Toxic shock syndrome caused by staphylococcus (MRSA detected)

Todd et al. 1978.

Toxic-Shock-Syndrome, TSS.

Superantigen-producing staphylococcal disease with scarlatinous exanthema and reduced general condition. In the process, it can lead to shock and multiorgan failure.

• Incidence: 0.8-3.4/100,000 (2000-2003).
• At present, a constant incidence can be assumed.
• Approximately half of all TSS triggered by Staphylococcus are NM-STSS.
• Initially, the M-STSS was particularly prevalent. Since patients have now been informed about the regular replacement of tampons and changes have also occurred in their production, the rate of "tampon-triggered toxic shock syndromes" has decreased.

• Non-menstrual-associated, staphylococcal-induced toxic shock syndrome (NM-STSS).
• Menstruation-associated, staphylococcal-induced toxic shock syndrome (M-STSS).

• NM-TSS is mainly caused by staphylococci of the skin (wounds, abscesses, boils), in the context of another gynaecological infection (e.g. postpartum), burns, sinusitis, osteomyelitis or arthritis, respiratory infections after influenza infection, enterocolitis and intravenously drug abuse.
• Staphylococci produce exotoxins such as Toxic Shock Syndrome Toxin-1 (TSST-1) and Staphylococci Enterotoxins B, C, D, E and H. All these toxins are superantigens and can activate a high number of T-lymphocytes, which then release an exceptionally high number of proinflammatory cytokines.
• As with all infections, the immune system is very important. Patients without TSST-1 neutralizing antibodies are far more likely to develop TSS than other patients.

• The initial symptoms include fever, pharyngitis, myalgia, diarrhea, vomiting. There is a macular, scarlatinous, generalized exanthema. Palmoplantar may show erythema. After 1-2 weeks desquamation occurs. Without exception, conjunctival hyperemia, pharyngitis and a "strawberry tongue" are visible. In some cases, the symptoms of the CNS can be determined.
• The hypotension associated with TSS is shown by a prominent exanthema on the trunk, orthostatic dysfunction and a shock with multiorgan failure.
• Early treatment often leads to less pronounced symptoms.
• Between the beginning of menstruation and TSS are on average 2-3 days, after operations often only 2 days, but TSS can still occur after 2 months!

• Clinical criteria (United States Centers for Disease Control and Prevention):
• Fever: Temperature ≥ 38.9°C.
• Blood pressure: Systolic blood pressure ≤ 90 mmHg (adults), less than 5th percentile for children under 16 years.
• Skin change: diffuse, macular (scalatiniform) exanthema.
• Desquamation: 1-2 weeks after onset of the disease, especially palmoplantar.
• Multi-organ system (participation of ≥ 3 systems).
• Gastrointestinal: vomiting, diarrhea.
• Muscular: Myalgia, ≥ 2-fold increased CK.
• Mucous membrane: Vaginal, oropharyngeal and hyperemia of the subjunctive.
• Renal: Urea or Creatinine ≥ 2-fold increased.
• Liver: Bilirubin or transaminases ≥ increased 2-fold.
• Hematological: < 100'000 platelets.
• CNS: disorientation, changes of consciousness without focal neurological signs without fever or hypotension.

• No other germ detection (except possibly Staphylococcus aureus, however the detection of S. aureus is not essential to make the diagnosis).

• Negative serological test (antibodies are often only determined in special laboratories) for Rocky Mountain Spotted Fever, leptospirosis or measles.

• Clinic.
• Bacterial smears (where focus is suspected: neck, vagina, skin lesions, nasal atrium, groin). S. aureus can be isolated from the suspicious focus in 80-90% of cases, but serological detection is only possible in 5% of cases

• Blood count (anemia, leukocytosis with neutrophilia, thrombocytopenia), coagulation (consumption coagulopathy, prolonged prothrombin time and partial thromboplastin time), creatinine, Urea (renal insufficiency), transaminases, bilirubin (liver insufficiency), creatinine kinase (myalgia), electrolytes (hyponatremia, hypalbuminemia, hypocalcemia, hypophosphatemia),

• Blood culture (pathogen detection), U status.

• CNS symptoms (encephalopathy with disorientation, confusion, epileptic seizures, cerebral edema, headache, memory loss, poor concentration): Neurological consil and cerebrospinal puncture.

• Breathing problems: Thoracic x-ray and, if necessary, internal consil.

• Exclusion of a vaginal/intrauterine foreign body.

• Vital parameter monitoring. .

• The mortality rate is between 1.8-6%, depending on the trigger and study.

• Women with M-STSS should no longer use tampons. Spirals for contraception should also be avoided.

• Recurrences occur days to months after the initial manifestation, in patients who have not received sufficient antibiotic treatment, do not produce their own antibodies and where the cause (the infection focus) has not been remedied. 

1. Staphylococcal Toxin-Mediated Scalded Skin and Toxic Shock Syndromes.  Deadly Dermatologic Diseases: Springer Science + Business Media:133-6.
2. Annane D, Clair B, Salomon J. Managing toxic shock syndrome with antibiotics. Expert Opinion on Pharmacotherapy 2004;5:1701-10.
3. Bach MC. Dermatologic signs in toxic shock syndrome—clues to diagnosis. Journal of the American Academy of Dermatology 1983;8:343-7.
4. Cassar SL, Wong AL, Jadavji TAJ, Leung AKC. Multiple splenic infarcts associated with toxic shock syndrome. Pediatric Emergency Care 2002;18:31-2.
5. Chi CY, Wang SM, Lin HC, Liu CC. A clinical and microbiological comparison of Staphylococcus aureus toxic shock and scalded skin syndromes in children. Clin Infect Dis 2006;42:181-5.
6. Lappin E, Ferguson AJ. Gram-positive toxic shock syndromes. The Lancet Infectious Diseases 2009;9:281-90.
7. McCormick JK, Yarwood JM, Schlievert PM. Toxic Shock Syndrome and Bacterial Superantigens: An Update. Annual Review of Microbiology 2001;55:77-104.
8. Sagraves R. Update on Menstrual Toxic Shock Syndrome. American Pharmacy 1995;35:12-7.
9. Shands KN, Schmid GP, Dan BB, et al. Toxic-Shock Syndrome in Menstruating Women. New England Journal of Medicine 1980;303:1436-42.
10. Stevens DL. THE TOXIC SHOCK SYNDROMES. Infectious Disease Clinics of North America 1996;10:727-46.
11. Todd J, Fishaut M, Kapral F, Welch T. TOXIC-SHOCK SYNDROME ASSOCIATED WITH PHAGE-GROUP-I STAPHYLOCOCCI. The Lancet 1978;312:1116-8.
12. Vuzevski VD, Joost Tv, Wagenvoort JHT, Dey JJM. Cutaneous Pathology in Toxic Shock Syndrome. International Journal of Dermatology 1989;28:94-7.
13. Warner JE, Onderdonk AB. Diversity of Toxic Shock Syndrome Toxin 1-Positive Staphylococcus aureus Isolates. Applied and Environmental Microbiology 2004;70:6931-5.
14. White MC, Thornton K, Young AER. Early diagnosis and treatment of toxic shock syndrome in paediatric burns. Burns 2005;31:193-7.
15. Schlievert PM, Tripp TJ , Peterson ML. Reemergence of staphylococcal toxic shock syndrome in Minneapolis-St. Paul, Minnesota, during the 2000-2003 surveillance period. J Clin Microbiol 2004;42:2875-6.
16. DeVries AS, Lesher L, Schlievert PM, Rogers T, Villaume LG, Danila R et al. Staphylococcal toxic shock syndrome 2000-2006: epidemiology, clinical features, and molecular characteristics. PLoS One 2011;6:e22997.
17. Smit MA, Nyquist AC , Todd JK. Infectious shock and toxic shock syndrome diagnoses in hospitals, Colorado, USA. Emerg Infect Dis 2013;19:1855-8.
18. Centers for Disease C. Reduced incidence of menstrual toxic-shock syndrome--United States, 1980-1990. MMWR Morb Mortal Wkly Rep 1990;39:421-3.
19. Gaventa S, Reingold AL, Hightower AW, Broome CV, Schwartz B, Hoppe C et al. Active surveillance for toxic shock syndrome in the United States, 1986. Rev Infect Dis 1989;11 Suppl 1:S28-34.