| Streptococcus pyogenes | |
|---|---|
_(52602981880).jpg) | |
| False-color scanning electron micrograph of chain ofStreptococcus pyogenes bacteria (yellow) | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Bacillati |
| Phylum: | Bacillota |
| Class: | Bacilli |
| Order: | Lactobacillales |
| Family: | Streptococcaceae |
| Genus: | Streptococcus |
| Species: | S. pyogenes |
| Binomial name | |
| Streptococcus pyogenes Rosenbach 1884 | |
Streptococcus pyogenes is aspecies ofGram-positive, aerotolerantbacteria in the genusStreptococcus. These bacteria areextracellular, and made up of non-motile and non-sporingcocci (round cells) that tend to link in chains. They are clinically important for humans, as they are an infrequent, but usuallypathogenic, part of theskin microbiota that can causegroup A streptococcal infection.S. pyogenes is the predominant species harboring theLancefield group Aantigen, and is often calledgroup AStreptococcus (GAS). However, bothStreptococcus dysgalactiae and theStreptococcus anginosus group can possess group A antigen as well. Group A streptococci, when grown onblood agar, typically produce small (2–3 mm) zones ofbeta-hemolysis, a completedestruction ofred blood cells. The namegroup A (beta-hemolytic)Streptococcus is thus also used.[1]
The species name is derived from Greek words meaning 'a chain' (streptos) of berries (coccus [Latinized fromkokkos]) andpus (pyo)-forming (genes), since a number of infections caused by the bacterium produce pus. The main criterion for differentiation betweenStaphylococcus spp. andStreptococcus spp. is thecatalase test. Staphylococci are catalase positive whereas streptococci are catalase-negative.[2]S. pyogenes can becultured on fresh blood agar plates. ThePYR test allows for the differentiation ofStreptococcus pyogenes from other morphologically similar beta-hemolytic streptococci (includingS. dysgalactiae subsp.esquismilis) asS. pyogenes will produce a positive test result.[3]
An estimated 700 million GAS infections occur worldwide each year. While the overall mortality rate for these infections is less than 0.1%, over 650,000 of the cases are severe and invasive, and these cases have a mortality rate of 25%.[4] Early recognition and treatment are critical;diagnostic failure can result insepsis and death.[5][6]S. pyogenes is clinically and historically significant as the cause ofscarlet fever, which results from exposure to the species'exotoxin.[7]
Unlike most bacterial pathogens,S. pyogenes only infects humans. Thus,zoonotic transmission from an animal (or animal products) to a human is rare.[8]
S. pyogenes typically colonizes the throat, genital mucosa,rectum, and skin. Of healthy adults, 1% to 5% have throat, vaginal, or rectal carriage, with children being more common carriers. Most frequently, transmission from one person to another occurs due to inhalation ofrespiratory droplets, produced by sneezing and coughing from an infected person. Skin contact, contact withobjects harboring the bacterium, and consumption of contaminated food are possible but uncommon modes of transmission.Streptococcal pharyngitis occurs most frequently in late winter to early spring in most countries as indoor spaces are used more often and thus more crowded. Disease cases are the lowest during autumn.[9]
MaternalS. pyogenes infection usually happens in late pregnancy, at more than 30 weeks ofgestation to four weekspostpartum. Maternal infections account for 2 to 4% of all clinically diagnosedS. pyogenes infections.[9] The risk ofsepsis is relatively high compared to other bacterial infections acquired during pregnancy, andS. pyogenes is a leading cause ofseptic shock and death in pregnant and postpartum women.[10]
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In 1928,Rebecca Lancefield published a method for serotypingS. pyogenes based on its cell-wall polysaccharide,[11] avirulence factor displayed on its surface.[12] Later, in 1946, Lancefield described the serologic classification ofS. pyogenes isolates based on components of their surfacepili (known as the T-antigen)[13] which are used by bacteria to attach to host cells.[14] As of 2016, a total of 120M proteins have been identified. These M proteins are encoded by 234 typeemm genes with greater than 1,200 alleles.[9]
All strains ofS. pyogenes are polylysogenized, in that they carry one or morebacteriophage in their genomes.[15] Some of the phages may be defective, but in some cases active phage may compensate for defects in others.[16] In general, the genome ofS. pyogenes strains isolated during disease are >90% identical, they differ by the phage they carry.[17]
S. pyogenes has severalvirulence factors that enable it to attach to host tissues, evade the immune response, and spread by penetrating host tissue layers.[18] A carbohydrate-basedbacterial capsule composed ofhyaluronic acid surrounds the bacterium, protecting it fromphagocytosis byneutrophils.[2] In addition, the capsule and several factors embedded in the cell wall, includingM protein,lipoteichoic acid, and protein F (SfbI) facilitate attachment to various host cells.[19] M protein also inhibitsopsonization by the alternativecomplement pathway by binding to host complement regulators. The M protein found on some serotypes is also able to prevent opsonization by binding tofibrinogen.[2] However, the M protein is also the weakest point in this pathogen's defense, asantibodies produced by theimmune system against M protein target the bacteria for engulfment byphagocytes. M proteins are unique to each strain, and identification can be used clinically to confirm the strain causing an infection.[20]
| Name | Description |
|---|---|
| Streptolysin O | Anexotoxin, 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 ofS. pyogenes: Thisstreptococcal 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 calledstreptopain.[21] |
| Streptokinase | Enzymatically activatesplasminogen, a proteolytic enzyme, intoplasmin, which in turn digestsfibrin and other proteins |
| Hyaluronidase | Hyaluronidase is widely assumed to facilitate the spread of the bacteria through tissues by breaking downhyaluronic acid, an important component ofconnective tissue. However, very few isolates ofS. 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.[22] Thus, the true role of hyaluronidase in pathogenesis, if any, remains unknown. |
| Streptodornase | Most strains ofS. pyogenes secrete up to four differentDNases, which are sometimes called streptodornase. The DNases protect the bacteria from being trapped inneutrophil extracellular traps (NETs) by digesting the NETs' web of DNA, to which are boundneutrophilserine proteases that can kill the bacteria.[23] |
| C5apeptidase | C5a peptidase cleaves a potentneutrophil chemotaxin calledC5a, which is produced by thecomplement system.[24] C5a peptidase is necessary to minimize the influx ofneutrophils early in infection as the bacteria are attempting to colonize the host's tissue.[25] C5a peptidase, although required to degrade the neutrophil chemotaxin C5a in the early stages of infection, is not required forS. pyogenes to prevent the influx of neutrophils as the bacteria spread through thefascia.[26] |
| Streptococcal chemokine protease | The affected tissue of patients with severe cases ofnecrotizing fasciitis are devoid of neutrophils.[27] Theserine protease ScpC, which is released byS. pyogenes, is responsible for preventing the migration of neutrophils to the spreading infection. ScpC degrades thechemokineIL-8, which would otherwise attractneutrophils to the site of infection.[25][26] |
The genomes of different strains were sequenced (genome size is 1.8–1.9 Mbp),[28] encoding about 1700-1900 proteins (1700 in strain NZ131,[29][30] 1865 in strain MGAS5005[31][32]). Complete genome sequences of the type strain ofS. pyogenes (NCTC 8198T =CCUG 4207T) are available inDNA Data Bank of Japan,European Nucleotide Archive, andGenBank under the accession numbersLN831034 andCP028841.[33]
Biofilms are a way forS. pyogenes, as well as other bacterial cells, to communicate with each other. In the biofilm gene expression for multiple purposes (such as defending against the host immune system) is controlled viaquorum sensing.[34] One of the biofilm forming pathways in GAS is the Rgg2/3 pathway. It regulates SHP's (short hydrophobic peptides) that are quorum sensing pheromones, a.k.a. autoinducers. The SHP's are translated to an immature form of the pheromone and must undergo processing, first by a metalloprotease enzyme inside the cell and then in the extracellular space, to reach their mature active form. The mode of transportation out of the cell and the extracellular processing factor(s) are still unknown. The mature SHP pheromone can then be taken into nearby cells and the cell it originated from via a transmembrane protein, oligopeptide permease.[34] In the cytosol the pheromones have two functions in the Rgg2/3 pathway. Firstly, they inhibit the activity of Rgg3 which is a transcriptional regulator repressing SHP production. Secondly, they bind another transcriptional regulator, Rgg2, that increases the production of SHP's, having an antagonistic effect to Rgg3. SHP's activating their own transcriptional activator creates a positive feedback loop, which is common for the production for quorum sensing peptides. It enables the rapid production of the pheromones in large quantities. The production of SHP's increases biofilm biogenesis.[34] It has been suggested that GAS switches between biofilm formation and degradation by utilizing pathways with opposing effects. Whilst Rgg2/3 pathway increases biofilm, theRopB pathway disrupts it. RopB is another Rgg-like protein (Rgg1) that directly activates SpeB (streptococcal pyrogenic exotoxin B), a cysteine protease that acts as a virulence factor. In the absence of this pathway, biofilm formation is enhanced, possibly due to the lack of the protease degrading pheromones or other Rgg2/3 pathway counteracting effects.[34]
S. pyogenes is the cause of many human diseases, ranging from mild superficial skin infections to life-threatening systemic diseases[35].
When the infection is of the throat,S. pyogenes causespharyngitis which is also known as strep throat. In rare cases, strep throat can develop into a condition known asscarlet fever. most striking symptom is a strawberry-like rash on the tongue.
Infections of the skin range from mild to life-threatening. Superficial infections ofS. pyogenes infections include and localized skin infection non-bullous (impetigo).Erysipelas andcellulitis are characterized by multiplication and lateral spread ofS. pyogenes in deep layers of the skin.S. pyogenes invasion and multiplication in thefascia beneath the skin can lead tonecrotizing fasciitis, a life-threatening surgical emergency.[36][37]
Colonization of the vagina by S. pyogenes can cause several illnesses, depending on the circumstances. The bacterium is a major cause ofpueperal fever in the mother[38] andinfection in newborns[39]. Newborns are susceptible to some forms of the infection that are rarely seen in adults, includingmeningitis.[40][41] Toxins produced byS. pyogenes may lead to streptococcaltoxic shock syndrome, a life-threatening emergency.[2]
Like many pathogenic bacteria,S. pyogenes may colonize a healthy person's respiratory system without causing disease, existing as acommensal member of the respiratory microbiota. It is commonly found in some populations as part of the mixedmicrobiome of the upper respiratory tract. Individuals who have the bacterium in their bodies but no signs of disease are known asasymptomatic carriers.[42][43][44] The bacteria may start to cause disease when the host's immune system weakens, such as during a viral respiratory infection, which may lead toS. pyogenessuperinfection.[43][44]
S. pyogenes can also cause disease in the form of post-infectious "non-pyogenic" (not associated with local bacterial multiplication and pus formation) syndromes. Theseautoimmune-mediated complications (sequela) follow a small percentage of infections and includerheumatic fever and acutepost-infectious glomerulonephritis. Both conditions appear several weeks following the initial streptococcal infection.S. pyogenes infections are commonly associated with the release of one or more bacterialtoxins. The release of endotoxins from throat infections has been linked to the development of scarlet fever which can lead to rheumatic fever.[7] Rheumatic fever is characterized by inflammation of the joints and/or heart following an episode ofstreptococcal pharyngitis. Acute glomerulonephritis, inflammation of therenal glomerulus, can follow streptococcal pharyngitis or skin infection.[45]
S. pyogenes is sensitive topenicillin, and has not developedresistance to it,[46] making penicillin a suitableantibiotic to treat infections caused by this bacterium. Failure of treatment with penicillin is generally attributed to other local commensal microorganisms producingβ-lactamase, or failure to achieve adequate tissue levels in the pharynx. Certain strains have developed resistance tomacrolides,tetracyclines, andclindamycin.[47]
There is a polyvalent inactivated vaccine against several types ofStreptococcus includingS. pyogenes called "vacuna antipiogena polivalente BIOL". It is recommended to be administered in a 5 week series. Two weekly applications are made at intervals of 2 to 4 days. The vaccine is produced by the Instituto Biológico Argentino.[48]
There is another potential vaccine being developed; the vaccine candidate peptide is called StreptInCor.[49]
ManyS. pyogenes proteins have unique properties, which have been harnessed in recent years to produce a highly specific "superglue"[50][51] and a route to enhance the effectiveness ofantibody therapy.[52]
TheCRISPR system from this organism[53] that is used to recognize and destroyDNA from invading viruses, thus stopping the infection, was appropriated in 2012 for use as a genome-editing tool that could potentially alter any piece of DNA and laterRNA.[54]
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