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Toxic shock syndrome

Last updated: April 29, 2021

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Toxic shock syndrome (TSS) is a rare toxin-mediated life-threatening acute condition caused by toxin-producing strains of Streptococcus pyogenes and Staphylococcus aureus. These bacterial strains produce superantigenic exotoxins, which trigger massive cytokine release and cause endothelial cell wall damage; this can lead to capillary leak syndrome and end-organ damage. Risk factors for TSS include prolonged tampon placement, wounds (including surgical wounds), and invasive/aggressive Group A Streptococcus (GAS) infections (e.g., necrotizing fasciitis). TSS initially manifests with flu-like prodromal symptoms followed rapidly by symptoms of a systemic inflammatory response syndrome, which may progress to shock and multiple organ failure. Diagnostic studies often demonstrate end-organ dysfunction, and positive cultures can help narrow antibiotic therapy. TSS is a clinical diagnosis and treatment should be initiated as soon as TSS is suspected. Rapid recognition of TSS, followed by fluid resuscitation, appropriate antibiotic selection, reduction/neutralization of the toxin load, and removal of the infection source are essential for the management of TSS. TSS can be fatal if treatment is not initiated promptly; streptococcal TSS has a mortality rate of ∼ 30–80%.

Streptococcus pyogenes and Staphylococcus aureus both cause TSS; however, streptococcal TSS and staphylococcal TSS often differ in their etiologies, clinical presentation, laboratory findings, and mortality rates.

Overview of toxic shock syndrome (TSS)
Streptococcal TSS Staphylococcal TSS
Menstrual TSS Nonmenstrual TSS
Etiology and risk factors
  • High-absorbency tampons
  • Prolonged placement of tampons, menstrual cups, and vaginal sponges
  • Postsurgical wound packing (especially nasal packing)
  • Burn and wound infections
  • Postpartum or postabortion infections
Superantigens implicated in TSS [1][2]
Onset
  • Variable
  • Typically within 48 hours postsurgery or postpartum [8]
Characteristic clinical features
  • Fever ≥ 38.9°C (102°F)
  • Features of underlying invasive GAS infection
  • Renal impairment [9]
  • Desquamating rash (uncommon;∼ 10%)
  • Fever ≥ 38.9°C (102°F)
  • Diffuse desquamating rash involving palms and soles (common;∼ 90%)
  • CNS involvement
  • Mucosal (conjunctival, oral, vaginal) involvement
Blood cultures
  • Typically positive (∼ 60%) [3]
  • Typically negative (positive in < 5%) [3][10]
Management
Mortality rates
  • 30–80% [1][3]
  • < 5% [3][7][10]
  • Up to 20% [3][7][10]
  • Incidence: ∼ 0.5–3/100,000 [7][11]
  • Age: Invasive GAS infections and subsequent complications are more common in young children and adults > 65 years of age. [3][9][12]

Epidemiological data refers to the US, unless otherwise specified.

TSS is most commonly caused by toxin-producing strains of Streptococcus pyogenes and Staphylococcus aureus [3]

Risk factors for TSS [1]
Streptococcal TSS Invasive GAS infections [3][9][12]
Noninvasive GAS infections
Others
Staphylococcal TSS Menstrual factors
(∼ 50% of cases) [14]
  • High-absorbency tampons
  • Prolonged placement of tampons, menstrual cups, and vaginal sponges
Nonmenstrual factors [1]
  • Burn and wound infections
  • Postpartum or postabortion infections
  • Postsurgical wound packing
Both Underlying medical conditions
Recent viral infections [8][15][16]

TSS is a systemic inflammatory response, similar to sepsis; see also “Pathophysiology” in “Sepsis.”

Very small amounts of superantigens can rapidly activate excessive numbers of T cells, triggering a massive release of proinflammatory cytokines, resulting in SIRS

TSS typically manifests as a prodrome of nonspecific symptoms, followed by hypotension and rapid progression (8–12 hours) to end-organ involvement. [3]

Onset

Prodrome [1]

Suspect underlying necrotizing fasciitis or myositis in patients with pain out of proportion to physical findings on examination.

Shock and end-organ dysfunction [3]

General principles

Initiate empiric antibiotic therapy for TSS as soon as TSS is suspected; do not wait for the results of laboratory studies.

Laboratory studies [21][22]

Workup for sepsis

Findings are typically nonspecific but may show evidence of infection and end-organ involvement.

Bacteriology

Blood cultures are typically negative in staphylococcal TSS.

Toxin-specific studies

Imaging

Imaging is not needed to make a diagnosis of TSS, but it may be considered if patients have the following symptoms:

The symptoms of TSS overlap with many other conditions, including the following:

Approach [1][3][11][26]

TSS is a life-threatening emergency that requires early diagnosis and a multidisciplinary approach to management.

Hemodynamic resuscitation

Management of source(s) of infection [3][8]

  • Examine for skin lesions and wounds.
  • Remove any foreign bodies (e.g., tampons, nasal packs, surgical packs).
  • Drain infected fluid collections (e.g., abscess).
  • Urgent surgical consult for suspected necrotizing fasciitis/myositis.

Obtain cultures from any potential site(s) of infection.

Antibiotic therapy [11][27][28]

Protein synthesis-inhibiting antibiotics inhibit toxin production but as they are bacteriostatic, they should be used in combination with a bactericidal antistreptococcal and/or antistaphylococcal antibiotic.

Empiric antibiotic therapy for TSS [11][27][28]

Causative organism unclear

(or penicillin allergy in confirmed TSS) [11][28][29]

Based on suspected pathogen
(i.e., based on history, clinical features, Gram stain, or cultures)
Suspected streptococcal TSS [28]
Suspected staphylococcal TSS [11][28]

Adjunctive therapy [11]

  • TSS is a reportable disease in the United States. [21][22]
  • The CDC has described features that are typical of streptococcal TSS and nonstreptococcal TSS for reporting purposes only; these criteria should not be used for diagnosis or to guide treatment.

Reporting criteria for toxic shock syndrome (TSS)

(based on the CDC reporting criteria for streptococcal TSS and nonstreptococcal TSS)

Streptococcal TSS [21] Nonstreptococcal (staphylococcal) TSS [22]

Clinical criteria
(all criteria need to be met)

Causative pathogen
  • Cultures are often negative, but S. aureus may be isolated from blood. [3]
  • No other identified cause

Use these criteria for reporting only, not diagnosis! Early, aggressive treatment is recommended to prevent dangerous sequelae even if not all criteria have been met.

We list the most important complications. The selection is not exhaustive.

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