Toxic Shock Syndrome

Authored by Dr Colin Tidy, 24 Nov 2014

Reviewed by:
Dr Helen Huins, 24 Nov 2014

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Synonyms: TSS, streptococcal toxic shock-like syndrome (STSS), 'toxic strep'

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.

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.

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 is usually nonspecific and patients generally present with flu-like symptoms and can develop a life-threatening 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.
  • 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.

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]
  • 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.

Further reading and references

  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 Jun42(6):2866-9.

  2. Hagiya H, Okita S, Kuroe Y, et al; A fatal case of streptococcal toxic shock syndrome due to Streptococcus dysgalactiae subsp. equisimilis possibly caused by an intramuscular injection. Intern Med. 201352(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 Mar8(3):174-81.

  4. Chuang YY, Huang YC, Lin TY; Toxic shock syndrome in children: epidemiology, pathogenesis, and management. Paediatr Drugs. 20057(1):11-25.

  5. Annane D, Clair B, Salomon J; Managing toxic shock syndrome with antibiotics. Expert Opin Pharmacother. 2004 Aug5(8):1701-10.

  6. Tilanus AM, de Geus HR, Rijnders BJ, et al; Severe group A streptococcal toxic shock syndrome presenting as primary peritonitis: a case report and brief review of the literature. Int J Infect Dis. 2010 Sep14 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 Mar9(1):101-3.

  8. McKinnon HD Jr, Howard T; Evaluating the febrile patient with a rash. Am Fam Physician. 2000 Aug 1562(4):804-16.

  9. Patel GP, Gurka DP, Balk RA; New treatment strategies for severe sepsis and septic shock. Curr Opin Crit Care. 2003 Oct9(5):390-6.

  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 Jul48(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 28329(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

Hi All,  I dont know if anyone has come across this.  I have a worm infestation in my face.  They travel around under the skin leaving tracks and bursting holes into my skin.  they create glass like...

nicolamc
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