To use all functions of this page, please activate cookies in your browser.
With an accout for my.bionity.com you can always see everything at a glance – and you can configure your own website and individual newsletter.
- My watch list
- My saved searches
- My saved topics
- My newsletter
Streptococcus pyogenes is a spherical gram-positive bacteria that grows in long chains  and is the cause of Group A streptococcal infections. S. pyogenes displays group A antigen on its cell wall and beta-hemolysis when cultured on blood agar plate. S. pyogenes typically produces large zones of beta-hemolysis, the complete disruption of erythrocytes and the release of hemoglobin, and it is therefore called Group A (beta-hemolytic) Streptococcus (abbreviated GAS). Streptococci are catalase-negative.
Additional recommended knowledge
In 1928, Rebecca Lancefield published a method for serotyping S. pyogenes based on its M protein, a virulence factor that is displayed on its surface. Later in 1946, Lancefield described the serologic classification of S. pyogenes isolates based on their surface T antigen. Four of the 20 T antigens have been revealed to be pili, which are used by bacteria to attach to host cells. Currently, over 100 M serotypes and approximately 20 T serotypes are known.
S. pyogenes is the cause of many important human diseases ranging from mild superficial skin infections to life-threatening systemic diseases. Infections typically begin in the throat or skin. Examples of mild S. pyogenes infections include pharyngitis ("strep throat") and localized skin infection ("impetigo"). Erysipelas and cellulitis are characterized by multiplication and lateral spread of S. pyogenes in deep layers of the skin. S. pyogenes invasion and multiplication in the fascia can lead to necrotizing fasciitis, a potentially life-threatening condition requiring surgical treatment.
Infections due to certain strains of S. pyogenes can be associated with the release of bacterial toxins. Throat infections associated with release of certain toxins lead to scarlet fever. Other toxigenic S. pyogenes infections may lead to streptococcal toxic shock syndrome, which can be life-threatening.
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 poststreptococcal glomerulonephritis. Both conditions appear several weeks following the initial streptococcal infection. Rheumatic fever is characterised by inflammation of the joints and/or heart following an episode of Streptococcal pharyngitis. Acute glomerulonephritis, inflammation of the renal glomerulus, can follow Streptococcal pharyngitis or skin infection.
This bacterium remains acutely sensitive to penicillin. Failure of treatment with penicillin is generally attributed to other local commensal organisms producing β-lactamase or failure to achieve adequate tissue levels in the pharynx. Certain strains have developed resistance to macrolides, tetracyclines and clindamycin.
S. pyogenes has several virulence factors that enable it to attach to host tissues, evade the immune response, and spread by penetrating host tissue layers. A carbohydrate capsule composed of hyaluronic acid surrounds the bacterium, protecting it from phagocytosis by neutrophils. In addition, the capsule and several factors embedded in the cell wall, including M protein, lipoteichoic acid, and protein F (SfbI) facilitate attachment to various host cells. M protein also inhibits opsonization by the alternative complement pathway by binding to host complement regulators. M protein found on some serotypes are also able to prevent opsonization by binding to fibrinogen. However, the M protein is also the weakest point in this pathogen's defense as antibodies produced by the immune system against M protein target the bacteria for engulfment by phagocytes. M proteins are unique to each strain, and identification can be used clinically to confirm the strain causing an infection.
S. pyogenes releases a number of proteins, including several virulence factors, into its host:
Usually, a throat swab is taken to the laboratory for testing. A Gram stain is performed to show Gram positive, cocci, in chains. Then, culture the organism on blood agar with added bacitracin antibiotic disk to show beta-haemolytic colonies and sensitivity (zone of inhibition around the disk) for the antibiotic. Then, perform catalase test, which should show a negative reaction for all Streptococci. S. pyogenes is cAMP and hippurate tests negative. Serological identification of the organism involves testing for the presence of group A specific polysaccharide in the bacterium's cell wall using the Phadebact test. As a precautionary measure tests are also carried out to check for illnesses including, but not limited to, Syphilis, and Avascular Necrosis, and Clubfoot.
The treatment of choice is penicillin, however in the absence of readily available penicillin, small incisions made to the infected area will relieve swelling and discomfort until proper medical assistance can be sought. There is no reported instance of penicillin-resistance reported to date, although since 1985 there have been many reports of penicillin-tolerance.
Macrolides, chloramphenicol, and tetracyclines may be used if the strain isolated has been shown to be sensitive, but resistance is much more common.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Streptococcus_pyogenes". A list of authors is available in Wikipedia.|