The Dept of Anaesthesia & Intensive Care, CUHK thanks

for an unrestricted education grant
BASIC instructor/provider course, Hong Kong, July 2nd-4th
Other upcoming courses
Home Feedback Contents

Toxic shock syndrome

Up Anaerobes Aspergillosis Botulism Candidiasis Cholera CMV infection Creutzfeldt Jakob Fever HIV Infection control Leptospirosis Line infection Malaria Meliodosis Meningococcal disease Microbiology Needle stick injury Neutropenic fever PIRO Rickettsia SDD Sepsis management Soft tissue Strongyloidiasis Toxic shock syndrome Tetanus Tuberculosis Viral diseases


Created in October, 2006

by Thomas Li

Staphylococcal toxic shock syndrome

Streptococcal toxic shock syndrome

Staphylococcal toxic shock syndrome

2 types

Menstrual type

It was first described in 1978, occurred in women during menstrual period and associated with use of highly absorbent tampons. Subsequent, sharp decrease in incidence of menstruation related staphylococcal toxic shock syndrome was related to the withdrawal of use of highly absorbent tampons.

Non-menstrual type

  • Postsurgical TSS (may be associated with relatively minor infection without pyrogenic response)
  • Influenza associated TSS (superinfection of Staphylococcus aureus of respiratory tract epithelium damaged by influenza virus)
  • Recalcitrant erythematous desquamating syndrome (occurs in AIDS patients)
  • Associated with contraceptive diaphragm
  • Normal childbirth usually with prior endometritis
  • Burns patients

It can occur after surgical wound infection, postpartum infection, cutaneous, subcutaneous infection or after pulmonary staphyloccal infections.

Pathogenetic mechanisms

Staphylococcus aureus produces exotoxins including toxic shock syndrome toxin-1 (TSST-1), enterotoxins A, C, D, E and H. They act as superantigens which can activate a large number of T cells (with specific b chain variable regions of the T cell antigen receptor) leading to production of massive amount of cytokines including interleukin 1, 2, tumour necrosis factor a,b and interferon-g.

Clinical manifestations and diagnosis

  1. Fever
  2. Hypotension
  3. Rash with diffuse macular erythroderma with subsequent desquamation
  4. Multiorgan dysfunction with 3 of the following:
    1. GI: vomiting and diarrhoea  
    2. Muscle: Myalgia and elevation of serum creatine phosphokinase level
    3. Mucous membrane: Conjunctival, oropharyngeal or vaginal mucosal congestion
    4. Renal dysfunction: elevation of serum creatinine by 2 times of normal
    5. Liver dysfunction: elevation of bilirubin or transaminase by 2 times of ULN
    6. CNS: confusion, change in conscious state
  5. Negative blood or CSF culture except Staphylococcus aureus. Negative serological tests for Rocky Mountain spotted fever, measles, leptospirosis

* Generalized non-pitting oedema is frequently observed (because of capillary leakage and fluid resuscitation), but it is not one of the diagnostic criteria

Management

  1. Resuscitation and organ support therapy (especially aggressive fluid resuscitation)
  2. Source control

    Removal of tampon, nasal pack if any

    Drainage of pus

    Debridement of wound

     

  3. Antibiotic therapy

    Clindamycin IV + cloxacillin IV

     

  4. IV immunoglobulin

Anecdotal experience

No randomized controlled trial to support its use

 

Streptococcal toxic shock syndrome

Usually associated with group A streptococcus infection, but can also be observed in group B or C streptococcus infection

Definition

Streptococcal toxic shock syndrome: Clinical syndrome with any Streptococcal infection (usually invasive Group A streptococci) with acute onset of shock and organ dysfunction.

Pathogenic mechanisms

Exotoxins released from streptococcus acts as superantigens activate the immune system to release massive quantities of inflammatory cytokines with increase in capillary permeability, tissue damage, shock and multiorgan failure

M protein: important virulent factor of Group A Streptococcal infection. It is a filamentous protein attached to bacterial cell membrane conferring antiphagocytic properties

Streptococcal pyrogenic exotoxins A, B and C

Streptococcal superantigens

Epidemiology

Affect persons of all ages

Risk factors

  • Diabetes mellitus

  • Alcohol abuse

  • Prior minor trauma

  • Pregnancy

  • Injuries causing haematoma or muscle injury

  • Prior surgical procedures like Caesarean section, normal vaginal delivery, dermatological procedures

  • Prior varicella infection

  • Prior use of NSAID

Clinical manifestations

  • Abrupt onset of severe diffuse or localized pain - may cause confusion with other clinical entities like AMI, peritonitis. Pain may be out of proportion to the injury

  • Fever or hypothermia, chills

  • GI symptoms: vomiting and diarrhoea

  • Hypotension

  • Diffuse skin rash occurs uncommonly  in only 10% of cases

Complications

  • ARDS

  • Acute renal failure

  • Disseminated intravascular coagulation

Laboratory investigations

  • Leukocytosis may be mild with increase in percentage of immature neutrophils

  • Elevation of serum creatinine

  • Elevation of serum creatine phosphokinase

  • Hypoalbuminaemia

  • Hypocalcaemia

  • Blood culture may be positive (in 60-100% of cases, more often than staphylococcal toxic shock syndrome)

Diagnostic criteria

  1. Isolation of streptococcus from normally sterile site

  2. Hypotension

  3. Two of the followings

    1. Renal impairment (2x elevation of baseline or upper limit of normal)

    2. Coagulopathy and/or thrombocytopenia

    3. Hepatic dysfunction (2x elevation of baseline or upper limit of normal)

    4. ARDS

    5. Erythematous macular rash (may desquamate 1 to 3 weeks later)

    6. Soft tissue necrosis

Differential diagnosis

Management

  1. Resuscitation and organ support therapy

  2. Source control - prompt identification, drainage or debridement of source of streptococcal infection

  3. Antibiotic therapy

    Clindamycin

    1. suppress synthesis of bacterial toxin

    2. facilitate phagocytosis by inhibiting bacterial synthesis of antiphagocytic M protein

    3. suppression of TNF

    4. longer postantibiotic effect

    5. not affected by the stage of growth of bacterial as in beta-lactam

    together with broad spectrum beta lactam such as piperacillin-tazobactam with subsequent de-escalation of antibiotics to high dose penicillin and clindamycin according to subsequent culture and sensitivity result

     

  4. Intravenous immunoglobulin

    1. Neutralization of circulating toxins

    2. Inhibit cytokine production

    3. Case reports and a prematurely terminated randomized placebo controlled trial

 

References

  1. McCormick JK. Toxic shock syndrome and bacterial superantigens: An update. Annual Review of Microbiology. 2001; 55: 77-104.

  2. Herzer CM. Toxic shock syndrome: broadening the differential diagnosis. J Am Board Fam Pract 2001; 14: 131-136

  3. Andrews MM et al. Recurrent nonmenstrual toxic shock syndrome. Clinical diagnosis, diagnosis and treatment. Clin Infect Dis 2001; 32: 1470-1479.

  4. Baxter F, McChesney J. Severe group A streptococcal infection and streptococcal toxic shock syndrome. Can J Anaes 2000; 47:1129

  5. Chuang YY et al. Toxic shock syndrome in children: epidemiology, pathogenesis and treatment. Paediatr Drugs 2005; 7: 11-25.

  6. Darenberg J et al. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: A European randomized, double-blinded, placebo-controlled trial. Clin Inf Dis 2003; 37: 333-340

     

     

     

     

 

 

 

 

 

 

 

 


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
Copyright policy    Contributors