Toxic Shock Syndrome

• TSS is a systemic illness caused by infection with toxin-producing strains of S. aureus or less often streptococci.

• Originally described in association with tampon use, TSS now occurs more commonly secondary to a local wound infection.

• TSS is the constellation of fever, rash, hypotension, and multisystem organ involvement (at least three organ systems) and its presentation ranges from mild to fatal disease.

• TSS typically presents with the sudden onset of high fever, muscle aches, vomiting, diarrhea, and headache.

• A diffuse macular erythema or a “scarlatiniform” (i.e., sandpaper-like feel) exanthem with accentuation in flexures develops first on the trunk and quickly spreads to the extremities.

• Other skin features that may be present include erythema and edema of the palms and soles, hyperemia of the conjunctiva and mucous membranes, and “strawberry tongue.”

• Desquamation of the palms and soles may occur 1 to 3 weeks after the onset of illness (Fig. 7.21).

• Hypotensive shock may occur.

• Decreased renal function, prolonged muscle aches, paresthesias, arthralgias, and amenorrhea can occur as a result of TSS.

• Months after recovery some patients may develop Beau lines, nail shedding, or telogen effluvium.

• Diagnosis is made when the characteristic clinical findings of fever, rash, and hypotension are present in patients who have an infection with S. aureus or Strepococcus.

• Blood urea nitrogen, creatinine, liver enzymes, and the white blood cell count may be elevated and thrombocytopenia may be present.

• Gram stain and cultures of vaginal exudate or wounds positive for S. aureus or, rarely, group A streptococci can support the diagnosis.

Staphylococcal Scalded Skin Syndrome (SSSS)

• Staphylococcal scalded skin syndrome (SSSS) is a generalized red, blistering eruption caused by infection with an exfoliative toxin-producing strain of S. aureus and primarily occurs in infants and young children.

• The exfoliative toxin derived from S. aureus spreads from the initial site of infection, usually the nasopharyx or conjunctiva, via the bloodstream.

• The toxin is epidermolytic and cleaves desmoglien 1, an important protein necessary for cell-to-cell adhesion in the granular layer of the epidermis, resulting in blister formation.

• The prodrome consists of fever, irritability, and skin pain.

• Sometimes evidence of the staphylococcal infection in the conjunctiva or nose may be present as conjunctivitis or rhinorrhea.

• The skin eruption begins as diffuse redness of the skin starting on the head and neck (with or without facial swelling) and flexures and becomes generalized over 1 to 2 days (Fig. 7.22).

• Soon thereafter, flaccid bullae develop that easily rupture with minimal pressure leaving behind moist superficial erosions (Fig. 7.23).

• Nikolsky sign, the easy separation of epidermis with minimal lateral pressure, is positive.

• Periorificial crusting and radial fissuring with sparing of the oral mucosa is a characteristic clinical feature.

• Desquamation can last 3 to 5 days, followed by complete healing without scarring.

• The diagnosis of SSSS is generally made clinically.

• Cultures taken from the bullae and erosions on the skin are negative but S. aureus may be cultured from the conjunctiva, nasopharynx, or perianal skin.