Toxic shock syndrome pathophysiology

Jump to navigation Jump to search

Toxic shock syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Toxic Shock Syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Toxic shock syndrome pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Toxic shock syndrome pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Toxic shock syndrome pathophysiology

CDC on Toxic shock syndrome pathophysiology

Toxic shock syndrome pathophysiology in the news

Blogs on Toxic shock syndrome pathophysiology

Directions to Hospitals Treating Toxic shock syndrome

Risk calculators and risk factors for Toxic shock syndrome pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

In both TSS (caused by S. aureus) and TSLS (caused by S. pyogenes), disease progression stems from a superantigen toxin that allows the non-specific binding of MHC II with T cell receptors, resulting in polyclonal T-cell activation.

Usually exotoxin producing strains of Staphylococcus aureus, a bacterium. S. aureus commonly colonizes skin and mucous membranes in humans. TSS has been associated with use of tampons and intravaginal contraceptive devices in women and occurs as a complication of skin abscesses or surgery. http://www.cdc.gov/ncidod/dbmd/diseaseinfo/toxicshock_t.htm

This infection can occur via the skin (e.g. cuts, surgery, burns), vagina (via tampon), or pharynx. However, most of the large number of individuals who are exposed to or colonized with toxin-producing strains of S. aureus or S. pyogenes do not develop toxic shock syndrome. One reason is that a large fraction of the population has protective antibodies against the toxins that cause TSS.[1] It is not clear why the antibodies are present in people who have never had the disease.

Toxin production by S. aureus requires a protein-rich environment, which is provided by the flow of menstrual blood, a neutral vaginal pH, which occurs during menstruation, and elevated oxygen levels, which is provided by the tampon that is inserted into the normally anaerobic vaginal environment.[2] Although ulcerations have been reported in women using super absorbent tampons, the link to menstrual TSS, if any, is unclear. The toxin implicated in menstrual TSS is capable of entering the bloodstream by crossing the vaginal wall in the absence of ulcerations.[3] Women may avoid problems by choosing a tampon with the minimum absorbency needed to control menstrual flow and using tampons only during active menstruation. Alternately, a woman may choose to use a different kind of menstrual product that may eliminate or reduce the risk of TSS, such as sanitary napkins or a menstrual cup.

References

  1. McCormick J, Yarwood J, Schlievert P. "Toxic shock syndrome and bacterial superantigens: an update". Annu Rev Microbiol. 55: 77–104. PMID 11544350.
  2. McCormick J, Yarwood J, Schlievert P. "Toxic shock syndrome and bacterial superantigens: an update". Annu Rev Microbiol. 55: 77–104. PMID 11544350.
  3. Schlievert P, Jablonski L, Roggiani M, Sadler I, Callantine S, Mitchell D, Ohlendorf D, Bohach G (2000). "Pyrogenic toxin superantigen site specificity in toxic shock syndrome and food poisoning in animals". Infect Immun. 68 (6): 3630–4. PMID 10816521.


Template:WikiDoc Sources