Streptococcus pyogenes is a species of Gram-positive, aerotolerant bacterium in the genus Streptococcus. These bacteria are extracellular, and made up of non-motile and non-sporing cocci. It is clinically important for humans. It is an infrequent, but usually pathogenic, part of the skin microbiota. It is the predominant species harboring the Lancefield group A antigen, and is often called group A Streptococcus (GAS). However, both Streptococcus dysgalactiae and the Streptococcus anginosus group can possess group A antigen. Group A streptococci when grown on blood agar typically produces small zones of beta-hemolysis, a complete destruction of red blood cells. (A zone size of 2–3 mm is typical.) It is thus also called group A (beta-hemolytic) Streptococcus(GABHS), and it can make colonies greater than 0.5 mm in size.[1]
Like other cocci, streptococci are round bacteria. The species name is derived from Greek words meaning 'a chain' (streptos) of berries (coccus [Latinized from kokkos]) and pus (pyo)-forming(genes), because streptococcal cells tend to link in chains of round cells (see image) and a number of infections caused by the bacterium produce pus. The main criterion for differentiation between Staphylococcus spp. and Streptococcus spp. is the catalase test. Staphylococci are catalase positive whereas streptococci are catalase-negative.[2] S. pyogenes can be cultured on fresh blood agar plates. Under ideal conditions, it has an incubation period of 1 to 3 days.[3]
An estimated 700 million GAS infections occur worldwide each year. While the overall mortality rate for these infections is 0.1%, over 650,000 of the cases are severe and invasive, and have a mortality rate of 25%.[4] Early recognition and treatment are critical; diagnostic failure can result in sepsis and death.[5][6]
| Streptococcus pyogenes | |
|---|---|
 | |
| S. pyogenes bacteria at 900× magnification | |
Scientific classification | |
| Domain: | Bacteria |
| Phylum: | Firmicutes |
| Class: | Bacilli |
| Order: | Lactobacillales |
| Family: | Streptococcaceae |
| Genus: | Streptococcus |
| Species: | S. pyogenes |
| Binomial name | |
| Streptococcus pyogenes Rosenbach 1884 | |
Serotyping[edit]
In 1928, Rebecca Lancefield published a method for serotyping S. pyogenes based on its cell-wall polysaccharide,[8] a virulence factor displayed on its surface.[9] Later, in 1946, Lancefield described the serologic classification of S. pyogenes isolates based on their surface T-antigen.[10] Four of the 20 T-antigens have been revealed to be pili, which are used by bacteria to attach to host cells.[11] As of 2016, a total of 120 M proteins are identified. These M proteins are encoded by 234 types emm gene with greater than 1,200 alleles.[7]
Lysogeny[edit]
All strains of S. pyogenes are polylysogenized, in that they carry one or more bacteriophage on their genomes.[12] Some of the 'phages may be defective, but in some cases active 'phage may compensate for defects in others.[13] In general, the genome of S. pyogenes strains isolated during disease are >90% identical, they differ by the 'phage they carry.[14]
Virulence factors[edit]
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.[15] A carbohydrate-based bacterial capsule composed of hyaluronic acid surrounds the bacterium, protecting it from phagocytosis by neutrophils.[2] 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.[16] 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.[2] However, the M protein is also the weakest point in this pathogen's defense, as antibodies produced by the immune systemagainst 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.[17]
| Name | Description |
|---|---|
| Streptolysin O | An exotoxin, one of the bases of the organism's beta-hemolytic property, streptolysin O causes an immune response and detection of antibodies to it; antistreptolysin O (ASO) can be clinically used to confirm a recent infection. It is damaged by oxygen. |
| Streptolysin S | A cardiotoxic exotoxin, another beta-hemolytic component, not immunogenic and O2 stable: A potent cell poison affecting many types of cell including neutrophils, platelets, and subcellular organelles. |
| Streptococcal pyrogenic 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, also known as toxic shock like syndrome (TSLS). |
| Streptococcal pyrogenic exotoxin C (SpeC) | |
| Streptococcal pyrogenic exotoxin B (SpeB) | A cysteine protease and the predominant secreted protein. Multiple actions, including degrading the extracellular matrix, cytokines, complement components, and immunoglobulins. Also called streptopain.[18] |
| Streptokinase | Enzymatically activates plasminogen, a proteolytic enzyme, into plasmin, which in turn digests fibrin and other proteins |
| Hyaluronidase | Hyaluronidase is widely assumed to facilitate 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 encodes the enzyme. Moreover, the few isolates capable of secreting hyaluronidase do not appear to need it to spread through tissues or to cause skin lesions.[19] 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 NETs' web of DNA, to which are bound neutrophil serine proteases that can kill the bacteria.[20] |
| C5a peptidase | C5a peptidase cleaves a potent neutrophil chemotaxin called C5a, which is produced by the complement system.[21] C5a peptidase is necessary to minimize the influx of neutrophils early in infection as the bacteria are attempting to colonize the host's tissue.[22] 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.[23] |
| Streptococcal chemokine protease | The affected tissue of patients with severe cases of necrotizing fasciitis are devoid of neutrophils.[24] The serine protease ScpC, which is released by S. pyogenes, is responsible for preventing the migration of neutrophils to the spreading infection. ScpC degrades the chemokine IL-8, which would otherwise attract neutrophils to the site of infection.[22][23] |
https://en.wikipedia.org/wiki/Streptococcus_pyogenes
Scarlet fever is a disease resulting from a group A streptococcus (group A strep) infection, also known as Streptococcus pyogenes.[1] The signs and symptoms include a sore throat, fever, headaches, swollen lymph nodes, and a characteristic rash.[1] The rash is red and feels like sandpaper and the tongue may be red and bumpy.[1] It most commonly affects children between five and 15 years of age.[1]
Scarlet fever affects a small number of people who have strep throat or streptococcal skin infections.[1] The bacteria are usually spread by people coughing or sneezing.[1] It can also be spread when a person touches an object that has the bacteria on it and then touches their mouth or nose.[1] The characteristic rash is due to the erythrogenic toxin, a substance produced by some types of the bacterium.[1][4] The diagnosis is typically confirmed by culturing the throat.[1]
As of 2020 there is no vaccine.[5] Prevention is by frequent handwashing, not sharing personal items, and staying away from other people when sick.[1] The disease is treatable with antibiotics, which prevent most complications.[1]Outcomes with scarlet fever are typically good if treated.[3] Long-term complications as a result of scarlet fever include kidney disease, rheumatic heart disease, and arthritis.[1] In the early 20th century, before antibiotics were available, it was a leading cause of death in children.[6][7] An antitoxin was produced before antibiotics; however, it was never made in sufficient quantities, and could not be used to treat any other disease as antibiotics can.
There have been signs of antibiotic resistance, and there have been recent outbreaks in Hong Kong in 2011 and in the UK in 2014, with occurrence rising 68% in the UK in the four years up to 2018. Research published in October 2020 has shown that infection of the bacterium by three viruses has led to stronger strains of the bacterium.[5]
| Specialty | Infectious disease |
|---|---|
| Symptoms | Sore throat, fever, headaches, swollen lymph nodes, characteristic rash[1] |
| Complications | Glomerulonephritis, rheumatic heart disease, arthritis[1] |
| Usual onset | 5–15 years old[1] |
| Causes | Strep throat, streptococcal skin infections[1] |
| Diagnostic method | Throat culture[1] |
| Prevention | Handwashing, not sharing personal items, staying away from sick people[1] |
| Treatment | Antibiotics[1] |
| Prognosis | Typically good[3] |
https://en.wikipedia.org/wiki/Scarlet_fever
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