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

Streptococcal Toxic Shock Syndrome

Created: 16/5/2007

 

Streptococcal Toxic Shock Syndrome

Dr John Griffiths DICM MRCP FRCA MA
CriticalCareUK Editor


Focus on Group A streptococcal infections

The incidence of Group A streptococcal (GAS) infections has been increasing worldwide since 1987. There is no obvious explanation for this phenomenon but it is probably related to virulence factors in the organism or lack of immunity in the host.

Three important types of infection are recognised:

  • necrotising fasciitis (NF)
  • myositis
  • streptococcal toxic shock syndrome (STSS).
Mortality rates are high, ranging from 20% for NF, 30-80% for STSS and 100% for myositis. Therapy consists of high doses of antibiotic combinations, aggressive surgery and in the case of STSS, intravenous administration of immunoglobulin.


Focus on Group A streptococcal infections

Group A streptococci produce a number of surface components and exo-toxins that make Group A streptococcal infections particularly virulent. These include:

  • M proteins that are expressed on the surface of the bacteria and are thought to confer the ability to resist phagocytosis. Fatal invasive fatal streptococcal infections are associated with expression of M protein types M1 and M3.
  • Superantigens that can activate T-cells without being initially processed by antigen-presenting cells. This results in the stimulation of a much greater proportion of T-cells (40% versus 0.01% of all T-cells) and therefore increased production of the cytokines which mediate STSS. Streptococcal pyrogenic exotoxins A-C, in particular SPE-A, appear to play a major role in severe disease.


Focus on STSS

STSS is well defined in the literature and has been defined using both clinical and laboratory criteria (Table 1). Laboratory findings include: leucocytosis, Gram-stain smears from an aspirate or debrided tissue containing Gram-positive cocci, elevated creatine kinase (in NF/myositis) and bacteraemia.
Adults between the ages of 20-50 years seem to be most commonly affected and tend to have no underlying disease. The acquisition is mainly through the mucous membranes of skin, but in up to 50% of patients no specific portal of entry can be identified. Approximately 50% of patients with STSS have NF. Complications occur frequently with 55% developing ARDS and 80% renal impairment.

Table 1. Diagnostic criteria for streptococcal toxic shock syndrome

Group A streptococcus isolated from a normally sterile site


AND


Hypotension


AND


At least 2 of the following:


renal impairment

coagulopathy

liver abnormality

ARDS

extensive tissue necrosis/necrotising fasciitis

erythematous rash


Focus on Necrotising fasciitis

The most common primary site for NF are the limbs, with the lower limbs affected in 53%, the upper limb in 29%, the trunk in 9%, perineum in 8% and the face in 1%
of cases. NF follows a set sequence of diffuse erythema and swelling associated with exquisite pain. The pain is out of proportion to the clinical findings and can therefore be differentiated from simple cellulitis. As NF progresses, anaesthesia of the overlying skin occurs as a consequence of the thrombosis of small blood vessels and destruction of superficial nerves located in the underlying subcutaneous tissues. This is followed by the appearance of bullae filled with clear fluid and a rapidly evolving frank gangrene.

Non-steroidal anti-inflammatory drugs may predispose to NF by inhibiting granulocyte function, augmenting cytokine production and attenuating the cardinal manifestations of inflammation.


Focus on Treatment

Empirical antibiotic therapy should be started as soon as the disease is suspected, and should have broad spectrum activity against Streptococcus, Clostridium and mixed aerobic-anaerobic organisms which can also cause NF. A combination of penicillin plus a beta-lactamase inhibitor and clindomycin is usually chosen. In animal models, penicillin is less effective against aggressive infections, such as those with a large innoculum, because there is less expression of penicillin-binding proteins in the stationary phase of the bacterial cell cycle. Clindamycin, by contrast, has shown greater efficacy in fulminant infection, because, by inhibiting protein synthesis it is not affected by innoculum size or the stage of bacterial growth. Tetanus toxoid should be considered for patients not up to date with immunization.

Expeditious surgery is vital. The aim of surgery is to remove all necrotic tissues by radical debridement, to preserve as much viable skin as possible and to maintain haemostasis. Amputation may be necessary to remove all non-viable tissues. A “second-look” procedure may be necessary within 12-24 hours to remove all further necrotic and infected tissue that may have been missed, and multiple debridements may be necessary.

Intravenous immunoglobulin (Sandoglobulin) has been shown to be beneficial, and this may be due to its ability to neutralise super-antigens. Patients with lethal infections lack neutralising antibodies to one or several toxins. The current dosage recommended is 2 g/kg daily for 2 days. However, immunoglobulins must not be administered to patients with IgA deficiency and those with circulating anti-IgA antibodies. Side-effects (dizziness, nausea, chills, dyspnoea) are rare and are usually minor. This promising avenue is becoming widely accepted practice in Canada.

Hyperbaric oxygen therapy has been advocated in GAS myositis by analogy with clostridial infection, but this is controversial and should never delay definitive surgery.

Contact prophylaxis
Secondary cases are rare, but have been reported among family members with intimate contact and also among medical personnel caring for patients. The risk of invasive GAS infection among members of the patient's household is nearly two hundred times higher than the risk to the general population. This rate of disease risk and case fatality is estimated to be similar to contacts of patients with sporadic meningococcal infection. Although optimal antibiotic regimens have not yet been formulated, a ten day course of a cephalosporin or a macrolide has been proposed. Large outbreaks in the community have not occurred because the vast majority of the population has acquired immunity to one or more of the streptococcal virulence factors. Nosocomial transmission of GAS to healthcare workers has been documented. Appropriate precautions, including gown, mask, gloves and meticulous hand washing, should be instituted to protect healthcare workers as well as other patients.

Key learning points

  • The incidence of Group A streptococcal (GAS) infections is increasing and they are often associated with high mortality
  • Three important types of GAS infection are recognised: necrotising fasciitis,  myositis and streptococcal toxic shock syndrome

  • Treatment of GAS infection includes appropriate early, empirical intravenous antibiotic therapy and expeditious surgery
  • Severe cases of Streptococcal toxic shock syndrome with necrotising fascitis may respond to intravenous immunoglobulin in addition to standard management

Key references

Baxter F, McChesney J.
Severe Group A streptococcal infection and streptococcal toxic shock syndrome (Review).
Can J Anaesth 2000; 47: 1129-1140.

Leitch H, Palepu A, Fernandes C.
Necrotising fasciitis secondary to Group A streptococcus. Morbidity and mortality still high (Review).
Can Fam Phys 2000; 46: 1460-1466

Perez C, Kubak B, Cryer H et al.
Adjunctive treatment of streptococcal toxic shock syndrome using intravenous immunoglobulin: case report and review.
Am J Med 1997; 102: 111-113

Shupak A, Shoshani O, Goldenberg I et al.
Necrotising fasciitis: an indication for hyperbaric oxygen therapy?
Surgery 1995; 118: 873-878

Weiss K, Laverdiere M.
Group A streptococcus invasive infections (Review).
Can J Surg 1997; 40: 18-25.


ArticleDate:20070516
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