Toxic Shock Syndrome
Two varieties – Staphylococcal TSS and Streptococcal TSS.
Both are essentially syndromes of acute multi-organ failure caused by toxins that act as superantigens, activating the immune system and causing a massive cytokine cascade that leads to capillary leak, tissue damage, shock, and multiorgan failure.
Streptococcal TSS is most often seen in association with invasive disease, such as necrotizing fasciitis (which is complicated by TSS in up to 50% of cases), pneumonia,and bacteremia. Of these, soft tissue infection is the most common source.
Staphylococcal TSS, on the other hand, traditionally was seen in association with highly absorbent tampons in the 1980s. Since recognition of this, however, tampons have been changed and this is less common than in the past. About 60% of causes are nonmenstrual, including surgical wounds, cutaneous lesions, burns, respiratory infections, and nasal packings (i.e. for epistaxis). The remaining 40% are menstrual related and have a better prognosis.
Staphylococcal TSS is defined by fever; diffuse macular rash; desquamation of the rash 1 to 2 weeks after the onset of illness with involvement of the palms and soles; hypotension; multiorgan system involvement; and lack of positive blood, throat, or cerebrospinal fluid cultures. A confirmed case is when all six of these criteria are met, whereas a probable case is when five of the six criteria are met.
Clinically, both present with acute onset of hypotension and multiorgan failure with a distributive shock physiology. Staph TSS more commonly has a diffuse erythematous rash that involves the palms and soles, and desquamates in 1-2 weeks if the patient survives; in Strep TSS, a diffuse scarlatina-like erythema is present in only ~10% of cases.
Some important differences between the two: In Strep TSS, bacteremia is much more common than in Staph TSS (~60% vs 5%), and prognosis is much much worse (~50% mortality or more vs ~5%).
Management:
1) Hemodynamic support – they require massive amounts of IVFs and usually pressors as well.
2) Surgery – for Strep TSS associated with invasive soft tissue infection, this is absolutely necessary, and the earlier the better. With abxs alone, mortality is basically 100%. Surgical exploration with biopsy and gram stain can often provide early definitive diagnosis.
3) Antibiotics
- Beta-lactam – Group A strep is uniformly sensitive to PCN. For staph, depends on MRSA or not: Nafcillin vs Vancomycin.
- Clindamycin – more effective than beta-lactams against Group A strep in invasive infections. Rationale is the so-called “Eagle Effect” described by Eagle in the 1950s – once there is a high inoculum of Strep and it reaches the stationary phase of growth, Strep does not express PCN-binding proteins and thus is less susceptible to beta-lactams. Clindamycin is not affected by inoculum size or stage of growth, suppresses synthesis of bacterial toxins, has a longer post-Abx effect than Beta-lactams, and may event modulate the immune response by suppressing TNF production.
- Linezolid - similar to Clindamycin, has anti-toxin effect that is likely more efficacious than Vancomycin or beta-lactams.
4) IVIG – small amounts of conflicting data on the efficacy, but generally is recommended. Rationale is that the immunoglobulins “soak up” the bacterial toxins and also modulate the immune response.
(Ellen Eaton MD, 5/19/11)
(Chanu Rhee MD, 1/7/11)