Search our site 
 
Advanced Search
 
Home | News | Exam dates | Contact us | About us | Testimonials |
 
 

map
You are in Home >> Intensive Care >> Sepsis >> Pathophysiology >> Pathophysiology: Articles

Staphylococcal Toxic Shock Syndrome

Created: 25/9/2007
Updated: 10/10/2007

 

Staphylococcal Toxic Shock Syndrome

Dr Andrew Walden MRCP PhD
SpR in ICU medicine, John Radcliffe hospital, Oxford

Focus on Staphylococcus aureus

Staphylococcus aureus is a gram-positive bacterium that is an immobile coccus able to grow in both aerobic and anaerobic media and which forms grape like clusters. It is commonly found on the skin and nasal mucous membranes of humans and is capable of causing a wide range of disease from mild skin infections to life threatening pneumonia, septic shock and bacterial endocarditis.

Staphylococcus aureus is capable of generating a large array of exotoxins and the clinical syndrome of toxic shock (TSS) has been well documented since the late 1970s. Menstrual TSS has been on the decline over the past 20 years following an aggressive advertising campaign however the incidence of non-menstrual TSS has remained the same. Non-menstrual TSS has been described in respiratory tract infections, skin and soft tissue infections, bone infections and after numerous operations. The incidence remains around 1:100,000

    The essential features of TSS are:

  • Fever
  • Scarlitiform rash
  • Cardiovascular collapse

Focus on Pathophysiology of TSS

TSS is mediated by a superantigen which can cross mucosal membranes into the bloodstream. Superantigens are a group of viral and bacterial protein toxins that exhibit potent polyclonal lymphocyte transforming properties to CD4 and CD8 positive T-lymphocytes. For standard antigens the process of presentation to T-cells involves degradation in antigen presenting cells to form peptides which are combined with major histocompatability complex (MHC) molecules. These are then expressed on the APC cell surface and are ‘recognised’ by a groove formed by the variable domains of the T-cell receptor (TcR) (Fig 1). As such each epitope presented with MHC molecules is destined to be recognised by a specific TcR structure. The response therefore is limited to the range of 1-100 T-cells per million.




Superantigens bind to the non-variable regions of the MHC molecules and subsequently bind to the vb variable domain of the TcR with little or no involvement of other regions of the TcR (Fig 1). In concentrations in the nano- to pico- ranges superantigens are capable of stimulating up to 30% of the T-cell population. The close proximity of APC’s and T-cells coupled with the large population of stimulated T-cells results in a massive and unchecked release of inflammatory cytokines. T-cell release of cytokines augments the release of monokines from the APC’s and vice versa resulting in an overwhelming inflammatory response in the host with the clinical manifestation of severe cardiovascular collapse and multiple organ failure.

Focus on the treatment of TSS

    Treatment of TSS involves:

  • Prompt antibiotic administration
  • Source control
  • Organ support

Antibiotic Therapy
There is no evidence base as to the correct antibiotic regimen. However, if the clinical syndrome is suspected then prompt administration of antibiotics is life-saving. To date the recommendation is to use a b-lactamase-resistant anti-staphylococcal agent and clindamycin to reduce the synthesis of TSST-1. The emergence of toxin producing MRSA has clear implications in the empirical treatment of this disorder and the use of Vancomycin should be considered in high risk patients.

Source control
Source control can be difficult since this infection does not have to be associated with a large collection. Clearly in female patients a full vaginal examination should be performed and tampons removed. Where appropriate in post-surgical patients wounds may need to be re-explored.

Organ Support
Organ support in the face of TSS is often required. Pressor and inotropic support may be essential and multi-organ failure may ensue with prolonged intensive care stay.

The outcome from staphylococcal toxic shock syndrome is good with mortality rates around 5% this compares favourably with streptococcal toxic shock where mortality rates can be as high as 50%.

Key Learning Points

  • Staphylococcal TSS presents with a triad of fever, scarlitiform rash and cardiovascular collapse
  • Prompt treatment with antibiotics is essential
  • Clindamycin should be given to offset the effects of the toxin
  • The outcome is good with prompt and appropriate treatment

Key references

Muller-Alouf H, Carnoy C, Simonet M, Alouf J.
Superantigen bacterial toxins: state of the art.
Toxicon 2001; 39:1691-1701.

Isaac NC, Thompson RL.
Staphylococcal toxic shock sundrome.
Postgrad Med 2001; 110:55-62.

Murray RJ.
Recognition and management of staphylococcus aureus toxin-mediated disease.
Intern Med J 2005; 35:S106-S119

Hajjeh RA, Reingold A, Weil A, Shutt K, Schuchat A, Perkins BA.
Toxic shock syndrome in the united states: surveillance update, 1979-1996.
Emerg Infect Dis 1999; 5:807-10


ArticleDate:20070925
SiteSection: Article
 
   
    
                                            
  Posting rules

     To view or add comments you must be a registered user and login  




Login Status  

You are not currently logged in.
UK/Ireland Registration
Overseas Registration

  Forgot your password?








 
All rights reserved © 2016. Designed by AnaesthesiaUK.

{Site map} {Site disclaimer} {Privacy Policy} {Terms and conditions}

 Like us on Facebook 

vp