Streptococcal & Staphylococcal Toxic Shock Syndrome (TSS)

David A Wininger, MDInternal Medicine Residency Program Director Associate Professor, Clinical Internal Medicine Division of Infectious DiseasesThe Ohio State University Wexner Medical Center614-293-3989 David.wininger@osumc.edu

Learning Objectives

Describe the nature and mechanisms of action of streptococcal and staphylococcal virulence factors as it related to Toxic Shock Syndrome (TSS)

Describe the role of molecular signals and cytokines involved in the pathophysiology of Toxic Shock Syndrome (TSS)

Compare and contrast the epidemiology, clinical manifestations, diagnosis, management and prognosis of streptococcal and staphylococcal Toxic Shock Syndrome (TSS)

Group A Streptococci: Virulence Factors

Toxins Pyrogenic exotoxins

SpeA, SpeB, SpeC, SpeF, etc.

Streptococcal TSS Scarlet Fever

Structural M-Protein Lipoteichoic acid F-Protein Capsule

Enzymes Streptolysin S Streptolysin O Streptokinases DNases C5a peptidase

Staphylococcus aureus TSST-1 & Enterotoxins are Superantigens

Or 2 separate slides

Superantigens in Staph and Strep

Staphylococcal

Toxic Shock Syndrome Toxin -1 (TSST-1)

Staphylococcal enterotoxins

At least 15 types

Staphylococcal exotoxins

Homologous to the enterotoxins

Streptococcal

SPE-A, SPE-C (Scarlet Fever- coded by bacteriophage)

SPE-B, SPE-E, SPE-G, etc.

SSA (Streptococcal Superantigen)

Superantigens (such as TSST-1)

Cytokine Release after Nonspecific Superantigen Stimulation of T-cells

Primarily CD4+ T cell response is triggered by superantigen

T-helper Th1 response IL-2, IFN-γ, IL-1β and TNF-α

Immune Response

Given lack of Th2 response, antibody expression is decreased during response to superantigens

Lack of protective antibody to TSST-1 after first episode leaves ~50% patients vulnerable to recurrence

Toxic Shock Syndrome Epidemiology

Staphylococcus aureus TSST-1 producing strains

Menstruating women Hyper absorbent tampons

Non-menstrual disease results from colonization of any site: Surgical wounds (may not look hot)

Post-influenza lung

Other skin/soft tissue

Contraceptive diaphragms

5% mortality now that condition is routinely recognized

Toxic Shock Syndrome Epidemiology

Streptococcus pyogenes (Group A) M-serotypes 1 or 3

Mucoid strains – prominent capsules

Produce SPE’s

Can occur in patients of any age

Patients at risk: HIV infection, Diabetes mellitus, Cancer, Heart or Lung disease, Chicken-pox/Shingles, Injection drug use, Ethanol abuse

Mortality almost 50%

Toxic Shock Syndrome: Clinical Manifestations(Staphylococcal or Streptococcal)

Streptococcal Toxic Shock SyndromeCommon Clinical Manifestations

Cellulitis Myositis Necrotizing fasciitis (“Flesh Eating Strep”)

Toxic Shock Syndrome (TSS): Diagnosis

Staphylococcal TSS

Usually a clinical diagnosis

Diagnostic criteria have been developed

Often lack positive cultures for staph

Staph can be cultured from colonized sites (mucosal surfaces)

Lack of anti-TSST1 antibodies during acute syndrome is expected.

Toxic Shock Syndrome (TSS): Diagnosis

Streptococcal TSS

Cultures from involved sites are usually positive

Positive growth from sterile site (blood, deep tissue) is more definitive than positive culture from non-sterile site like superficial skin

Clinical diagnostic criteria are similar to those for Staph TSS

Toxic Shock Syndrome (TSS): Management

Staphylococcal TSS

Supportive care

IV fluids, other blood pressure support, intensive care as needed (ventilator, renal dialysis, etc.)

Removal of potential focus

Anti-staphylococcal antibiotics even if cultures are negative.

Consider IVIG for more severe cases but usually not necessary

Toxic Shock Syndrome (TSS): Management

Streptococcal TSS

Supportive care as with staph

Aggressive surgical debridement or other removal of infected source (site is usually overt)

Anti-streptococcal antibiotics (penicillin + clindamycin)

Clindamycin blocks protein synthesis (↓ toxin production)

IVIG more likely to be used, since cases are often more severe

Summary

Toxic Shock Syndrome (TSS) is mediated by superantigen toxins produced by Staphylococcus aureus and Group A Streptococcus.

Staphylococcal TSS is more likely to be a culture negative presentation of septic shock, while Streptococcal TSS is likely to manifest with a severe overt localizable infection of soft tissue or another body site.

Both aggressive supportive care and antimicrobial coverage of the causative organism are critical for successful management of TSS.

Intravenous immunoglobulin is a consideration for the management of severe TSS, since one hallmark of the acute condition is absence of antibodies against the superantigen toxin.

Quiz

Thank you for completing this module

If you have any questions, write to me at david.wininger@osumc.edu or try my office at 614-293-3989.

David Wininger, MD

References

Medical Microbiology, 7th Ed. Murray, Rosenthal & Pfaller; Chapter 18 & 19, selected pages.

Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases, Seventh Edition Chapter 195 and Chapter 198 selected pages (available electronically in Prior Health Sciences Library among the Core 25 Textbooks)

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