How?
How does TSS Occur?
The pathogenesis of TSS proceeds as follows: (1) human colonisation or infection by a strain of S. aureus capable of producing a TSS toxin ("toxigenic strain"), (2) toxin production, (3) toxin absorption, and (4) intoxication.
The cross-sectional carriage rate of S. aureus is 15-40 percent. The anterior nasopharynx is the principal site of carriage; others include the axillae, vagina, and perineum. Among normal postmenarcheal European women, the rate of vaginal colonisation is 5-20 percent and is greatest during the menses. Tampon use does not influence that rate, nor do tampons enhance vaginal staphylococcal growth. About 25 percent of all S. aureus strains are toxigenic. Roughly 4-10 percent of normal people harbour toxigenic strains at any given time.
Although toxigenic strains have the genetic potential to produce toxins, they actually do so only at limited times, times when toxin production serves the bacterium’s survival needs. The exact nature of the environmental signals that cue the bacterium to produce toxin in vivo are not fully understood. Even less is known about the requirements and mechanisms for toxin uptake, but circulating toxin can be demonstrated in human TSS patients.
Intoxication by the TSS toxins is a very complex process. The toxins affect the host immune system, causing an exuberant and pathological host inflammatory response. Antibodies directed at the TSS toxins protect against TSS, these are thought to have developed by early adolescence in the majority of people. Interestingly, TSS is often not immunising; recurrent menstrual TSS is well-described.
