| Streptococcus pyogenes | |
|---|---|
| S. pyogenes bacteria at 900x magnification. | |
| Scientific classification | |
| Kingdom: | Eubacteria |
| Phylum: | Firmicutes |
| Class: | Cocci |
| Order: | Lactobacillales |
| Family: | Streptococcaceae |
| Genus: | Streptococcus |
| Species: | S. pyogenes |
| Binomial name | |
| Streptococcus pyogenes Rosenbach 1884 |
|
Streptococcus pyogenes is a spherical, Gram-positive bacterium that is the cause of group A streptococcal infections.[1] S. pyogenes displays streptococcal group A antigen on its cell wall. S. pyogenes typically produces large zones of beta-hemolysis (the complete disruption of erythrocytes and the release of hemoglobin) when cultured on blood agar plates, and are therefore also called Group A (beta-hemolytic) Streptococcus (abbreviated GABHS).
Streptococci are catalase-negative. In ideal conditions, S. pyogenes has an incubation period of approximately 1–3 days.[2] It is an infrequent, but usually pathogenic, part of the skin flora.
It is estimated that there are more than 700 million infections each year and over 650,000 cases of severe, invasive infections that have a mortality rate of 25 %.[3]
Contents |
In 1928, Rebecca Lancefield published a method for serotyping S. pyogenes based on its M protein, a virulence factor displayed on its surface.[4] Later in 1946, Lancefield described the serologic classification of S. pyogenes isolates based on their surface T antigen.[5] Four of the 20 T antigens have been revealed to be pili, which are used by bacteria to attach to host cells.[6] Over 100 M serotypes and approximately 20 T serotypes are known. The disease was widely publicized in the early 90's as it was the cause of death of Jim Henson.
S. pyogenes is the cause of many important human diseases, ranging from mild superficial skin infections to life-threatening systemic diseases.[1] 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.[1]
S. pyogenes can also cause disease in the form of postinfectious "nonpyogenic" (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 postinfectious 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.[7] A carbohydrate-based bacterial capsule composed of hyaluronic acid surrounds the bacterium, protecting it from phagocytosis by neutrophils.[1] 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.[8] M protein also inhibits opsonization by the alternative complement pathway by binding to host complement regulators. The M protein found on some serotypes is also able to prevent opsonization by binding to fibrinogen.[1] 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:[1]
| Name | Description |
|---|---|
| Streptolysin O | An exotoxin that is one of the bases of the organism's beta-hemolytic property. |
| Streptolysin S | A cardiotoxic exotoxin that is another beta-hemolytic component. Streptolysin S is not immunogenic and O2 stable. A potent cell poison affecting many types of cell including neutrophils, platelets, and sub-cellular organelles, streptolysin S causes an immune response and detection of antibodies to it; antistreptolysin O (ASO) can be clinically used to confirm a recent infection. |
| Streptococcal pyogenic exotoxin A (SpeA) | Superantigens secreted by many strains of S. pyogenes. This pyrogenic exotoxin is responsible for the rash of scarlet fever and many of the symptoms of streptococcal toxic shock syndrome. |
| Streptococcal pyogenic exotoxin C (SpeC) | |
| Streptokinase | Enzymatically activates plasminogen, a proteolytic enzyme, into plasmin, which in turn digests fibrin and other proteins. |
| Hyaluronidase | It is widely assumed hyaluronidase facilitates the spread of the bacteria through tissues by breaking down hyaluronic acid, an important component of connective tissue. However, very few isolates of S. pyogenes are capable of secreting active hyaluronidase due to mutations in the gene that encode the enzyme. Moreover, the few isolates that are capable of secreting hyaluronidase do not appear to need it to spread through tissues or to cause skin lesions.[9] Thus, the true role of hyaluronidase in pathogenesis, if any, remains unknown. |
| Streptodornase | Most strains of S. pyogenes secrete up to four different DNases, which are sometimes called streptodornase. The DNases protect the bacteria from being trapped in neutrophil extracellular traps (NETs) by digesting the NET's web of DNA, to which are bound neutrophil serine proteases that can kill the bacteria.[10] |
| C5a peptidase | C5a peptidase cleaves a potent neutrophil chemotaxin called C5a, which is produced by the complement system.[11] C5a peptidase is necessary to minimize the influx of neutrophils early in infection as the bacteria are attempting to colonize the host's tissue.[12] |
| Streptococcal chemokine protease | The affected tissue of patients with severe cases of necrotizing fasciitis are devoid of neutrophils.[13] The serine protease ScpC, which is released by S. pyogenes, is responsible for preventing the migration of neutrophils to the spreading infection.[14] ScpC degrades the chemokine IL-8, which would otherwise attract neutrophils to the site of infection. C5a peptidase, although required to degrade the neutrophil chemotaxin C5a in the early stages of infection, is not required for S. pyogenes to prevent the influx of neutrophils as the bacteria spread through the fascia.[12][14] |
Usually, a throat swab is taken to the laboratory for testing. A Gram stain is performed to show Gram-positive cocci in chains. Then, the organism is cultured on blood agar with an added bacitracin antibiotic disk to show beta-hemolytic colonies and sensitivity (zone of inhibition around the disk) for the antibiotic. Culture on non-blood containing agar then, perform catalase test, which should show a negative reaction for all Streptococci. S. pyogenes is CAMP (not to be confused with 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.
The treatment of choice is penicillin and the duration of treatment is well established as being 10 days minimum.[15] There has been no reported instance of penicillin-resistance to date, although since 1985, there have been many reports of penicillin-tolerance.[16]
Macrolides, chloramphenicol and tetracyclines may be used if the strain isolated has been shown to be sensitive, but resistance is much more common.
No vaccines are currently available to protect against S. pyogenes infection, but specific protective antibody has been shown to persist as long as 45 years after the original infection.[17]
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||