DermNet provides Google Translate, a free machine translation service. Note that this may not provide an exact translation in all languages


Toxic shock syndrome and toxic shock-like syndrome

Author: Dr Amanda Oakley, Dermatologist, Hamilton, New Zealand, 2002. Updated by Dr Jannet Gomez, January 2016. DermNet NZ Revision October 2021


What is toxic shock syndrome?

Toxic shock syndrome is an uncommon but severe acute illness due to exotoxins produced by specific strains of Staphylococcus aureus or Streptococcus pyogenes. 

What causes toxic shock syndrome?

Toxic shock syndrome featured in general public news in the early 1980s when an epidemic occurred. It was linked to the prolonged use of highly absorbent tampons in menstruating women. Since then manufacturers have made changes to tampon production and the number of cases of tampon-induced toxic shock syndrome has dropped significantly. Other causes for toxic shock syndrome include the use of contraceptive diaphragms and vaginal sponges (by women), as well as wound infections.

Toxic shock syndrome is caused by the release of exotoxins from toxigenic strains of the bacteria Staph aureus and Strep pyogenes in a person that lacks anti-toxin antibodies. These exotoxins act as superantigens.

Toxin-producing strains of Staph aureus causing toxic shock syndrome were first formally described in 1978. Prior to this time the syndrome was known as staphylococcal scarlet fever. Both menstrual and non-menstrual forms of toxic shock syndrome are caused by these toxins, which release massive amounts of cytokines that produce fever, rash, low blood pressure, tissue injury, and shock. Strains of Staph aureus producing toxic shock syndrome toxin-1 (TSST-1) cause almost all of the cases of menstrual toxic shock syndrome. Non-menstrual toxic shock syndrome are caused by strains producing either TSST-1 or staphylococcal enterotoxin B or C.

Toxic shock syndrome starts from a localised staphylococcal infection which produces the causative exotoxins.

When tampons are used, bacteria can gain entry into the uterus via the cervix or through mucosal splits or erosions in the vagina permitting access of bacteria into the tissues.

Non-menstrual toxic shock syndrome is now the more common form and may occur as a complication of other localised or systemic infections such as pneumonia, osteomyelitis, sinusitis, and skin wounds (surgical, traumatic, or burns).

In the late 1980s a disease that showed similar signs and symptoms to toxic shock syndrome but was caused by exotoxins released by toxin-producing M-protein strains of Strep pyogenes, was described. This disease although sometimes also referred to as toxic shock syndrome is more correctly known as streptococcal toxic shock-like syndrome (STSS).

STSS usually develops from a streptococcal soft-tissue infection such as bacterial cellulitis, necrotising fasciitis, or pyomyositis. Recent influenza A infection or chickenpox may predispose to secondary streptococcal infection.

Who gets toxic shock syndrome and STSS?

Toxic shock syndrome associated with menstrual tampons is now relatively rare, as most adults have developed protective antibodies to the exotoxin TSST-1. Women who have had toxic shock syndrome are at greatest risk, as the recurrence rate is reported to be between 30–40%.

Non-menstrual toxic shock syndrome and STSS occur in males and females of all age groups, associated with localised or systemic infections. The majority of cases are in healthy persons aged between 20 to 50 years, despite those most susceptible to staphylococcal and streptococcal infections being infants and young children, elderly, and immunocompromised individuals.

Other risk factors include:

  • Recent childbirth, miscarriage, or abortion. and the use of birth control devices such as the diaphragm or contraceptive sponges.
  • Foreign bodies, including nasal packing to stop nosebleeds and wound packing after surgery.
  • Wound infection after surgery. 

What are the clinical features of toxic shock syndrome and STSS?

Toxic shock syndrome and STSS share similar symptoms and signs.

  • Fever, diffuse macular red rash, low blood pressure, and multiple organ involvement are the hallmarks of these diseases.
  • Shedding of the skin in large sheets, especially from the palms and soles, is usually seen 1–2 weeks after the onset of illness.
  • Symptoms and signs are variable.

Centers for Disease Control and Prevention (CDC) have clinical criteria for toxic shock syndrome and STSS.

CDC Criteria for toxic shock syndrome and STSS
CDC case definition for toxic shock syndrome requires presence of the following 5 clinical criteria:
  1. Fever: temperature =/> 38.9 C
  2. Low blood pressure (including fainting or dizziness on standing)
  3. Widespread red flat rash
  4. Shedding of skin, especially on palms and soles, 1–2 weeks after onset of illness
  5. Abnormalities in 3 or more of the following organ systems:
  • gastrointestinal: vomiting or diarrhoea
  • muscular: severe muscle pain
  • hepatic: impaired liver function
  • renal: raised urea or creatinine levels
  • haematologic: bruising due to low blood platelet count
  • central nervous system: disorientation or confusion
  • mucous membranes: red eyes, mouth, vagina
CDC case definition for STSS requires isolation of group A streptococci and hypotension with 2 or more of the following clinical criteria:
  1. Renal impairment: decreased urine output
  2. Coagulopathy: bleeding problems
  3. Liver problems
  4. Rash that may shed, especially on palms and soles, 1–2 weeks after onset of illness
  5. Difficulty breathing
  6. Soft tissue necrosis including necrotising fasciitis, myositis and gangrene

How are toxic shock syndrome and STSS diagnosed?

Toxic shock syndrome diagnosis is confirmed if all 5 CDC clinical criteria are fulfilled. A probable case fulfils 4 of the 5 criteria.

To meet CDC criteria for toxic shock syndrome and STSS, diagnostic tests may include:

  • bacterial swabs from infected site of origin
  • blood cultures
  • blood tests: full blood count, renal and liver function, creatine kinase, coagulation
  • urine tests: urinalysis

What is the treatment of toxic shock syndrome and STSS?


Women who have had toxic shock syndrome should avoid using tampons during menstruation as reinfection can occur. If worn, they should be changed every 4–8 hours. The use of diaphragms and vaginal sponges may also increase the risk of toxic shock syndrome.

Prompt and thorough wound care will help to avoid toxic shock syndrome and STSS.

General measures

  • Removing the source of infection ie, tampons, vaginal sponges, nasal packing

  • Draining and cleaning the site of wound

  • Supportive measures may include:

    • Intravenous fluids to treat shock and prevent organ damage

    • Medications for very low blood pressure

    • Dialysis for renal failure

    • Administration of blood products

    • Infusions of intravenous immunoglobulin in severe resistant cases

    • Oxygen and mechanical ventilation to assist with breathing.

Specific measures

Treatment requires hospitalisation and intravenous antibiotics active against the causative organisms are given to eradicate the focus of the infection.

Flucloxacillin, nafcillin, oxacillin, linezolid, and first generation cephalosporin are the usual choices. Vancomycin can be used in patients sensitive to penicillin.

For STSS, penicillin plus clindamycin is the most effective combination treatment.

What is the outcome of toxic shock syndrome and STSS?

Toxic shock syndrome is a medical emergency that requires prompt treatment.

Early diagnosis and appropriate treatment prevents progression of the disease and possible complications such as heart problems, acute renal failure, adult respiratory distress syndrome, and disseminated intravascular coagulation.

The mortality rate of toxic shock syndrome is approximately 5–15%, and recurrences have been reported in as many as 30–40% of cases. Mortality rates of STSS are more than 5 times higher than in toxic shock syndrome.



  • Celie KB, Colen DL, Kovach SJ 3rd. Toxic Shock Syndrome after Surgery: Case Presentation and Systematic Review of the Literature. Plast Reconstr Surg Glob Open. 2020;8(5):e2499.  doi:10.1097/GOX.0000000000002499. PubMed Central 
  • DeVries AS, Lesher L, Schlievert PM, et al. Staphylococcal toxic shock syndrome 2000-2006: epidemiology, clinical features, and molecular characteristics. PLoS One. 2011;6(8):e22997. doi:10.1371/journal.pone.0022997. Journal 
  • Lappin E, Ferguson AJ. Gram-positive toxic shock syndromes. Lancet Infect Dis. 2009;9(5):281–90. doi:10.1016/S1473-3099(09)70066-0. PubMed 
  • Norrby-Teglund A, Muller MP, Mcgeer A, et al. Successful management of severe group A streptococcal soft tissue infections using an aggressive medical regimen including intravenous polyspecific immunoglobulin together with a conservative surgical approach. Scand J Infect Dis. 2005;37(3):166-72. doi:10.1080/00365540410020866. PubMed 
  • Poudel B, Zhang Q, Trongtorsak A, et al. An overlooked cause of septic shock: Staphylococcal Toxic Shock Syndrome secondary to an axillary abscess. IDCases. 2020;23:e01039.  doi:10.1016/j.idcr.2020.e01039. Journal 
  • Sharma H, Smith D, Turner CE, et al. Clinical and molecular epidemiology of Staphylococcal Toxic Shock Syndrome in the United Kingdom. Emerg Infect Dis. 2018;24(2):258–66. doi:10.3201/eid2402.170606. Journal 

On DermNet

Other websites

Books about skin diseases


Related information

Sign up to the newsletter