This acute febrile illness with severe multisystem derangement has a case-fatality rate of 10 to 15 percent. Fever, headache, mental confusion, difuse macular erythematous rash, subcutaneous edema, nausea, vomiting, watery diarrhea, and marked hemoconcentration are usual findings. Renal failure followed by hepatic failure, disseminated intravascular coagulopathy, and circulatory collapse may follow in rapid sequence. During recovery, the rash-covered areas undergo desquamation. For some time, Staphylococcus aureus was recovered from almost all aHicted persons. Specifically, a staphylococcal exotoxin, termed toxic shock syndrome toxin-l (TSST-l), was found to cause the clinical manifestations by provoking profound endothelial injury. A very small amount ofTSST-1 has been shown to activate T cells to create a "cytokine storm" as described by Que (2005) and Heying (2007) and their coworkers.
During the 1990s, sporadic reports of virulent group A 3-hemolytic streptococcal infection began to appear (Anderson, 2014). Heavy colonization or infection is complicated in some cases by streptococcal toxic shock syndrome, which is produced when pyrogenic exotoxin is elaborated. Serotypes MI and M3 are particularly virulent (Beres, 2004; Okumura, 2004). Finally, almost identical indings of toxic shock were reported by Robbie and associates (2000) in women with Clos tridium sordellii colonization.
Thus, in some cases of toxic shock syndrome, infection is not apparent and colonization of a mucosal surface is the pre sumed source. At least 10 to 20 percent of pregnant women have vaginal colonization with S aureus. And Clostridium petingens and sordellii are cultured from 3 to 10 percent of asymptomatic women (Chong, 2016). Thus, it is not surprising that the disease develops in postpartum women when growth of vaginal bacteria is luxuriant (Chen, 2006; Guerinot, 1982).
Delayed diagnosis and treatment may be associated with maternal mortality (Schummer, 2002). Crum and colleagues shock syndrome. Principal therapy is supportive, while allow ing reversal of capillary endothelial injury. Ant�microbial ther apy that includes staphylococcal and streptococcal coverage is given. With evidence of pelvic infection, antimicrobial therapy must also include agents used for polymicrobial infections.
Women with these infections may require extensive wound debridement and possibly hysterectomy. Because the toxin is so potent, the mortality rate is correspondingly high (Hotch kiss, 2003).