Toxic shock syndrome (TSS) is caused by exotoxin-producing cocci. Strains of phage-group 1 Staphylococcus aureus elaborate the TSS toxin-1 (TSST-1) or related exotoxins; certain strains of Streptococcus pyogenes produce at least 2 exotoxins.
At highest risk of staphylococcal TSS are
Mechanical or chemical factors related to tampon use probably enhance production of the exotoxin or facilitate its entry into the bloodstream through a mucosal break or via the uterus. Estimates suggest about 3 cases/100,000 menstruating women still occur, and cases are still reported in women who do not use tampons and in women who have infection after childbirth, abortion, or surgery. About 15% of cases occur postpartum or as a complication of postoperative staphylococcal wound infections that appear insignificant. Cases have also been reported in both men and women with any type of S. aureus infection.
Mortality from staphylococcal TSS is < 3%. Recurrences are common among women who continue to use tampons during the first 4 months after an episode.
Streptococcal TSS is similar to that caused by S. aureus, but mortality is higher (20 to 60%) despite aggressive therapy. In addition, about 50% of patients have S. pyogenes bacteremia, and 50% have necrotizing fasciitis (neither is common with staphylococcal TSS). Patients are usually otherwise healthy children or adults.
Primary infections in skin and soft tissue are more common than in other sites. In contrast to staphylococcal TSS, streptococcal TSS is more likely to cause acute respiratory distress syndrome (ARDS) and less likely to cause a typical cutaneous reaction.
S. pyogenes TSS is defined as any group A beta-hemolytic streptococci (GABHS) infection associated with shock and organ failure.
Risk factors for GABHS TSS include
Onset of toxic shock syndrome is sudden, with
Staphylococcal TSS is likely to cause vomiting, diarrhea, myalgia, elevated creatine kinase, mucositis, hepatic damage, thrombocytopenia, and confusion. The staphylococcal TSS rash is more likely to desquamate, particularly on the palms and soles, between 3 and 7 days after onset.
Streptococcal TSS commonly causes acute respiratory distress syndrome (in about 55% of patients), coagulopathy, and hepatic damage and is more likely to cause fever, malaise, and severe pain at the site of a soft-tissue infection.
Renal impairment is frequent and common to both. The syndrome may progress within 48 hours to syncope, shock, and death. Less severe cases of staphylococcal TSS are fairly common.
Diagnosis of toxic shock syndrome (TSS) is made clinically and by isolating the organism from blood cultures (for Streptococcus) or from the local site.
TSS resembles Kawasaki disease, but Kawasaki disease usually occurs in children < 5 years of age and does not cause shock, azotemia, or thrombocytopenia; the rash is maculopapular. Other disorders to be considered are scarlet fever, Reye syndrome, staphylococcal scalded skin syndrome, meningococcemia, Rocky Mountain spotted fever, leptospirosis, and viral exanthematous diseases. These disorders are ruled out by specific clinical differences, cultures, and serologic tests.
Specimens for culture should be taken from any lesions, the nose (for staphylococci), throat (for streptococci), vagina (for both), and blood.
MRI or CT of soft tissue is helpful in localizing sites of infection.
Continuous monitoring of renal, hepatic, bone marrow, and cardiopulmonary function is necessary.
Patients suspected of having TSS should be hospitalized immediately and treated intensively. Tampons, diaphragms, and other foreign bodies should be removed at once.
Suspected primary sites should be decontaminated thoroughly. Decontamination includes
Fluids and electrolytes are replaced to prevent or treat hypovolemia, hypotension, and shock. Because fluid loss into tissues can occur throughout the body (because of systemic capillary leak syndrome and hypoalbuminemia), shock may be profound and resistant. Aggressive fluid resuscitation and circulatory, ventilatory, and/or hemodialysis support are sometimes required.
Obvious infections should be treated with antibiotics (for indications and doses, see Table: Antibiotic Treatment of Staphylococcal Infections in Adults). Pending culture results, clindamycin or linezolid (to suppress toxin production) plus vancomycin, daptomycin, linezolid, or ceftaroline—empiric choices that cover the most likely etiologic organisms—should be used. If a pathogen is isolated on culture, the antibiotic regimen is adjusted as needed, as for the following:
Antibiotics given during the acute illness may eradicate pathogen foci and prevent recurrences. Passive immunization to TSS toxins with IV immune globulin (2 g/kg, followed by 0.4 g/kg daily for up to 5 days) has been helpful in severe cases of both types of TSS and lasts for weeks, but the disease may not induce active immunity, so recurrences are possible.
If a test for seroconversion of the serum antibody responses to TSST-1 in acute- and convalescent-phase paired sera is negative, women who have had staphylococcal TSS should probably refrain from using tampons and cervical caps, plugs, and diaphragms. Advising all women, regardless of TSST-1 antibody status, to change tampons frequently or use napkins instead and to avoid hyperabsorbent tampons seems prudent.
Toxic shock syndrome (TSS) is caused by exotoxin-producing strains of Staphylococcus aureus and Streptococcus pyogenes.
Although classically described as occurring with tampon use, TSS may occur after many staphylococcal or streptococcal soft-tissue infections.
Onset of symptoms is sudden; symptoms include high fever, hypotension (which can be refractory), diffuse erythematous rash, and multiple organ dysfunction.
Provide aggressive supportive care, and decontaminate and/or debride the source site.
Give antibiotics (eg, clindamycin plus vancomycin or daptomycin) pending culture and susceptibility testing.
Give IV immune globulin if TSS is severe.