Pathophysiology

ETIOLOGY AND PATHOGENESIS Most cases of TSS have been directly associated with colonization or infection with S. aureus. An exotoxin, toxic shock syndrome toxin (TSST-1) has been implicated as a significant factor in the production of symptoms associated with TSS, either through direct toxic effects on the host or through stimulation of secondary mediators in response to TSST-1. The biologic properties of TSST-1 include the ability to (1) induce fever directly on the hypothalamus or indirectly via interleukin 1 (IL-1) and tumor necrosis factor (TNF) production, (2) promote T-lymphocyte "superantigenization" and overstimulation, (3) induce interferon production, (4) enhance delayed hypersensitivity, (5) suppress neutrophil migration and immunoglobulin secretion, and (6) enhance host susceptibility to endotoxins.

Ninety percent of menstrual-related cases of TSS (MRTSS) are caused by S. aureus strains that produce TSST-1, which is present in less than half of nonmenstrual-related TSS (NMTSS) cases. Enterotoxins B and C have been identified from isolates of NMTSS and have a biochemical structure almost identical to that of TSST-1. This explains the similarity in clinical manifestations of MRTSS and NMTSS. NMTSS may be mediated by unidentified precursors and toxins or by-products of TSST-1.3

The amount of TSST-1 produced by toxigenic strains of S. aureus in MRTSS is enhanced by certain vaginal conditions: temperature of 39 to 40°C (102.2 to 104°F), a neutral pH, a Po2 of greater than 5 percent, and supplemental C02. These conditions can be met with the change in vaginal pH from acidic to neutral during menses and an increase in 02 and C02 content of the vagina with the introduction of tampons or intravaginal devices. Other influences include synthetic fibers in tampon composition and a synergistic relationship between S. aureus and Escherichia coli.4

The most impressive aspect of the pathophysiology is the massive vasodilatation and rapid movement of the serum proteins and fluids from the intravascular to the extravascular space. Hypotension is accounted for by (1) decreased vasomotor tone, causing pooling of blood in the periphery and therein decreased central venous pressure and pulmonary capillary wedge pressure; (2) nonhydrostatic leakage of fluid into the interstitium, causing decreased intravascular volume and generalized nonpitting edema, primarily of the head and neck; (3) depressed cardiac function, including decreased wall motion and decreased shortening fraction; and (4) total body-water deficits secondary to vomiting, diarrhea, and fever.

Hypoalbuminemia, hypoferrinemia, and proteolysis caused by IL-1 are consistent with the peripheral edema, anemia, and rhabdomyolysis seen in TSS. TNF induces profound acidosis, shock, and multisystem organ failure in animal models similar to the effects of TSS. The multisystem organ failure may be a reflection of either a direct effect of the toxin on tissues or the rapid onset of hypotension and decreased perfusion.

The immunologic status of an individual plays a role in the pathogenesis of TSS, especially in cases of recurrence. Low convalescent titers to TSST-1 and enterotoxins B and C are found in the majority of patients with TSS for up to 1 year after infection.3

EPIDEMIOLOGY CDC surveillance of TSS from 1979 through 1996 reported 5296 definite and probable cases ( Fig, 138-1). From 1981 through 1987, there was a dramatic decrease in the number of reported cases. In 1992, only 44 definite cases, 51 probable cases, and 3 deaths occurred from TSS. Of the 44 definite cases, 20 occurred during menstruation. The decrease in cases is presumably due to changes in the composition of tampons, general public awareness of the risks of tampon use, and increased medical awareness and detection. Although the use of contraceptive sponges and diaphragms places the individual at risk, their exact contribution to the development of TSS is unclear.

TSS was initially a disease of young, healthy, menstruating women; 50 percent of cases reported in 1986 and 1987 were found in this group. Tampon use increased the risk of TSS in susceptible females by 33 times. S. aureus has been isolated from the vaginas of 98 percent of women with TSS, compared to an 8 to 10 percent carrier rate in control subjects. It is presumed that women who develop menstrual TSS are colonized with S. aureus before the onset of menstruation.

The proportion of NMTSS cases has increased since 1980 (59 percent), primarily because of the decrease in the number of menstruation-related cases. The absolute number of cases of NMTSS has remained relatively constant, however. Nearly 25 percent of NMTSS cases are associated with postpartum and S. aureus vaginal infections.5 There is an increasing incidence of NMTSS in males. Men constitute one-third of patients with TSS, with a mortality rate 3.3 times that of MRTSS in women. A 50 percent mortality rate has been reported in non-TSST-1 S. aureus infections (i.e., enterotoxin B or C), while a 10 percent rate has been reported in TSST-1-producing S. aureus infections.

The means by which S. aureus enters the host in TSS are numerous and have been well documented in a wide variety of clinical settings. TSS has also been reported following influenza and influenza-like illnesses and is associated with a significant mortality rate (43 percent). Nasal packing (nasal tampons) is also associated with TSS, with 20 to 40 percent of the adult population carrying S. aureus in the nasal vestibule.

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