Toxic Shock Syndrome (TSS)

Onset of toxic shock syndrome is sudden, with (1):

• Fever (39 to 40.5° C, which remains elevated)

• Hypotension (systolic blood pressure < 90 mm Hg for adults or less than the fifth percentile for age in children; it can be refractory)

• A diffuse macular erythroderma (especially on the palms and soles, 1 to 2 weeks after onset)

• Involvement of at least 3 other organ systems (eg, gastrointestinal, muscular, mucous membrane, renal, hepatic, hematologic, central nervous system)

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, coagulopathy, and hepatic damage and is more likely to cause high fever, malaise, tachycardia, tachypnea, and severe pain at the site of a soft-tissue infection (2).

Renal impairment is frequent and common in both types of TSS.

Although less severe cases of staphylococcal TSS are fairly common, severe cases of TSS may progress within 48 hours to syncope, tissue necrosis, shock, disseminated coagulation, multisystem organ failure, and death.

Staphylococcal Toxic Shock Syndrome

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Staphylococcal toxic shock syndrome causes a diffuse erythematous rash. Later in the course of the disease, the rash desquamates, especially on the palms and soles.

Image courtesy of the Public Health Image Library of the Centers for Disease Control and Prevention.

• Primarily history and physical examination

• Cultures

• Sometimes imaging (MRI, CT)

• Sometimes adjunctive measurement of anti-TSST-1 antibody

Diagnosis of toxic shock syndrome (TSS) is made clinically and by isolating the organism from blood cultures (for Streptococcus) or from the local site.

Specimens for culture should be taken from any lesions, the nose (for staphylococci), throat (for streptococci), vagina (for both), and blood. Microbiological confirmation is not required for diagnosis, as blood cultures are often negative, but isolation of either organism from a relevant site supports the diagnosis.

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.

Measuring anti-TSST-1 antibody levels for seroconversion after infection may help guide vaccine development efforts and ultimately prevent recurrence (1).

• Local measures (decontamination of infected sites, including debridement and irrigation)

• Fluid resuscitation and circulatory support

• Empiric antibiotic therapy (eg, beta-lactams or vancomycin, daptomycin, or ceftaroline (if MRSA proven or suspected) plus protein inhibitors (clindamycin or linezolid) pending culture resultsEmpiric antibiotic therapy (eg, beta-lactams or vancomycin, daptomycin, or ceftaroline (if MRSA proven or suspected) plus protein inhibitors (clindamycin or linezolid) pending culture results

• Adjunctive treatment with IV immune globulin (IVIG)

Patients suspected of having TSS should be hospitalized immediately and treated intensively. Tampons, diaphragms, and other foreign bodies suspected to be contributing to the infection should be removed at once.

Suspected primary sites should be decontaminated thoroughly. Decontamination includes:

• Reinspection and irrigation of surgical wounds, even if they appear healthy

• Repeated debridement of devitalized tissues

• Irrigation with normal saline of potential naturally colonized sites (sinuses, vagina)

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), subsequent 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. Pending culture results, clindamycin or linezolid (to suppress toxin production) plus vancomycin, daptomycin, Obvious infections should be treated with antibiotics. Pending culture results, clindamycin or linezolid (to suppress toxin production) plus vancomycin, daptomycin,linezolid (if clindamycin used), or ceftaroline should be used; these antibiotics are empiric choices that cover the most likely etiologic organisms. If a pathogen is isolated on culture, the antibiotic regimen is adjusted as needed, as for the following:used), or ceftaroline should be used; these antibiotics are empiric choices that cover the most likely etiologic organisms. If a pathogen is isolated on culture, the antibiotic regimen is adjusted as needed, as for the following:

• For group A streptococci: Clindamycin or linezolid plus a beta-lactamFor group A streptococci: Clindamycin or linezolid plus a beta-lactam

• For methicillin-susceptible S. aureus (MSSA): Clindamycin plus oxacillin or nafcillin(MSSA): Clindamycin plus oxacillin or nafcillin

• For methicillin-resistant Staphylococcus aureus (MRSA): Vancomycin or daptomycin plus clindamycin or linezolid, depending on the susceptibility(MRSA): Vancomycin or daptomycin plus clindamycin or linezolid, depending on the susceptibility

Antibiotics given during the acute illness may eradicate pathogen foci and prevent recurrences. Passive immunization to TSS toxins with IVIG 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. It may reduce mortality from staphylococcal TSS, especially when coadministered with clindamycin (Antibiotics given during the acute illness may eradicate pathogen foci and prevent recurrences. Passive immunization to TSS toxins with IVIG 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. It may reduce mortality from staphylococcal TSS, especially when coadministered with clindamycin (1).

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 may have a genetically higher risk of TSS due to associations with HLA class II genes (2). Such women (with higher genetic risks and negative seroconversion) should refrain from using tampons and menstrual cups, cervical caps, contraceptive sponges, intrauterine devices, diaphragms, and pessaries. Advising all women, regardless of TSST-1 antibody status, to change tampons or other vaginally inserted materials frequently or use napkins instead and to avoid hyperabsorbent tampons seems prudent.

In cases of S. aureus nasal carriage, topical mupirocin may be used. In cases of extra-nasal colonization, bathing with additional chlorhexidine antiseptic for 1 week is warranted.nasal carriage, topical mupirocin may be used. In cases of extra-nasal colonization, bathing with additional chlorhexidine antiseptic for 1 week is warranted.