Toxic shock syndrome in Adult
- Erythema of the palms and soles that desquamates 1-3 weeks after the initial onset
- Diffuse scarlatiniform exanthem that begins on the trunk and spreads toward the extremities
- Erythema of the mucous membranes (strawberry tongue and conjunctival hyperemia)
Staphylococcal TSS is caused by S. aureus strains that can produce the toxic shock syndrome toxin-1 (TSST-1). TSST-1 is believed to cause disease via direct effects on end organs, impairing clearance of gut flora derived endotoxins, with TSST-1 acting as a superantigen leading to massive nonspecific activation of T-cells and subsequent inflammation and vascular leakage. In this form of TSS, risk factors include lack of an antibody to TSST-1, surgical packing, abscesses, surgical mesh, and tampon use. A late 1980s study showed a lower rate of tampon usage among African American and Mexican American women compared to white women, and while this may help explain the lower incidence of TSS in African American women, the authors did not believe the findings were sufficient to explain the discrepancy entirely. They hypothesized that perhaps the erythema of TSS is more difficult to see on darker skin phototypes, thus resulting in clinicians failing to recognize or report TSS because they failed to recognize one of the criteria for diagnosis.
Streptococcal TSS is also caused by exotoxins that cause massive stimulation of T-cells via a superantigen mechanism. Clinically, the most common presenting symptom is severe pain in an extremity with or without underlying soft tissue infection. A prodrome of fever, diarrhea, and myalgias is often seen. The macular exanthem seen in staphylococcal TSS is much less commonly found in streptococcal TSS. Approximately 48-72 hours after the initial onset, shock and multiorgan failure follow. In this form of TSS, risk factors include varicella infection, bites, and lacerations.
Epidemiological studies from 2000-2004 in the United States show the incidence of invasive group A Streptococcus infections, such as streptococcal TSS, are higher among African Americans than other groups. The case fatality rate, however, was not different between groups.
Interestingly, there is an emerging pathogen, Streptococcus suis, which can be transmitted from pigs to humans and has been responsible for several large outbreaks of disease, including toxic shock syndrome, in Asia, specifically Thailand and China. The consumption of raw or undercooked pork is the number one risk factor. In one Thai study, 23% of patients with positive cultures developed TSS, and the mortality rate from infection with certain serotypes of S. suis has proven to be exceptionally high. Thus, this new pathogen has been cause of great concern worldwide.
All forms of TSS can result in confusion and coma, renal impairment, liver impairment, adult respiratory distress syndrome, and disseminated intravascular coagulation. Supportive measures (eg, intravenous fluids, vasopressors) and appropriate antibiotics are the mainstays of treatment.
A multisystem inflammatory syndrome potentially linked to COVID-19 has been reported in children and young adults; clinical features include Kawasaki-like and toxic shock syndrome-like presentations.
Immunocompromised Patient Considerations
Although infections with S. aureus are common in human immunodeficiency virus (HIV)-infected people, the complication of TSS is rare. This is thought to be related to the immune deficits and T-helper cell dysfunction in HIV-infected people. However, in cases that have been reported, they tend to present with a recurrent and prolonged disease course. Attributed to delayed antibody production against TSST-1 by HIV-infected individuals, a protracted disease course has been reported in HIV-infected teens, adults, and children.
A48.3 – Toxic shock syndrome
18504008 – Toxic shock syndrome
- Staphylococcal scalded skin syndrome
- Drug hypersensitivity syndrome (DRESS)
- Exanthematous drug eruption
- Drug-induced erythroderma
- Toxic epidermal necrolysis (TEN) – Drug induced, high fevers, skin tenderness, mucosal erosions, and skin detachment about 1-3 weeks after the inciting medication is started.
- Stevens-Johnson syndrome – Drug induced, high fevers, skin tenderness, mucosal erosions, and skin detachment about 1-3 weeks after the inciting medication is started.
- Scarlet fever – 1-mm erythematous papules, always elevated WBC with left shift, eosinophilia in up to 20% of patients.
- Erythrodermic psoriasis
- Atopic dermatitis with erythroderma
- Contact dermatitis
- Pemphigus erythematosus
- Pityriasis rubra pilaris
- Sezary syndrome (see cutaneous T-cell lymphoma)
- Necrotizing fasciitis – Rapidly progressing necrosis of fascia and subcutaneous fat.
- Kawasaki disease – Fever lasting for more than 5 days with oral mucosal changes, conjunctival injection, and cervical lymphadenopathy.
- Meningococcemia – Rapid decompensation, characteristic petechial eruption caused by N. meningitidis.
- Rocky Mountain spotted fever – Characteristic retiform purpura; check for serologies.