These bacteria are extracellular, and made up of non-motile and non-sporing cocci (round cells) that tend to link in chains.

They are clinically important for humans, as they are an infrequent, but usually pathogenic, part of the skin microbiota that can cause group A streptococcal infection.

The PYR test allows for the differentiation of Streptococcus pyogenes from other morphologically similar beta-hemolytic streptococci (including S. dysgalactiae subsp.

[5][6] S. pyogenes is clinically and historically significant as the cause of scarlet fever, which results from exposure to the species' exotoxin.

Streptococcal pharyngitis occurs most frequently in late winter to early spring in most countries as indoor spaces are used more often and thus more crowded.

[9] The risk of sepsis is relatively high compared to other bacterial infections acquired during pregnancy, and S. pyogenes is a leading cause of septic shock and death in pregnant and postpartum women.

[10] In 1928, Rebecca Lancefield published a method for serotyping S. pyogenes based on its cell-wall polysaccharide,[11] a virulence factor displayed on its surface.

[12] Later, in 1946, Lancefield described the serologic classification of S. pyogenes isolates based on components of their surface pili (known as the T-antigen)[13] which are used by bacteria to attach to host cells.

[18] A carbohydrate-based bacterial capsule composed of hyaluronic acid surrounds the bacterium, protecting it from phagocytosis by neutrophils.

Complete genome sequences of the type strain of S. pyogenes (NCTC 8198T = CCUG 4207T) are available in DNA Data Bank of Japan, European Nucleotide Archive, and GenBank under the accession numbers LN831034 and CP028841.

In the biofilm gene expression for multiple purposes (such as defending against the host immune system) is controlled via quorum sensing.

RopB is another Rgg-like protein (Rgg1) that directly activates SpeB (Streptococcal pyrogenic exotoxin B), a cysteine protease that acts as a virulence factor.

S. pyogenes invasion and multiplication in the fascia beneath the skin can lead to necrotizing fasciitis, a life-threatening surgical emergency.

[39][40][41] The bacteria may start to cause disease when the host's immune system weakens, such as during a viral respiratory infection, which may lead to S. pyogenes superinfection.

[2] S. pyogenes can also cause disease in the form of post-infectious "non-pyogenic" (not associated with local bacterial multiplication and pus formation) syndromes.

These autoimmune-mediated complications follow a small percentage of infections and include rheumatic fever and acute post-infectious glomerulonephritis.

[43] There is a polyvalent inactivated vaccine against several types of Streptococcus including S. pyogenes called " vacuna antipiogena polivalente BIOL" it is recommended an administration in a series of 5 weeks.

[45] Many S. pyogenes proteins have unique properties, which have been harnessed in recent years to produce a highly specific "superglue"[46][47] and a route to enhance the effectiveness of antibody therapy.