[1] S. pyogenes is a species of beta-hemolytic Gram-positive bacteria that is responsible for a wide range of infections that are mostly common and fairly mild.

[8] The diseases that may be caused as a result of this include streptococcal toxic shock syndrome (STSS), necrotizing fasciitis (NF), pneumonia, and bacteremia.

[4] In addition, infection of GAS may lead to further complications and health conditions, namely acute rheumatic fever and poststreptococcal glomerulonephritis.

This increased risk may be due to a combination of shared genetic susceptibility within the family, close contact with carriers, and the virulence of the Group A streptococcal strain that is involved.

[15] Public health policies internationally reflect differing views of how the close contacts of people affected by severe Group A streptococcal infections should be treated.

Health Canada[16] and the US CDC recommend close contacts see their doctor for full evaluation and may require antibiotics;[17] current UK Health Protection Agency guidance is that, for a number of reasons, close contacts should not receive antibiotics unless they are symptomatic but that they should receive information and advice to seek immediate medical attention if they develop symptoms.

The rapid pyrrolidonyl arylamidase (PYR) test is commonly used, wherein a positive reaction confers a presumptive identification of group A beta-hemolytic streptococci if the appearance and clinical context is consistent.

[30] In later years, a positive test result for the presence of group A streptococci was found in 32.1 percent of individuals after throat cultures were carried out in a 20-year-long (1953/1954–1973/1974) study performed in Nashville, Tennessee.

[30] Environmental factors, such as less crowding and the increase of family living space, can account for the reduction in incidence and severity of group A streptococci.

This is especially important considering an estimated 500,000 deaths worldwide all occurring after acute rheumatic fever, invasive infection, or subsequent heart disease can be accredited to GAS.

[31] This number is quite large, often leaving the health care system encumbered, since 91 percent of patients infected with invasive GAS need to be hospitalized with 8950–11,500 episodes and 1050–1850 deaths taking place each year.

The M-protein generates antibodies that cross-react with autoantigens on interstitial connective tissue, in particular of the endocardium and synovium, that can lead to significant clinical illness.

Although common in developing countries, ARF is rare in the United States, possibly secondary to improved antibiotic treatment, with small isolated outbreaks reported only occasionally.

It is most common among children between 5 and 15 years old and occurs 1–3 weeks after an untreated GAS pharyngitis, but caution is advised when interpreting the demographics of the contemporary picture of pediatric cases in the United States.

[32] ARF is often clinically diagnosed based on Jones Criteria, which include: pancarditis, migratory polyarthritis of large joints, subcutaneous nodules, erythema marginatum, and sydenham chorea (involuntary, purposeless movement).

Chronic rheumatic heart disease mostly affects the mitral valve, which can become thickened with calcification of the leaflets, often causing fusion of the commissures and chordae tendineae.

Other findings of ARF include erythema marginatum (usually over the spine or other bony areas) and a red expanding rash on the trunk and extremities that recurs over weeks to months.

A neurological disorder, Sydenham chorea, can occur months after an initial attack, causing jerky involuntary movements, muscle weakness, slurred speech, and personality changes.

Clinical findings may include dark-colored urine, swelling of different parts of the body (edema), and high blood pressure.

[35][36] The CANS/PANS hypotheses include different possible mechanisms underlying acute-onset neuropsychiatric conditions, but do not exclude GABHS infections as a cause in a subset of individuals.

[34][35][36] Note: Elements of the original text of this article are taken from the NIH Fact Sheet "Group A Streptococcal Infections", dated March 1999.