Toxic shock syndrome

Toxic shock syndrome
Classification and external resources
Specialty	Infectious disease
ICD-10	A48.3
ICD-9-CM	040.82
DiseasesDB	13187
MedlinePlus	000653
eMedicine	med/2292 emerg/600 derm/425 ped/2269
Patient UK	Toxic shock syndrome
MeSH	D012772
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Toxic shock syndrome (TSS) is a potentially fatal illness caused by a bacterial toxin. Different bacterial toxins may cause toxic shock syndrome. The causative bacteria include Staphylococcus aureus, where TSS is caused by enterotoxin type B or TSST-1, and , where it is caused by streptococcal pyrogenic exotoxins. Streptococcal TSS is sometimes referred to as toxic shock-like syndrome (TSLS) or streptococcal toxic shock syndrome (STSS).

Symptoms of toxic shock syndrome vary depending on the underlying cause. TSS resulting from infection with the bacterium Staphylococcus aureus typically manifests in otherwise healthy individuals via signs and symptoms including high fever, accompanied by low blood pressure, malaise and confusion, which can rapidly progress to stupor, coma, and multiple organ failure. The characteristic rash, often seen early in the course of illness, resembles a sunburn, and can involve any region of the body including the lips, mouth, eyes, palms and soles. In patients who survive the initial phase of the infection, the rash desquamates, or peels off, after 10–14 days.

In contrast, TSS caused by the bacterium , or TSLS, typically presents in people with pre-existing skin infections with the bacteria. These individuals often experience severe pain at the site of the skin infection, followed by rapid progression of symptoms as described above for TSS. In contrast to TSS caused by Staphylococcus, streptococcal TSS less often involves a sunburn-like rash.

For staphylococcal toxic shock syndrome, the diagnosis is based strictly upon CDC criteria defined in 2011, as follows:

Cases are classified as confirmed or probable based on the following:

In both TSS (caused by S. aureus) and TSLS (caused by S. pyogenes), disease progression stems from a superantigen toxin that allows the nonspecific binding of MHC II with T-cell receptors, resulting in polyclonal T-cell activation. In typical T-cell recognition, an antigen is taken up by an antigen-presenting cell, processed, expressed on the cell surface in complex with class II major histocompatibility complex (MHC) in a groove formed by the alpha and beta chains of class II MHC, and recognized by an antigen-specific T-cell receptor.

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