In the early 1980s, TSS was recognized as an illness primarily in women at or within 2 days of their menstrual period and particularly in women using higher-absorbency tampons. However, even at that time cases were being reported in women who were not menstruating and in children and men. With the removal ofthe highest- absorbency tampons from the market, there was an associated drop in the reported incidence ofmenstrual, tamponassociated TSS, though there are still significant numbers of cases. Nearly all cases ofmenstrual TSS in which the site of staphylococcal infection is the cervix or vagina are associated with production of TSST-l. Although not completely clarified, the association oftampon use with TSS may have resulted from introduction of oxygen or in certain cases surfactants on tampons into the vagina. These agents stimulate production ofTSST-1.
As well, limitation of nutrients, such as magnesium, may simulate environmental conditions present in late-logarithmic phase of growth, in which TSST-1 is maximally made. Some tampons bind magnesium and thus may limit its availability to the microbe. Unlike menstrual TSS, the number of cases seen in nonmenstruating women, children, and men has remained constant over the same time period, although there have been changes in the subsets of nonmenstrual TSS. Postsurgical TSS is well-recognized as occurring after nearly any type of surgical procedure. In these cases it may be difficult to identity the source of the infection, since many TSS-associated S. aureus are not pyogenic, in contrast to typical S. aureus, and thus the incision site may heal over and not reveal an important subcutaneous abscess. Fast et al. have proposed that this lack of pyogenic response comes in part from the massive release of tumor necrosis factor-a (TNFa) from macrophages as a result of the superantigenicity. Others have noted the lack of production of highly inflammatory virulence factors by the causative organism, thus allowing the organism to resemble coagulase-negative staphylococci.
Since the early 1980s, two important new categories of nonmenstrual TSS have been recognized, influenza-associated TSS and recalcitrant erythematous desquamating syndrome. Influenza TSS appears to be a consequence of influenza virus damage to the upper respiratory tract and subsequent superinfection by S. aureus ofthe damaged sites. In many cases, these infection sites are not pyogenic and many appear only as very minor infections. Influenza virus infection in the respiratory tract may cause the pH to rise to near neutrality as a result of the buffering capacity ofblood. TSST-1 and staphylococcal exotoxins are made only at pHs near neutrality so would likely be made in the throat only in necrotic centers (formed by the infection) with neutral pH.