Toxic Shock Syndrome
Question 1 from the second paper of 2007 asks specifically about the features of staphylococcal toxic shock syndrome. Both streptococci and staphylococci produce superantigens, and because of this the summary below expends little effort to help discriminate between them.
The information for this summary has been scraped together among the following sources:
- This NEJM case report (2013)
- A review article from PLOS (2011)
- Donald Low' overview from Critical Care Clinics (2013)
Pathogenesis of toxic shock syndrome
Some staphylococci and some Group A streptococci produce a characteristic protein (the Toxic Shock Syndrome Toxin, or TSST-1, 2 and 3).
- TSST activates T-cells directly, acting as a "superantigen"
- Massive inflammatory cytokine release is the result
- Endothelial dysfunction and vasodilatory shock ensues, which is out of proportion to the severity of the initiating infection.
In Low's article, staphylococcal TSS is separated into "menstrual" and "non-menstrual" categories. Apparently, the tampon introduces oxygen, which is required for TSS-1 production.
In contrast, streptococcal toxic shock as typically associated with a streptococcal pneumonia or with necrotising fasciitis.
Clinical manifestations of toxic shock syndrome
According to the CDC, there are four stereotypical criteria for toxic shock syndrome, all of which must be met:
- High fever (> 38.9°)
- Hypotension and shock
- Rash consistent with diffuse macular erythroderma
- Desquamation, particularly of the palms and soles
There are also non-diagnostic associated features:
- Rapid onset: ~ 2 days
- One might expect
- Multisystem organ involvement
- Staphylococcus may grow in the blood (but blood cultures otherwise negative)
- Staphylococcus aureus is only rarely (5%) recovered from blood cultures in toxic shock, in contrast to Group A Streptococci which are typically easily cultured from the blood.
- Vigorous resuscitation
- Source control
- Immediate debridement of the necrotic tissue if it is a streptococcal necrotising fasciitis
- Immediate removal of the tampon
- β-lactam antibiotics
- Clindamycin as an adjunct (prevents the synthesis of TSST)
- Intravenous immunoglobulin (to bind circulating TSST)
- IVIG also decreases in the production of proinflammatory cytokines and causes a downregulation of adhesion molecules and chemokines.
The Oh's Manual chapter on severe soft tissue infections (Ch. 71, p. 736) brings up some interesting points about the use of IV immunoglobulin in toxic shock:
- All the evidence in support of this therapy comes from the same group of researchers
- The mortality benefit was a trend, and was non-significant
- The dose of IVIG varies;
- Some give a single dose of 2g/kg
- Others give 1g/kg and then 0.5g/kg for two more days
- The effect of the polyspecific IVIG might vary from bottle to bottle, as the immunoglobulin infusion is a pooled product, representing a mixture of immunoglobulins from the population. Populations might vary in their expression of anti-TSST antibodies. One might call this the "Soylent Green Effect" (flavour varies from person to person).