Epidemiology[edit]
S. pyogenes typically colonizes the throat, genital mucosa, rectum, and skin. Of healthy individuals, 1% to 5% have throat, vaginal, or rectal carriage. In healthy children, such carriage rate varies from 2% to 17%. There are four methods for the transmission of this bacterium: inhalation of respiratory droplets, skin contact, contact with objects, surface, or dust that is contaminated with bacteria or, less commonly, transmission through food. Such bacteria can cause a variety of diseases such as streptococcal pharyngitis, rheumatic fever, rheumatic heart disease, and scarlet fever. Although pharyngitis is mostly viral in origin, about 15 to 30% of all pharyngitis cases in children are caused by GAS; meanwhile, 5 to 20% of pharyngitis in adults are streptococcal. The number of pharyngitis cases is higher in children when compared with adults due to exposures in schools, nurseries, and as a consequence of lower host immunity. Such cases Streptococcal pharyngitis occurs more frequently from December to April (later winter to early spring) in seasonal countries, possibly due to changing climate, behavioural changes or predisposing viral infection. Disease cases are the lowest during autumn.[7]
MT1 (metabolic type 1) clone is frequently associated with invasive Streptococcus pyogenes infections among developed countries. The incidence and mortality of S. pyognes was high during the pre-penicillin era, but had already started to fall prior to the widespread availability of penicillin. Therefore, environmental factors do play a role in the S. pyogenes infection. Incidence of S. pyogenes is 2 to 4 per 100,000 population in developed countries and 12 to 83 per 100,000 population in developing countries. S. pyogenes infection is more frequently found in men than women, with highest rates in the elderly, followed by infants. In people with risk factors such as heart disease, diabetes, malignancy, blunt trauma, surgical incision, virus respiratory infection, including influenza, S. pyogenes infection happens in 17 to 25% of all cases. GAS secondary infection usually happens within one week of the diagnosis of influenza infection. In 14 to 16% of childhood S. pyogenes infections, there is a prior chickenpox infection. Such S. pyogenes infection in children usually manifests as severe soft tissue infection with onset 4 to 12 days from the chickenpox diagnosis. There is also 40 to 60 times increase in risk of S. pyogenes infection within the first two weeks of chickenpox infection in children. However, 20 to 30% of S. pyogenes infection does occur in adults with no identifiable risk factors. The incidence is higher in children (50 to 80% of S. pyogenes infection) with no known risk factors. The rates of scarlet fever in UK was usually 4 in 100,000 population, however, in 2014, the rates had risen to 49 per 100,000 population. Rheumatic fever and rheumatic heart disease (RHD) usually occurs at 2 to 3 weeks after the throat infection, which is more common among the impoverished people in developing countries. From 1967 to 1996, the global mean incidence of rheumatic fever and RHD was 19 per 100,000 with the highest incidence at 51 per 100,000.[7]
Maternal S. pyogenes infection usually happens in late pregnancy; at more than 30 weeks of gestation to four weeks post partum, which accounts for 2 to 4% of all the S. pyogenes infections. This represents 20 to 100 times increase in risk for S. pyogenes infections. Clinical manifestations are: pneumonia, septic arthritis, necrotizing fasciitis, and genital tract sepsis. According to a study done by Queen Charlotte's hospital in London during the 1930s, the vagina was not the common source of such infection. On the contrary, maternal throat infection and close contacts with carriers were the more common sites for maternal S. pyogenes infection.[7]
Bacteriology[edit]
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 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.[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 encode 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] |
Genome[edit]
The genome of different strains were sequenced (genome size is 1.8–1.9 Mbp)[25] encoding about 1700-1900 proteins (1700 in strain NZ131,[26][27] 1865 in strain MGAS5005[28][29]).
Disease[edit]
S. pyogenes is the cause of many human diseases, ranging from mild superficial skin infections to life-threatening systemic diseases.[2] Infections typically begin in the throat or skin. The most striking sign is a strawberry-like rash. 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 life-threatening condition requiring surgery.[citation needed] [30] The bacterium is found in neonatal infections.[31]
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.[2]
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 post-infectious glomerulonephritis. Both conditions appear several weeks following the initial streptococcal infection. Rheumatic fever is characterized 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.
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