Toxic Shock Syndrome

Pathophysiology
S. aureus exotoxins now are recognized to be superantigens, and the endogenous mediators produced by these exotoxins appear to mediate manifestations of the disease

Risk factors for menstrual TSS

Median age of patients 21 years 97 percent of such cases have occurred in whites Tampons composition

Risk factors for Non-menstrual TSS

Acquisition of non-menstrual disease include
Colonization (or acquisition) of a toxin-producing strain of S. aureus
individual must be colonized with or acquire a strain of S. aureus that produces TSST-I or one of the staphylococcal enterotoxins

Absence of protective antitoxin antibody, and

development of TSS is the absence of protective antibody levels for the toxin (TSST-I or enterotoxin) produced by the isolate associated with TSS.

An infected site
Interruption of a Mucosal or Skin Surface

Presence of a Foreign Body

 Numerous patients with TSS have been reported for whom no obvious focus of infection was found. Trauma or surgery in areas of the body frequently colonized with S. aureus (nose, skin, vagina) places individuals at enhanced risk for infection and subsequent TSS.

 TSS has unique clinical manifestations not generally noted in septic shock, including diffuse erythroderma, delayed desquamation of the palms and soles, conjunctival and pharyngeal hyperemia, muscle injury, rapidly accelerated renal failure, and gastrointestinal symptoms.

Case Definition of Toxic Shock Syndrome

1. 2. 3. 4. 5. Fever: Temperature 38.9C Rash: Diffuse macular erythroderma Desquamation: 1-2 wk after onset of illness, particularly on palms, soles, fingers, and toes Hypotension: SBP90 mm Hg for adults; <5th centile <16 yr old; orthostatic drop in diastolic blood pressure 15 mm Hg from lying to sitting; orthostatic syncope or orthostatic dizziness Involvement of three or more of the following organ systems:
I. II. Gastrointestinal: Vomiting or diarrhea at onset of illness Muscular: Severe myalgia or creatinine phosphokinase level greater than twice the upper limit of normal for the laboratory III. Mucous membrane: Vaginal, oropharyngeal, or conjunctival hyperemia IV. Renal: BUN or serum creatinine greater than twice the upper limit of normal or 5 white blood cells per high-power field in the absence of a urinary tract infection V. Hepatic: Total bilirubin, AST, or ALT greater than twice the upper limit of normal for the laboratory VI. Hematologic: platelets <100,000/mm 3 VII. Central nervous system: disorientation or alterations in consciousness without focal neurologic signs when fever and hypotension are absent

6.

Blood, throat, or cerebrospinal fluid cultures; blood culture may be positive for Staphylococcus aureus Serologic tests for Rocky Mountain spotted fever, leptospirosis, or measles

Negative results on the following tests, if obtained:

Case Classification

Probable: A case with 5 of the 6 clinical findings described above Confirmed: A case with all 6 of the clinical findings described above, including desquamation, unless the patient dies before desquamation could occur

From Wharton, M., Chorba, T. L., Vogt, R. L., et al.: Case definitions for public health surveillance. M. M. W. R. Recomm. Rep. 39(RR-13): 1-43, 1990.

Therapeutic Principles for Management

1. Identify the focus of infection: debride and irrigate extensively and remove any foreign material 2. Isolate the organism for antimicrobial susceptibility studies 3. Administer parenteral antimicrobial therapy
Stop enzyme/toxin production with a protein synthesis inhibitor (e.g., clindamycin, erythromycin, gentamicin) and Eradicate the organism with a bacterial cell wall inhibitor (e.g., - lactamaseresistant antistaphylococcal antimicrobial agent)

Consider IVIg, Methylprednisolone in severe disease

4.

Anticipate the management of multisystem organ failure

Recurrences
High rate of recurrence in patients with inadequately treated menstrual or nonmenstrual disease The use of antistaphylococcal antimicrobial therapy to which the organism is susceptible in doses recommended for serious infections for 10 to 14 days and discontinuation of tampon use can reduce the rate of recurrence significantly absent or delayed antibody response to TSST-I superantigenic toxins are not processed by antigen-processing cells and T lymphocytes as conventional antigens

PREVENTION AND PROPHYLAXIS

minimize their use of high-absorbency tampons frequency of changing tampons during a menstrual period has not been associated with risk for the development of TSS the use of an individual tampon for no more than 12 hours at a time might decrease the risk for menstrual TSS.L postoperative TSS: recognize early; to open, explore extensively, and irrigate wounds; and to provide immediate antimicrobial and supportive therapy for suspected TSS