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Toxic shock syndrome is caused by infection with the bacteria Staphylococcus aureus. The exotoxins produced by the bacteria cause the individual to experience the characteristic symptoms of the syndrome, such as shock and fever.
The initial stage of the pathogenesis of toxic shock syndrome involves the colonization of the bacteria Staphylococcus aureus. It is not clearly understood how this occurs in all cases of the syndrome, however in some high-risk population groups the cause is more obvious.
For example, menstruating women who use tampons are more likely to suffer from toxic shock syndrome, particularly if they leave the tampon in for an extended period of time. This is likely to be a result of the tampon contain absorbed menstrual fluid is an optimal breeding ground for the bacteria to grow.
When the bacterial infection is established, the production of exotoxins may begin causing the syndrome to become problematic.
There are several possible exotoxins that may be responsible for causing toxic shock syndrome, including:
The vast majority of cases of toxic shock syndrome are associated with the exotoxin toxic shock syndrome toxin type-1 (TSST-1), which account for nearly all cases of menstrual women and half of other cases. Staphylococcal enterotoxin B also commonly causes the syndrome and is the second most common exotoxin involved.
Approximately three-quarters of all patients develop antibodies against TSST-1 by adolescence and the vast majority has antibody protection by adulthood, which affects the likelihood of being affected by the syndrome.
In addition to the immunity of the individual against the presenting toxins, there are several other factors that affect the clinical expression and, therefore, severity of the syndrome. The levels of pH, glucose and magnesium in the blood all have an effect on the individual’s ability to mediate the toxins, as well as age.
When the exotoxins are produced as a result of infection with Staphylococcus aureus, they can be absorbed into the systemic circulation to cause significant effects in individuals that do not possess sufficient antitoxin antibodies to offer protection.
Although the specific mediators of the exotoxins are not known with certainty, it is likely that cytokines including interleukin 1 (IL-1) and tumor necrosis factor (TNF) are involved.
The exotoxins stimulate a response from the T-cells in the body and affect their ability to bind to receptors and class II major histocompatibility complex of antigen presenting cells. As a result, the T-cells proliferate extensively in the body, leading to symptoms of shock and tissue destruction.
Additionally, polyclonal immunoglobulin production is inhibited by the production of interferon-gamma. This reduces the patient’s ability to develop antibodies for the toxins and explains why some patients experience a relapse of toxic shock syndrome.