In children the case-fatality rate for influenza TSS appears to be — 90%, with a lower rate in adults. It is likely that infection with other viruses, such as parainfluenza virus, could result in similar TSS. Recalcitrant erythematous desquamating syndrome represents an unrelenting TSS that occurs in AIDS patients. This illness may continue for > 70 days, often resulting in the patient’s death. Recently, there has been a resurgence of severe invasive group A streptococcal infections, including a toxic shocklike syndrome (TSLS). TSLS is defined by hypotension or shock including evidence oftwo or more multiorgan components (renal impairment, coagulopathy, liver involvement, adult respiratory distress syndrome, rash, soft tissue necrosis) and the presence ofgroup A streptococci. If the group A streptococci are isolated from an otherwise sterile body site the patient is considered to have a definite case, whereas if the organism is isolated from a nonsterile body site, the case is considered probable since it cannot be determined with complete certainty that the streptococci were the causative agent rather than simply being carried by the patient.
Risk factors for development of TSLS appear to include the following: chickenpox in children, prior use of nonsteroidal antiinflammatory agents, penetrating and nonpenetrating wounds, and infections of the genital tract in women. Chickenpox results in a transient state of immunosuppression and causes skin lesions that increase susceptibility to infection; both factors are likely to contribute significantly to the increased risk ofTSLS. The reason for the apparent association of TSLS with individuals who use nonsteroidal antiinflammatory agents remains unknown. Infections of the postpartum endometrium occur; also, some evidence suggests that women are more susceptible to scarlet fever during their menstrual periods. Thus, it is possible that hormone changes, combined with changes in mucosal pH that occur during menstruation and postpartum, increase a woman’s susceptibility to TSLS. Several studies have investigated the possible toxin association with development of TSLS. Studies in our laboratory and in collaboration with Musser et al. suggest that the majority of TSLS streptococcal isolates make SPE A or contain the gene, speA, for that toxin, compared with only –15% of streptococci in general. All of the TSLS isolates make SPE B or contain the speB gene, but this is also true ofnon-TSLS streptococci. There has been considerable interest in the potential that SPEB’s close relationship to streptococcal protease may in part account for the large amount of tissue damage seen in many patients. However, TSLS is a very aggressive streptococcal infection and several other factors, including those of host origin, may be contributing. Many studies have found SPE C or speC present in a relatively small number ofcases, but exceptions have been noted. For example, Leggiadro et al. found that 58% of isolates had spec’ and a recent study ofMI isolates from Europe found that most had speC as well as speA.