Streptococcuspyogenes

Streptococcus pyogenes (group A beta streptococci)

Organism

Streptococcus pyogenes, a group A beta streptococcus, is a gram-positive coccus typically arranged in chains.
Facultative anaerobe (def).

Habitat

Asymptomatic colonization of the upper respiratory tract in humans.

Source

Pharyngitis is pread person to person primarily by respiratory droplets; skin infections are spread by direct contact with an infected person or through fomites (def).

Epidemiology

The group A beta hemolytic streptococci are responsible for most acute human streptococcal infections. Between 5% and 20% of children are asymptomatic carriers. The most common infection is pharyngitis (def) with the organism usually being limited to the mucous membranes and lymphatic tissue of the upper respiratory tract. Children are at greatest risk for infection.

Clinical Disease

The most common infection is pharyngitis (streptococcal sore throat) with the organism usually being limited to the mucous membranes and lymphatic tissue of the upper respiratory tract. From the pharynx, however, the streptococci sometimes spread to other areas of the respiratory tract resulting in laryngitis (def), bronchitis (def), pneumonia, and otitis media (def).
Occasionally, it may enter the lymphatic vessels or the blood and disseminate to other areas of the body, causing septicemia (def), osteomyelitis (def), endocarditis(def), septic arthritis (def), and meningitis (def).
If it enters injured skin, it may cause pyogenic (def) cutaneous infections such as impetigo , erysipelas (def), orcellulitis (def).
Group A beta streptococcus infections can result in two autoimmune diseases (def), rheumatic fever and acute glomerulonephritis, where antibodies made against streptococcal antigens cross react with joint membranes and heart valve tissue in the case of rheumatic fever, or glomerular cells and basement membranes of the kidneys in the case of acute glomerulonephritis.
Certain strains of S. pyogenes cause invasive group A beta streptococcal infections. Each year in the U.S. there are between 750 and 1500 cases of necrotizing fasciitis where a streptococcal-coded protease called Exotoxin B destroys the muscle (myositis) or the muscle covering (necrotizing fasciitis). There are another 750 - 1500 cases of toxic shock-like syndrome (def) due to group A beta streptococci producing Streptococcal pyrogenic exotoxin (Spe).

Pathogenicity

A capsule of hyaluronic acid enables the bacterium to resist phagocytic engulfment.
Peptidoglycan fragments and teichoic acids from its gram-positive cell wall can lead to excessive cytokine production and a massive inflammatory response. Inflammation in lung tissue results in the alveoli (def) becoming filled with plasma (def) which, in turn, prevents gas exchange.
Lipoteichoic acid binds to fibronectin on epithelial cells.
M protein functions as an adhesin (def) and is antiphagocytic by leading to the degradation of the complement protein C3b, a protein that promotes attachment of microbes to phagocytes.
M-like proteins bind the antibodies IgM and IgG.
F protein is an adhesin (def) that binds to fibronectin on epithelial cells.
M protein and F protein rnable S. pyogenes to invade epithelial cells and this helps maintain persistent infections and spread to deeper tissues.
Streptococcal pyrogenic exotoxin (Spe), is a superantigen (def) produced by rare invasive strains and scarlet fever strains of Streptococcus pyogenes causes toxic shock-like syndrome (TSLS). Excessive cytokine (def) production leads to fever, rash, and shock.
Streptolysin S and Streptolysin O can lyse white blood cells, platelets, and red blood cells.
Streptokinase can lyse fibrin clots and facilitate the spread of bacteria through tissue.
C5a peptidase degrades the complement protein C5a that promotes inflammation and the chemotaxis of phagocytes to the infected site.
DNase degrades cell-free DNA in purulent abcesses to reduce viscosity of the pus and facilitate spread of the bacteria.

Treatment

Treatment includes penicillins, cephalosporins, and erythromycin* (see antibiotic table).

*Drugs may change with time.

For a more detailed article on Streptococcus pyogenes, see Streptococcus Group A Infections, by Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM, Program Director, Associate Professor, Department of Internal Medicine, Divisions of Pulmonary and Critical Care Medicine, University of Manitoba; Site Coordinator of Respiratory Medicine, St Boniface General Hospital; and Godfrey Harding, MD, FRCPC, Program Director of Medical Microbiology, Professor, Department of Medicine, Section of Infectious Diseases and Microbiology, St Boniface Hospital, University of Manitoba, Canada.