated by enterotoxins produced by Staphylococcus aureus or Streptococcus pyogenes.Generally when we say TSS we mean Toxic shock syndrome caused by Staphylococcus aureus & only when we specify it as STSS we mean Toxic shock syndrome caused by Streptococcus pyogenes.
Clinical case definition of TSS
An illness with the following clinical manifestations:
  • Fever: temperature greater than or equal to 102.0°F (greater than or equal to 38.9°C)
  • Rash: diffuse macular erythroderma
  • Desquamation: 1-2 weeks after onset of illness, particularly on the palms and soles
  • Hypotension: systolic blood pressure less than or equal to 90 mm Hg for adults or less than fifth percentile by age for children aged less than16 years; orthostatic drop in diastolic blood pressure greater than or equal to 15 mm Hg from lying to sitting, orthostatic syncope, or orthostatic dizziness
  • Multisystem involvement (three or more of the following):
    • Gastrointestinal: vomiting or diarrhea at onset of illness 
    • Muscular: severe myalgia or creatine phosphokinase level at least twice the upper limit of normal
    • Mucous membrane: vaginal, oropharyngeal, or conjunctival hyperemia
    • Renal: blood urea nitrogen or creatinine at least twice the upper limit of normal for laboratory or urinary sediment with pyuria (greater than or equal to 5 leukocytes per high-power field) in the absence of urinary tract infection
    • Hepatic: total bilirubin, alanine aminotransferase enzyme, or asparate aminotransferase enzyme levels at least twice the upper limit of normal for laboratory
    • Hematologic: platelets less than 100,000/mm3
    • Central nervous system: disorientation or alterations in consciousness without focal neurologic signs when fever and hypotension are absent.



Staphylococcal TSS presents with a triad of fever, scarlitiform rash and cardiovascular collapse


In the early 1980s, the incidence of staphylococcal TSS among healthy, young, menstruating women increased. Eventually, it was discovered that a specific manufacturing defect in tampons linked staphylococcal TSS to their use. The tampons were believed to neutralize the acidic vaginal environment during menstruation, thus promoting oxygen tension and raising carbon dioxide levels in the vagina, providing a proper medium for the growth of S aureus.[reference from emedicine]


Case definition for streptococcal TSS :

  1. Isolation of group A Streptococcus from a normally sterile site (ie, blood, cerebrospinal fluid, pleural or peritoneal fluid)
  2. Hypotension
  3. Two or more of the following:
      1. 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.
      2. 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.
      3. 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.
      4. 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.
      5. A generalized erythematous macular rash that may desquamate.
      6. Soft-tissue necrosis, including necrotizing fasciitis or myositis, or gangrene.

The following risk factors have been reported to be associated with STSS:

  • Patients with HIV, diabetes, cancer, ethanol abuse, and other chronic diseases
  • Patients with a recent history of varicella infection (chicken pox)
  • Patients who used nonsteroidal anti-inflammatory drugs (NSAIDs)

Differntiate between TSS & STSS clinically & lab studies:

Differentiating between staphylococcal and streptococcal TSS is often difficult at the initial presentation. On the other hand, there appears to be some symptoms and signs that may assist in distinguishing between the 2 etiologies.

  1. Patients with staphylococcal TSS tend to present with diarrhea, vomiting, generalized erythroderma, conjunctival injection, and/or severe myalgia.
  2. Patients with streptococcal TSS, however, often have a form of soft tissue necrosis (eg, cellulitis, abscess, myositis, or necrotizing fasciitis), influenza-like symptoms, and (as previously described) varicella in those patients who have not been vaccinated against it.


Laboratory tests are often the only way to distinguish between the 2 etiologies. As previously mentioned, both types of TSS are mediated by enterotoxins.

  • In staphylococcal TSS, toxic shock syndrome toxin–1 (TSST-1) is responsible for nearly 75% of cases. Testing for this toxin involves detecting the presence of antibodies against it. If TSST-1 antibodies are present in the laboratory studies, the specificity of TSS being caused by S aureus is up to 90%.
  • S pyogenes TSS, on the other hand, is mediated by different enterotoxins, but all are linked to the M-protein found in the cell membrane of the bacterium. Streptococcal pyrogenic exotoxins (SPEs) A, B, and C are present in only about 13% of S pyogenes–mediated TSS-related cases; however, laboratory testing suggests that the M-protein is present in about 75% of these cases. Unfortunately, no reliable tests detecting M-protein exist at this time. Streptolysin O, however, is another toxic immunogenic protein produced by S pyogenes. Its presence during an infection can be measured using the titer against antistreptolysin antibody (ASO titer). The sensitivity of this test ranges from 62-76%, with a specificity of 79-85%; therefore, elevated titer levels will often identify S pyogenes as the etiologic bacterium.

TREATMENT:Regardless of the bacteria causing TSS, the treatment remains the same.

Crystalloids and inotropic agents are used to aggressively treat the hypovolemic shock, with close monitoring of the patient's mean arterial pressure (MAP) and central venous pressure (CVP).

Furthermore, targeted antibiotics are indicated;

  • penicillin or a beta-lactam antibiotic is used for treating group A streptococci, and
  • vancomycin or a semisynthetic antistaphylococcal penicillin is used for staphylococcal TSS.
  • Clindamycin(800 mg IV every 8 hours), however, has emerged as a key portion of the standard treatment. When utilized, clindamycin has an 83% more favorable outcome when compared with penicillin or beta-lactam antibiotics (14%). As opposed to penicillin, clindamycin is not affected by the size of the inoculum, it has a longer postantibiotic effect, and it better facilitates phagocytosis by inhibiting the production of the antiphagocytic M-protein. In addition, clindamycin reduces TSST-1 levels by up to 90%, whereas penicillin or other beta-lactam antibiotics have the potential to raise TSST-1 levels because they will lyse or alter the bacterial cell membrane, which often causes further release of the toxin into the bloodstream.clindamycin often is considered the drug of first choice for invasive group A streptococcal infections such as STSS

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