What is the superantigens produced by Streptococcus pyogenes?

Superantigens produced by Streptococcus pyogenes have been implicated with streptococcal toxic shock syndrome (STSS). We analyzed 19 acute-phase serum samples for mitogenic activity from patients with severe streptococcal disease.

What do superantigens do?

Superantigens are bacterial proteins that generate a powerful immune response by binding to Major Histocompatibility Complex class II molecules on antigen-presenting cells and T cell receptors on T cells.

What are the characteristics of Streptococcus pyogenes?

Both S pyogenes and S pneumoniae are Gram-positive cocci, nonmotile, and nonsporulating; they usually require complex culture media. S pyogenes characteristically is a round-to-ovoid coccus 0.6-1.0 μm in diameter (Fig. 13-1).

Does Group A streptococcus produce the superantigen toxin exotoxin A?

Group A streptococci can produce up to 11 serologically distinct superantigens (8, 15, 63–67). The streptococcal superantigens include SPE (serotypes A, C, and G to M), streptococcal superantigen (SSA), and streptococcal mitogenic exotoxin Zn (SMEZn) (8, 15).

Why do bacteria have superantigens?

Superantigens are defined by their ability to stimulate a large fraction of T cells via interactions with the TCR Vβ domain (Fig. 4.11). Superantigens are predominantly bacterial in origin, such as staphylococcal enterotoxins and toxin-1, which are responsible for toxic shock syndrome.

What are examples of superantigens?

Examples of superantigens include toxic shock syndrome toxin-1 (TSST-1), Streptococcal pyrogenic exotoxins (SPE), Staphylococcal enterotoxins (SE), and enterotoxogenic E. coli (ETEC) enterotoxin.

How do superantigens benefit bacteria?

Specifically it causes non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release. SAgs are produced by some pathogenic viruses and bacteria most likely as a defense mechanism against the immune system.

What infections does Streptococcus pyogenes cause?

Life-threatening infections caused by Streptococcus pyogenes (group A streptococcus) include scarlet fever, bacteremia, pneumonia, necrotizing fasciitis, myonecrosis and Streptococcal Toxic Shock Syndrome (StrepTSS).

How does Streptococcus pyogenes spread in body?

These bacteria are spread by direct contact with discharges from the nose and throat of infected people or by contact with infected wounds or sores on the skin. The risk of spreading the infection is highest when a person is ill, such as when people have “strep throat” or an infected wound.

What is the difference between streptolysin O and Streptolysin s?

Streptolysin O is oxygen-labile whereas streptolysin S is oxygen-stable. This means that streptolysin S is stable in the presence of atmospheric oxygen. In blood agar, the streptolysin S forms a zone of β hemolysis around the colonies of streptococci grown under routine aerobic conditions.

Is streptolysin a hemolysin?

Streptolysins are two hemolytic exotoxins from Streptococcus. Types include streptolysin O (SLO; slo), which is oxygen-labile, and streptolysin S (SLS; sagA), which is oxygen-stable. SLO is part of the thiol-activated cytolysin family.

How does superantigen production corrupt the immune response?

Evolution of superantigen production. SAg production effectively corrupts the immune response, allowing the microbe secreting the SAg to be carried and transmitted unchecked. One mechanism by which this is done is through inducing anergy of the T-cells to antigens and SAgs.

How is superantigen related to gastrointestinal toxicity?

One such effect is vomiting. This effect is felt in cases of food poisoning, when SAg-producing bacteria release the toxin, which is highly resistant to heat. There is a distinct region of the molecule that is active in inducing gastrointestinal toxicity.

Which is the most important cytokine produced by superantigen?

Superantigen. More importantly, the large number of activated T-cells secrete large amounts of cytokines, the most important of which is Interferon gamma. This excess amount of IFN-gamma in turn activates the macrophages. The activated macrophages, in turn, over-produce proinflammatory cytokines such as IL-1, IL-6 and TNF-alpha.

How are synthetic antibodies used to block SAg binding?

Synthetic antibodies and peptides have been created to mimic SAg-binding regions on the MHC class II, blocking the interaction and preventing T cell activation. Immunosuppressants are also employed to prevent T-cell activation and the release of cytokines.