eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Toxic Shock Syndrome

Author: Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Coauthor(s): Vinod K Dhawan, MD, FACP, FRCP(C), Professor, Department of Clinical Medicine, University of California at Los Angeles; Professor of Medicine, Charles R Drew University of Medicine and Science; Chief, Division of Infectious Diseases, MLK-Harbor Hospital
Contributor Information and Disclosures

Updated: Jan 27, 2009

Introduction

Background

Toxic shock syndrome (TSS) is a multisystem disease manifested by sudden onset of fever, chills, hypotension, and rash. Multisystem involvement may cause vomiting, diarrhea, myalgia, mucous membrane hyperemia, mental confusion, renal dysfunction, hepatic abnormalities, and thrombocytopenia. Toxic shock syndrome is caused by toxin-producing strains of staphylococci (staphylococcal toxic shock syndrome) and streptococci (streptococcal toxic shock syndrome). Both causes are discussed in this article. Todd et al first described staphylococcal toxic shock syndrome in 1978.1 The association of toxic shock syndrome with menstruation and tampon use was established in 1980. Cases of toxic shock syndrome caused by streptococci were first reported in the mid 1980s.

Pathophysiology

Staphylococcal toxic shock syndrome is caused by certain toxin-producing strains. Toxic shock syndrome toxin-1 (TSST-1) is implicated in 75% of patients with toxic shock syndrome, enterotoxin B is implicated in 23% of patients with toxic shock syndrome, and enterotoxin C is implicated in 2% of patients with toxic shock syndrome. Evidence implicating Staphylococcus aureus in toxic shock syndrome is as follows:

  • More than 90% of females with menses-associated toxic shock syndrome have vaginal colonization by S aureus, compared with a 10% carriage rate in healthy control subjects.
  • Toxin-producing staphylococci can be recovered in the vast majority of patients with nonmenstrual toxic shock syndrome.
  • Toxic shock syndrome recurs more frequently in the absence of antistaphylococcal therapy.
  • TSST-1 produced by most S aureus strains is detected in patients with toxic shock syndrome using titers of TSST-1 antibodies.

TSST-1 and the enterotoxins are superantigens. They result in nonspecific T-lymphocyte stimulation without normal antigenic recognition. This massive activation of lymphocytes leads to release of cytokines that contribute to the development of toxic shock syndrome.

Use of hyperabsorbent tampons creates conditions conducive to the production of staphylococcal toxic shock syndrome. Tampons increase the vaginal partial pressure of oxygen, stimulating toxin synthesis. They supply surfactants that can increase toxin production. Tampons also bind magnesium and shift the growth kinetics of S aureus to increase toxin production.

Streptococci that produce streptococcal pyrogenic exotoxin A (SPEA) (which has a 50% amino acid homology to staphylococcal enterotoxins B and C) and/or streptococcal pyrogenic exotoxin B (SPEB) cause streptococcal toxic shock syndrome. SPEA-producing organisms are more common in the United States, whereas SPEB-producing streptococci are recovered more frequently from patients with streptococcal toxic shock syndrome in Sweden and the United Kingdom. The predominant streptococcal serotype that produces toxic shock syndrome is M-1 (80% of strains in Sweden), although other serotypes, such as M-2, M-3, M-12, and M-28, may also produce toxic shock syndrome.

SPEs trigger a cascade of inflammatory cytokines, such as tumor necrosis factor-a, interleukin (IL)–2, and IL-6, leading to multiorgan injury and shock. Inflammatory cytokines may also be produced by other streptococcal components, such as peptidoglycan and lipoteichoic acid. Recently, streptococcal superantigen (SSA), a novel pyrogenic exotoxin, was isolated from an M-3 strain.

Most patients with streptococcal toxic shock syndrome do not have any underlying disease. Person-to-person spread of streptococcal toxic shock syndrome has been described.

Frequency

United States

Annual incidence of staphylococcal toxic shock syndrome is 1-5 cases per 100,000 menstruating women. An estimated 77-93% of cases occur in women (41% occur in females aged 13-19 y). Incidence of menstrual toxic shock syndrome has decreased since the discontinuation of hyperabsorbent tampon marketing. Similarly, the mortality rate has declined from 5.6% to 3.3%.

Incidence of streptococcal toxic shock syndrome is 5-10 cases per 100,000 population.

Mortality/Morbidity

The mortality rate in patients with S aureus toxic shock syndrome is approximately 3.3%. The mortality rate in patients with streptococcal toxic shock syndrome is approximately 30%.

Sex

Staphylococcal toxic shock syndrome is more common in females during menstruation. Nonmenstrual toxic shock syndrome is 3 times more common in females than in males. Streptococcal toxic shock syndrome equally affects males and females.

Age

Staphylococcal toxic shock syndrome is common in people aged 15-35 years. More than 90% of cases in women occur in those aged 15-19 years. Streptococcal toxic shock syndrome is seen in all age groups; however, most cases occur in people aged 20-50 years.

Clinical

History

Staphylococcal toxic shock syndrome

Staphylococcal toxic shock syndrome (TSS) is frequently seen in women during menstruation. More recently, with the decline in use of hyperabsorbent tampons, recognition of nonmenstrual toxic shock syndrome has been increasing. Various wounds, many appearing relatively benign, may harbor toxin-producing staphylococci. Thus, herniorrhaphy, mammoplasty, arthroscopy, and other surgical wound infections may be complicated by the development of toxic shock syndrome. Manifestations of toxic shock syndrome usually begin 2 days after surgery.

Onset of staphylococcal toxic shock syndrome is usually abrupt. Symptoms include fever, chills, myalgia, malaise, headache, sore throat, muscle tenderness, fatigue, vomiting, watery diarrhea, and abdominal discomfort. In a review of staphylococcal toxic shock syndrome by Davis and colleagues (1982), clinical findings included the following:2

  • Fever - 100%
  • Erythroderma - 100%
  • Diarrhea - 98%
  • Myalgia - 96%
  • Vomiting - 92%
  • Temperature higher than 40°C - 87%
  • Headache - 77%
  • Sore throat - 75%
  • Conjunctival hyperemia - 57%
  • Decreased sensorium - 40%
  • Vaginal hyperemia - 33%
  • Vaginal discharge - 28%
  • Rigors - 25%

Criteria for the diagnosis of staphylococcal toxic shock syndrome include the following:

  • Temperature higher than 38.9°C
  • Systolic blood pressure lower than 90 mm Hg
  • Rash with subsequent desquamation, especially on the palms and soles
  • Involvement of 3 or more of the following organ systems:
    • GI tract - Vomiting and profuse diarrhea
    • Muscles - Severe myalgia or a greater than 5-fold increase in creatine kinase levels
    • Mucous membranes (vagina, conjunctivae, pharynx) - Frank hyperemia
    • Renal system - BUN or creatinine levels at least twice the upper reference range limit or pyuria in the absence of urinary tract infection
    • Hepatic system - Bilirubin, serum aspartate aminotransferase (AST), or serum alanine aminotransferase (ALT) levels at least twice the upper reference range limit
    • Blood - Thrombocytopenia (platelet count <100,000/mL)
    • CNS - Disorientation without focal neurologic signs
  • Negative results of the serologic tests for Rocky Mountain spotted fever, leptospirosis, and measles when appropriate

Staphylococcal toxic shock syndrome associated with menstruation occurs more frequently in communities without a history of prior antibiotic exposure and is caused primarily by TSST-1–producing organisms. By contrast, nonmenstrual staphylococcal toxic shock syndrome is more common in hospitalized patients who have received prior antibiotic therapy. TSST-1 production is noted in only 50% of the patients. Enterotoxin B and C production is associated with the remainder of nonmenstrual staphylococcal toxic shock syndrome cases.

Streptococcal toxic shock syndrome

Onset is abrupt in patients with streptococcal toxic shock syndrome. An influenzalike syndrome, consisting of fever, chills, myalgia, nausea, vomiting, and diarrhea, may be noted in 20% of patients. Streptococcal toxic shock syndrome is defined by the following criteria:

  • A: Isolation of group A streptococci
    1. From a sterile site, such as blood, cerebrospinal fluid (CSF), pleural fluid, peritoneal fluid, or a tissue biopsy specimen
    2. From a nonsterile body site, such as the throat, vagina, sputum, or superficial skin lesions
  • B: Clinical signs of severity
    1. Hypotension - In adults, systolic blood pressure lower than or equal to 90 mm Hg; in children, systolic blood pressure lower than the fifth percentile for age
    2. Clinical and abnormal laboratory test results (requires 2 or more of the following criteria)
      • Renal impairment - Creatinine levels higher than or equal to 177 mol/L (>2 mg/dL) for adults or 2 or more times the upper reference range value for age; in patients with renal disease, a 2-fold or higher elevation over the baseline level
      • Coagulopathy - Platelet count less than 100 X 109/L (<100,000/μL) or disseminated intravascular coagulation
      • Liver abnormalities - AST, ALT, or total bilirubin levels 2 or more times the upper reference range value for age; in patients with liver disease, a 2-fold or higher elevation over the baseline level
      • Acute respiratory distress syndrome (ARDS) - Defined by (1) acute onset of diffuse pulmonary infiltrates and hypoxemia in the absence of cardiac failure, (2) evidence of diffuse capillary leaking manifested by acute onset of generalized edema, or (3) pleural or peritoneal effusions with hypoalbuminemia
      • Soft tissue necrosis, such as necrotizing fasciitis,3 myositis, or gangrene
      • A generalized erythematous macular rash that may desquamate

The diagnosis of streptococcal toxic shock syndrome is definite when criteria A1, B1, and B2 are met. The diagnosis of streptococcal toxic shock syndrome is probable when criteria A2, B1, and B2 are met.

Physical

  • Staphylococcal toxic shock syndrome: Patients with staphylococcal toxic shock syndrome SS develop rash, hypotension, and hyperemic conjunctival, pharyngeal, and vaginal mucosae. Diffuse erythroderma, cyanosis, and edema of extremities may be noted. Desquamation, especially of the palms and soles, may follow. Alteration in mental status may result in somnolence, agitation, disorientation, and obtundation.
  • Streptococcal toxic shock syndrome: In patients with streptococcal toxic shock syndrome, fever is the most common early sign, although hypothermia may be present in patients with shock. Almost 50% of patients may have normal blood pressure (systolic pressure >110 mm Hg) upon admission but develop hypotension within the subsequent 4 hours. In virtually all patients, shock is apparent at the time of admission or within 4-8 hours. A diffuse scarlatina-like erythema occurs in only 10% of patients.
    • Soft tissue infection occurs in 80% of patients and may progress from localized swelling and erythema to necrotizing fasciitis or myositis in 70% of these patients. Pain is abrupt at onset and is usually preceded by tenderness or other localized physical findings.
    • Non–soft tissue infections occur in 20% of patients and may include endophthalmitis, myositis, perihepatitis, peritonitis, and myocarditis. Confusion (55% of patients), coma, or combativeness may be noted.
  • Features of Staphylococcal and Streptococcal Toxic Shock Syndrome

    Open table in new window

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    Table
    FindingsStaphylococcal Toxic Shock SyndromeStreptococcal Toxic Shock Syndrome
    Age15-35 y20-50 y
    SexMore common in femalesMales and females
    Local invasive diseaseAbsentPresent
    Generalized erythrodermaPresentAbsent
    Nausea, vomiting, or diarrhea>90% of patientsUncommon
    BacteremiaUncommon60% of patients
    Toxins implicatedTSST-1; enterotoxins B and CStreptococcal pyrogenic exotoxins A and B
    Mortality rate3.3%30%
    FindingsStaphylococcal Toxic Shock SyndromeStreptococcal Toxic Shock Syndrome
    Age15-35 y20-50 y
    SexMore common in femalesMales and females
    Local invasive diseaseAbsentPresent
    Generalized erythrodermaPresentAbsent
    Nausea, vomiting, or diarrhea>90% of patientsUncommon
    BacteremiaUncommon60% of patients
    Toxins implicatedTSST-1; enterotoxins B and CStreptococcal pyrogenic exotoxins A and B
    Mortality rate3.3%30%

Causes

Staphylococcal toxic shock syndrome

Staphylococcal toxic shock syndrome is caused by certain toxin-producing strains. TSST-1 is implicated in 75% of patients with staphylococcal toxic shock syndrome, enterotoxin B is implicated in 23% of patients, and enterotoxin C is implicated in 2% of patients with staphylococcal toxic shock syndrome. Staphylococcal toxic shock syndrome has been associated with the following conditions:

  • Menstruation
  • Nonmenstrual conditions
    • Vaginal - Postpartum or following abortion
    • Surgical wounds, such as hernia repair, mammoplasty, and arthroscopy
    • Respiratory infections
    • Varicella infection4
    • Nasal packing

Streptococcal toxic shock syndrome

Streptococcal toxic shock syndrome is caused by one or both of the following toxins:

  • Pyrogenic exotoxin A (common in the United States and has a 50% amino acid homology to staphylococcal enterotoxins B and C)
  • Pyrogenic exotoxin B (common in Sweden and the United Kingdom)

The predominant streptococcal serotype producing toxic shock syndrome is M-1 (80% of strains in Sweden), although other serotypes, such as M-2, M-3, M-12, and M-28, may also produce toxic shock syndrome. Streptococcal toxic shock syndrome has been associated with the following conditions:

  • Skin infections
  • Surgical wounds
  • Pharyngitis5
  • Varicella infection
  • Influenza virus infection
  • Nonsteroidal anti-inflammatory agents: The use of nonsteroidal anti-inflammatory agents has been associated with streptococcal toxic shock syndrome, which is presumably caused by suppressing the early signs of streptococcal infection, thus delaying more specific antibacterial therapy.

More on Toxic Shock Syndrome

Overview: Toxic Shock Syndrome
Differential Diagnoses & Workup: Toxic Shock Syndrome
Treatment & Medication: Toxic Shock Syndrome
Follow-up: Toxic Shock Syndrome
Multimedia: Toxic Shock Syndrome
References
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Further Reading

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Keywords

toxic shock syndrome, TSS, acute respiratory distress syndrome, conjunctival hyperemia, cyanosis, endophthalmitis, erythroderma, hypotension, leptospirosis, measles, menses, menstruation, myocarditis, myositis, perihepatitis, peritoneal effusions, peritonitis, pleural effusions, Rocky Mountain spotted fever, soft tissue necrosis, staphylococcal infection, staphylococcal TSS, Staphylococcus aureus, S aureus, streptococcal infection, streptococcal TSS, Streptococcus pyogenes, S pyogenes, tampon use, TSS toxin-1, TSST-1, vaginal hyperemia

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Contributor Information and Disclosures

Author

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Coauthor(s)

Vinod K Dhawan, MD, FACP, FRCP(C), Professor, Department of Clinical Medicine, University of California at Los Angeles; Professor of Medicine, Charles R Drew University of Medicine and Science; Chief, Division of Infectious Diseases, MLK-Harbor Hospital
Vinod K Dhawan, MD, FACP, FRCP(C) is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada
Disclosure: Pfizer Inc None None

Medical Editor

David Jaimovich, MD, Chief Medical Officer, Joint Commission International and Joint Commission Resources
David Jaimovich, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Larry I Lutwick, MD, Professor of Medicine, State University of New York, Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus
Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

CME Editor

Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine
Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine
Disclosure: Baxter Honoraria Consulting; Pfizer Honoraria Consulting

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

 
 
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