Toxic Shock Syndrome

Key Features

• Multiple organisms that can cause toxic shock syndrome (TSS) include

  • Staphylococcus aureus

  • Streptococcus

  • Certain Clostridium species (C perfringens, C sordellii)

Staphylococcus aureus

• Strains of staphylococci may produce toxins that can cause three important entities

  • Scalded skin syndrome, typically in children, or bullous impetigo in adults

  • TSS

  • Enterotoxin food poisoning

• Although originally associated with tampon use, any focus (eg, nasopharynx, bone, vagina, rectum, abscess, or wound) harboring a toxin-producing S aureus strain can cause TSS

• Fatality rates may be as high as 15%

Streptococcal infection

• Any streptococcal infection—and necrotizing fasciitis in particular, can cause TSS

• TSS is due to pyrogenic erythrotoxin superantigen that stimulates massive release of inflammatory cytokines believed to mediate the shock

• Invasive disease

  • Risk factors are age (very young or older persons) and underlying medical conditions

  • Bacteremia occurs in most cases

Clostridium sordellii

• C sordellii is a rare cause of endometritis and toxic shock syndrome following childbirth

• Fatal cases of uterine infection following medically induced abortion with mifepristone have been reported

Clinical Findings

S aureus

• Toxic shock is characterized by abrupt onset of high fever, vomiting, and watery diarrhea

• Sore throat, myalgias, and headache are common

• A diffuse macular erythematous rash and nonpurulent conjunctivitis are common, and desquamation, especially of the palms and soles, is typical during recovery

Streptococcal TSS

• Invasion of skin or soft tissues

• Acute respiratory distress syndrome

• Kidney failure

• Skin rash and desquamation may not be present

C sordellii

• Abdominal pain

• Absence of fever

• Onset of illness was within 4–5 days of ingestion of mifepristone

• Clinical course is fulminant

• Infection appeared to be limited to the uterus, which shows

  • Necrosis

  • Edema

  • Hemorrhage

  • Acute inflammatory changes

Diagnosis

S aureus

• Blood cultures classically are negative because symptoms are due to the effects of the toxin and not to the invasive properties of the organism

C sordellii

• Tachycardia, severe hypotension, capillary leak syndrome with edema

• Profound leukocytosis, hemoconcentration

Treatment

S aureus

• Rapid rehydration, antistaphylococcal antibiotics (eg, parenteral nafcillin or oxacillin or, in the penicillin allergic patient, clindamycin), management of kidney or heart failure, and most importantly removal of sources of toxin (eg, removal of tampon, drainage of abscess)

• Intravenous clindamycin, 900 mg every 8 hours, is often added to inhibit toxin production

• Intravenous immune globulin may be considered, although there are limited data compared to streptococcus TSS