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Toxic Shock Syndrome
Synonyms: TSS, streptococcal toxic shock-like syndrome (STSS), 'toxic strep'
Definition
Toxic shock syndrome (TSS) is a multisystem inflammatory response to the presence of bacterial exotoxins.
Todd first described it amongst children in 1978; the toxins were secreted by Staphylococcus aureus.
Subsequently it was found to be associated with tampon use in menstruating women and Group A streptococcal
infections - the streptococcal toxic shock-like syndrome (STSS). It is now recognised as a consequence of a
range of infections associated with toxin-secreting staphylococci and streptococci. Enhanced surveillance of the
rate of Group A infections is undertaken by microbiologists in the UK and several European countries.
Pathogenesis
The infecting staphylococcal or streptococcal exotoxin acts as a superantigen, setting off a reactive inflammatory
cascade, mediated predominantly by tumour necrosis factor alpha and interleukin-1.
Epidemiology
In the early 1990s there were roughly 40 cases per year in the UK, with 2-3 deaths per year. This has since
declined due to change in tampon manufacture, and increased awareness.
Group C and Group G streptococci have been reported to cause invasive disease similar to that classically
associated with group A streptococcus. [1, 2]
The incidence of both TSS and STSS appeared to increase through the 1980s and 1990s but has now
stabilised. A UK series showed an incidence of STSS increasing from 1 to 9.5 per million population
per year in the 1990s. [3]
Infections not associated with menstruation have become more common as menstrual cases have
declined. The incidence in children is lower than that in adults. [4]
Both conditions are relatively rare; worldwide background prevalence of TSS is approximately
3/100,000 people. [5]
Possible risk factors
S. aureus cellulitis.
Wounds (including burns).
Tampon use (now less relevant) or gynaecological infection.
Puerperal sepsis.
Postoperative infections (classical signs of infection may be absent in wound).
Packed wounds - eg, nasal.
Sinusitis.
Tracheitis.
Recreational intravenous drug use.
HIV.
Allergic contact dermatitis.
Varicella spp.
Influenza A virus.
There is debate around an association with non-steroidal anti-inflammatory drug use. [4]
Presentation
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Presentation
Presentation is usually nonspecific and patients generally present with flu-like symptoms and can develop a lifethreatening TSS in just a few hours. [6] Features may include:
Fever: this is usually high at approximately 39ºC.
Rash: this is usually diffuse, macular and erythrodermic (intense widespread reddening of skin). A
scarlatiniform eruption, ie widespread fine, red, papular - 'sandpaper-like' with flexural accentuation,
may also be seen.
Hypotension: this may be profound and is due to suppression of myocardial contractility by the toxin. [7]
Multiorgan dysfunction.
Desquamation of palms and soles of feet 1-2 weeks after onset.
Palms, soles of feet, mucous membranes and tongue may be bright red.
Nausea, vomiting and diarrhoea are relatively frequent presenting features.
Myalgia and muscle weakness are common.
Confusion and disorientation may indicate encephalopathy.
Examination should seek evidence of the source of the infection by:
Close examination of the skin.
Checking for tampons; gynaecological examination.
Respiratory examination.
Differential diagnosis
Cellulitis.
Any patient with a fever and a rash. [8]
Meningococcal disease.
Gram-negative septic shock.
Erythema multiforme/Stevens-Johnson syndrome/toxic epidermal necrolysis (as drug reaction).
Heat-related illness.
Infectious mononucleosis.
Infective endocarditis.
Kawasaki disease.
Viral infection and exanthem.
Leptospirosis.
Typhus/other rickettsial infections.
Cardiogenic shock.
Listeria monocytogenes infection.
Typhoid.
Dengue fever.
Investigations
Blood cultures are positive in 5-15% of cases of TSS and in approximately 50% of STSS.
FBC often shows leukocytosis and low platelets.
U&Es may show raised urea and creatinine, electrolyte disturbance and hypocalcaemia.
CK and LFTs may be elevated.
Urinalysis may show microscopic haematuria/myoglobinuria.
Any wounds should be swabbed for culture.
Throat swab/others as per clinical suspicion of focus of infection.
CXR may be useful if there is suspected pneumonic focus.
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Management
Early diagnosis and rapid intervention are the key to arresting the cascade of inflammation that leads to rapid
deterioration:
Any persisting focus of infection, such as abscess, wound pack, wound slough or tampon, should be
removed immediately, with surgical assistance if necessary.
Aggressive haemodynamic resuscitation, preferably with central fluid volume monitoring and regular
electrolyte testing is crucial.
Vasopressor agents may be used to manage shock, under expert guidance.
Any abnormality of glucose levels should be closely managed and normalised. [9]
Antibiotics should be given early and in sufficient doses:
Choice of agent depends on suspected pathogen and local patterns of prevalence and
resistance. [10] Cephalosporins and clindamycin provide broad cover that should be
effective against relevant organisms. [5]
Steroids may play a role in improving survival. [11] Research has shown that a long course of low-dose
corticosteroids reduces 28-day all-cause mortality, and intensive care unit and hospital mortality. [12]
There is no evidence for the use of activated protein C for treating patients with severe sepsis or
septic shock. Activated protein C was therefore withdrawn in 2011. [13]
Prognosis
Mortality rate for TSS is around 5-15%.
A fatality rate of up to 64% has been noted in cases of STSS in the UK. [3]
Recurrence of TSS is found in 30-40% of cases.
Complications
Recurrence.
Cardiomyopathy.
Rhabdomyolysis.
Acute kidney injury.
Encephalopathy and cerebral oedema.
Acute respiratory distress syndrome.
Hepatic necrosis.
Thrombocytopenia and marrow suppression.
Disseminated intravascular coagulopathy (DIC).
Metabolic acidosis, electrolyte disturbance.
Further reading & references
Toxic Shock Syndrome Information Service
1. Korman TM, Boers A, Gooding TM, et al; Fatal case of toxic shock-like syndrome due to group C streptococcus associated
with superantigen exotoxin. J Clin Microbiol. 2004 Jun;42(6):2866-9.
2. Hagiya H, Okita S, Kuroe Y, et al; Afatal case of streptococcal toxic shock syndrome due to Streptococcus dysgalactiae
subsp. equisimilis possibly caused by an intramuscular injection. Intern Med. 2013;52(3):397-402. Epub 2013 Feb 1.
3. Barnham MR, Weightman NC, Anderson AW, et al ; Streptococcal toxic shock syndrome: a description of 14 cases from
North Yorkshire, UK. Clin Microbiol Infect. 2002 Mar;8(3):174-81.
4. Chuang YY, Huang YC, Lin TY; Toxic shock syndrome in children: epidemiology, pathogenesis, and management. Paediatr
Drugs. 2005;7(1):11-25.
5. Annane D, Clair B, Salomon J; Managing toxic shock syndrome with antibiotics. Expert Opin Pharmacother. 2004
Aug;5(8):1701-10.
6. Tilanus AM, de Geus HR, Rijnders BJ, et al; Severe group Astreptococcal toxic shock syndrome presenting as primary
peritonitis: a case report and brief review of the literature. Int J Infect Dis. 2010 Sep;14 Suppl 3:e208-12. doi:
10.1016/j.ijid.2009.07.014. Epub 2009 Nov 13.
7. Marik PE, Lipman J; The definition of septic shock: implications for treatment. Crit Care Resusc. 2007 Mar;9(1):101-3.
8. McKinnon HD Jr, Howard T; Evaluating the febrile patient with a rash. Am Fam Physician. 2000 Aug 15;62(4):804-16.
9. Patel GP, Gurka DP, Balk RA; New treatment strategies for severe sepsis and septic shock. Curr Opin Crit Care. 2003
Oct;9(5):390-6.
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10. British National Formulary
11. Nguyen HB, Rivers EP, Abrahamian FM, et al; Severe sepsis and septic shock: review of the literature and emergency
department management guidelines. Ann Emerg Med. 2006 Jul;48(1):28-54. Epub 2006 May 2.
12. Annane D, Bellissant E, Bollaert PE, et al; Corticosteroids for severe sepsis and septic shock: a systematic review and
meta-analysis. BMJ. 2004 Aug 28;329(7464):480. Epub 2004 Aug 2.
13. Martí-Carvajal AJ et al; Human recombinant activated protein C for severe sepsis and septic shock in adult and paediatric
patients, Cochrane Library, Dec 2012
Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical
conditions. EMIS has used all reasonable care in compiling the information but makes no warranty as to its
accuracy. Consult a doctor or other healthcare professional for diagnosis and treatment of medical conditions.
For details see our conditions.
Original Author:
Dr Sean Kavanagh
Current Version:
Dr Colin Tidy
Peer Reviewer:
Dr Helen Huins
Document ID:
2879 (v22)
Last Checked:
24/11/2014
Next Review:
23/11/2019
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