Staphylogenic toxin shock syndromeA48.3

Author:Prof. Dr. med. Peter Altmeyer

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Last updated on: 20.05.2022

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Synonym(s)

Shock syndrome toxic; STSS; Tampon Disease; Toxic Shock Syndrome; Toxic Shock Syndromes; Toxin Shock Syndrome; TSS

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HistoryThis section has been translated automatically.

Todd et al., 1978

DefinitionThis section has been translated automatically.

Severe, life-threatening clinical picture (see below superantigen) caused by the exotoxin TSST-1 (toxic shock syndrome toxin 1) formed by certain Staphylococcus aureus strains (see also exfoliatin) with scarlet-like skin symptoms, shock symptoms and multiple organ symptoms (see below)

A distinction must be made:

  • a menstrual STSS

by a

  • Non-central STSS

Both clinical pictures differ only in the localization of staphylococcal colonization (vaginal in menstrual STSS and non-vaginal = bursitis, abscesses) with analogous clinical symptoms.

Note: A similar clinical picture is caused by certain pyrogenic exotoxins produced by streptococci (see below Streptococcal toxic shock syndrome). Previously severe soft tissue infection. Clinical picture with severe pain, high fever, redness and erythema, followed by hypotension and shock symptoms.

PathogenThis section has been translated automatically.

Mainly staphylococci of phage group I

Occurrence/EpidemiologyThis section has been translated automatically.

Rare, prevalence is 0.5/100,000 per year

EtiopathogenesisThis section has been translated automatically.

A TSS only develops if toxin-producing organisms in abscess cavities or foreign bodies are protected by the body's own defence system and can thus produce a critical amount of toxins.TSS-1 is a 29kD protein and, as a superantigen, causes massive direct T-cell stimulation and a fulminant release of mediators.

ManifestationThis section has been translated automatically.

Mainly occurring in younger women who use vaginal tampons, also occurring after delivery (detection of Staphylococcus aureus from vaginal swabs). More rarely also men in connection with furuncles, abscesses, osteomyelitis . Increased production and/or absorption of the exotoxin is suspected).

Clinical featuresThis section has been translated automatically.

General: Temperatures > 39.6 °C, hypotension, orthostatic dysregulation, involvement of 3 or more of the following organ systems: gastrointestinal(vomiting, diarrhea), skeletal (myalgia, CK elevation), renal (urea and creatinine elevation, leukocyturia), hepatic (enzyme and bilirubin elevation), blood (thrombocytopenia), CNS (disorientation, impaired consciousness).

Integument: Palmoplantar erythema and generalized scarlatiniform exanthema with tendency to erythroderma. Desquamation 1-2 weeks after onset, predominantly on palms and soles. Hyperemia of the mucous membranes. In menstruating women, also initial vaginitis and vulvitis with purulent fluoride.

Criteria for the diagnosis of staphylogenic toxin shock syndrome (varies according to D. Abeck).

  • Fever > 38.90C
  • Exanthema (diffuse macular exanthema).
  • Hypotension (systolic blood pressure <90mmHg for adults).
  • Systemic infestation =/> 3 of the following organs.
    • Musculature (severe myalgias, CK rise to 2 times normal value)
    • Mucous membranes (vaginal, oropharyngeal or conjunctival hyperemia)
    • Kidney (urea level and creatinine level >2 times normal)
    • Liver (enzyme and bilirubin increase)
    • Blood count (platelet count decrease <100,000/ul)
    • CNS (disorientation, cloudiness of consciousness)
  • Microbiology (staphylococcal cultures neg. blood, throat, CSF).

Diagnosis likely if 5 of 6 criteria are met.

LaboratoryThis section has been translated automatically.

Negative blood culture, throat swab, CSF puncture, thrombocytopenia, elevation of liver and kidney values.

DiagnosisThis section has been translated automatically.

Cultural evidence of TSST-1-forming staphylococci; smear from vagina or other mucous membranes. Serological detection of TSST-1 antibodies is also possible.

Differential diagnosisThis section has been translated automatically.

Complication(s)This section has been translated automatically.

Renal failure; disseminated intravascular coagulation.

TherapyThis section has been translated automatically.

Cooperation with internists. Stage-dependent shock treatment (see below shock, anaphylactic). In addition, penicillinase-resistant penicillin such as Flucloxacillin (e.g. Staphylex Kps.) 4 times/day 1-2 g p.o. for 7 days. For resistance Linezolid (Zyvoxid) 2 times/day 600 mg p.o. or i.v.

Progression/forecastThis section has been translated automatically.

Varying degrees of difficulty. The lethality rate is about 6%. Good prognosis with timely treatment.

Case report(s)This section has been translated automatically.

A school class with 16-year-old girls from NRW is going on a skiing holiday to Austria for 1 week. They are accommodated there in 2-bed rooms in a pension, which is structurally damaged. (walls and floors are damp). Several schoolgirls develop a catarrhal infection of the respiratory tract after 2 days. 2 schoolgirls, who are accommodated in one room, stay away from skiing lessons on Thursday because they do not feel well because of their menstruation. The next day they both feel really ill with fever, malaise and circulation problems. The sports teacher as a supervisor prescribes bed rest for this "flu-like" infection, but this does not affect the condition, especially one of the students.

However, since the return journey is planned for the weekend, no medical help is required. During the bus trip, the condition of these 16-year-olds deteriorates rapidly. Arriving at home, a high respiratory rate and cyanosis are noticeable. She is weak and hardly reacts to calls. The emergency doctor who was called immediately referred the patient to the intensive care unit of the clinic.

There, despite intensive care measures and antibiotic therapy, the patient died after 2 days of septic shock with ARDS(acute respiratory distress syndrome), which was accompanied by hepatisation of the lung (in the X-ray image a "white" lung), so that oxygenation was not possible.

S. aureus was detectable in cultures of sputum and vaginal secretion. This strain produced TSST-1 and enterotoxin B. The massive toxin production was responsible for the lethal outcome.

LiteratureThis section has been translated automatically.

  1. Abeck D (2018) Staphylococcus and streptococcus infections of the skin. In: Braun-Falco`s Dermatology, Venerology Allergology G. Plewig et al. (Hrsg) Springer Verlag S 169
  2. Annane D et al (2004) Managing toxic shock syndrome with antibiotics. Expert Opinion Pharmacother 5: 1701-1710
  3. Barran W et al (1983) Toxic shock syndrome. Dermatologist 34: 55-58
  4. Hikone M et al(2015) Streptococcal toxic shock syndrome secondary to group A Streptococcus vaginitis. J Infect Chemother 21:873-876
  5. Lin YJ et al (2015) Early Differentiation of Kawasaki DiseaseShock Syndrome and Toxic Shock Syndrome in a Pediatric Intensive Care Unit. Pediatric Infect Dis J 34:1163-1167
  6. March WC et al (1986) Toxic shock syndrome. dermatologist 37: 410-412
  7. Todd J, Fishaut M, Kapral F (1978) Toxic-shock syndrome associated with phage-group-I staphylococci. Lancet 2: 1116-1118
  8. Torda A (2005) Postpartum toxic shock syndrome associated with multiple splenic infarcts. Med J Aust 182: 93
  9. Warner JE, Onderdonk AB (2004) Diversity of toxic shock syndrome toxin 1-positive Staphylococcus aureus isolates. Appl Environ Microbiol 70: 6931-6935
  10. White MC et al (2005) Early diagnosis and treatment of toxic shock syndrome in paediatric burns. Burns 31: 193-197

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Last updated on: 20.05.2022