Materiały źródłowe

• #1 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-Causes-Strep-Throat.aspx

  Beta-hemolytic group A streptococcus or Streptococcus pyogenes, a gram-positive human pathogen that habitually colonizes the throat or skin of the host, is a cause of streptococcal pharyngitis more commonly known as strep throat. Infections with this microorganism are underpinned by a panoply of virulence factors that are produced in direct response to environmental signals in the host. […] Adherence and subsequent growth of Streptococcus pyogenes on pharyngeal mucosal surfaces are usually sufficient to cause the clinical entity of streptococcal pharyngitis. Adhering to epithelial cells is a prerequisite event in the disease pathogenesis, which is facilitated by fibronectin-binding protein or protein F (although M-protein and peptidoglycan may also contribute). […] Together with M-protein, think capsules formed of hyaluronic acid found in some strains of Streptococcus pyogenes confer resistance to phagocytosis. The microorganism can also stimulate T cell responses and cytokine induction, resulting in fever and further tissue injury. This can be especially important in the development of complications that can be provoked by certain strains of streptococci.

• #1 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-Causes-Strep-Throat.aspx

  The immunological response of the host to streptococcal infection is characterized by the production of antibodies against a myriad of streptococcal cellular and extracellular constituents. Host responses against the aforementioned M-protein serotype can protect from reinfection with that specific serotype.

• #2 Pathogenesis, epidemiology and control of Group A Streptococcus infection | Nature Reviews Microbiology

  https://www.nature.com/articles/s41579-023-00865-7

  Streptococcus pyogenes (Group A Streptococcus; GAS) is exquisitely adapted to the human host, resulting in asymptomatic infection, pharyngitis, pyoderma, scarlet fever or invasive diseases, with potential for triggering post-infection immune sequelae. […] GAS deploys a range of virulence determinants to allow colonization, dissemination within the host and transmission, disrupting both innate and adaptive immune responses to infection. […] The recent identification of clinical GAS isolates with reduced penicillin sensitivity and increasing macrolide resistance threatens both frontline and penicillin-adjunctive antibiotic treatment. […] This paper reports demonstrating that SpeB triggers keratinocyte pyroptosis by cleaving GSDMA, providing a mechanism for inflammatory response stimulation at the epithelial cell layer.

• #2 Pathogenesis, epidemiology and control of Group A Streptococcus infection | Nature Reviews Microbiology

  https://www.nature.com/articles/s41579-023-00865-7

  This study utilizes biomimetic virulomics to show that GAS S protein captures lysed red blood cell membranes to cloak the bacterial cell surface, which allows bacteria to evade host immunity. […] This comprehensive report demonstrates that M1 protein triggers caspase 1-dependent NLRP3 inflammasome activation, leading to pyroptotic macrophage cell death. […] This comprehensive report details the molecular basis of natural selection of hypervirulent bacterial variants with increased risk of systemic dissemination. […] This important study demonstrates that epithelial cytokine IL-36 is a global sensor of pathogen-derived proteases during epithelial infection. […] This work demonstrates how GAS exploits neuro-immunological signalling to cause invasive infection. […] This study uses a combination of in vitro evolution and metabolic rescue experiments to demonstrate that a new antimicrobial resistance mechanism undetectable using traditional laboratory testing methods is responsible for high levels of resistance to sulfamethoxazole in GAS.

• #3 Pathogenesis of Group A Streptococcal Infections

  https://pmc.ncbi.nlm.nih.gov/articles/PMC88944/

  Group A streptococci are model extracellular gram-positive pathogens responsible for pharyngitis, impetigo, rheumatic fever, and acute glomerulonephritis. […] The strong resistance of the group A streptococcus to phagocytosis is related to factor H and fibrinogen binding by M protein and to disarming complement component C5a by the C5a peptidase. […] Molecular mimicry appears to play a role in autoimmune mechanisms involved in rheumatic fever, while nephritis strain-associated proteins may lead to immune-mediated acute glomerulonephritis. […] The adhesion process involves multiple group A streptococcal adhesins reported by several investigators as detailed below and described in excellent reviews. […] High-frequency invasion requires expression of M protein and/or fibronectin-binding proteins such as SfbI.

• #3 Pathogenesis of Group A Streptococcal Infections

  https://pmc.ncbi.nlm.nih.gov/articles/PMC88944/

  It is well established that group A streptococci are antiphagocytic due to surface exposed M protein and hyaluronic acid capsule. […] The antiphagocytic behavior of group A streptococci is also mediated by the binding of fibrinogen to the surface of M protein. […] The group A streptococcal capsule is composed of a polymer of hyaluronic acid containing repeating units of glucuronic acid and N-acetylglucosamine. […] The M protein is a major surface protein and virulence factor of group A streptococci, with more than 80 distinct serotypes identified. […] The M protein extends from the cell surface as an alpha-helical coiled-coil dimer which appears as fibrils on the surface of group A streptococci. […] The M proteins inhibit phagocytosis, which is a primary virulence mechanism for survival in tissues.

• #3 Pathogenesis of Group A Streptococcal Infections

  https://pmc.ncbi.nlm.nih.gov/articles/PMC88944/

  The C5a peptidase is a proteolytic enzyme found on the surface of group A streptococci. […] The C5a peptidase cleaves the complement-derived chemotaxin C5a at its PMN-binding site. […] The C5a peptidase is encoded by a gene which is regulated by mga in concert with M protein. […] The M protein has been and will continue to be the subject of intensive investigation due to its role as a major virulence factor and its potential as a vaccine against streptococcal infections.

• #4 Pathogenesis of Group A Streptococcal Infections – Anna Henningham – Discovery Medicine

  https://www.discoverymedicine.com/Anna-Henningham/2012/05/16/pathogenesis-of-group-a-streptococcal-infections/

  Group A Streptococcus (GAS; Streptococcus pyogenes) is a Gram-positive human pathogen which typically colonizes the throat or skin of the host. […] GAS diseases are underpinned by an extensive repertoire of virulence determinants that are differentially regulated in direct response to a battery of environmental signals within the host. […] The trigger for rapidly progressive invasive GAS disease has also been linked to the capacity of GAS to hijack host molecules for redeployment as virulence factors. […] It is thought there are three stages in the pathogenesis of GAS pharyngitis: i) adherence to the host pharyngeal epithelial tissue, often followed by invasion into and persistence in host epithelial cells, ii) nutrient acquisition to enable proliferation in the host, and iii) evasion of the host immune response.

• #4 Pathogenesis of Group A Streptococcal Infections – Anna Henningham – Discovery Medicine

  https://www.discoverymedicine.com/Anna-Henningham/2012/05/16/pathogenesis-of-group-a-streptococcal-infections/

  Several adhesins and GAS molecules have been implicated in GAS adhesion to and invasion of host epithelial cells (both cutaneous and mucosal) including C5a peptidase, FbaA, FBP54, hyaluronic acid capsule, Lbp, Lsp, LTA, M protein, pili, Protein F1, Protein F2, SEN, SlaA, and SOF. […] Intracellular persistence of GAS has been linked to recurrent cases of pharyngitis and may potentially contribute to the failure of penicillin during treatment. […] In addition to the capacity to internalize into host cells, GAS strains have evolved a number of other mechanisms to avoid the host immune response. […] The transition from superficial to invasive infection requires substantial changes in gene expression to facilitate bacterial evasion of sub-epithelial innate immune functions and dissemination into deeper tissues.

• #5 Pharyngitis

  https://www.atsu.edu/faculty/chamberlain/website/lectures/lecture/uriphyn.htm

  In viral pharyngitis, viruses gain access to the mucosal cells lining the nasopharynx and replicate in these cells. Damage to the host is often caused by damage to the cells where the viruses are replicating. […] In bacterial pharyngitis, S pyogenes attaches to the mucosal epithelial cells using M protein, lipoteichoic acid, and fibronectin-binding protein (protein F). It has a capsule composed of hyaluronic acid that prevents phagocytosis by host macrophages; because the hyaluronic acid in the bacterial capsule is identical to host hyaluronic acid. The capsule facilitates bacterial survival by covering the bacterial antigens. Extracellular factors produced by S pyogenes during the infection include protease and hyaluronidase. These extracellular factors assist the bacteria in invading the mucosa. Direct extension to other sites can occur but due to the use of antibiotic therapy, this is now quite rare.

• #5 Pharyngitis

  https://www.atsu.edu/faculty/chamberlain/website/lectures/lecture/uriphyn.htm

  Nonsuppurative lesions resulting in rheumatic fever and glomerulonephritis still occur following throat infections caused by S pyogenes. It is believed that several bacterial antigens from S pyogenes share antigenic epitopes with the heart and renal tissues. An autoimmune reaction occurs in some patients following production of an immune response to these cross-reactive bacterial antigens and damages the patients heart or kidneys. Note: Rheumatic fever and glomerulonephritis can occur after an episode of pharyngitis; only glomerulonephritis occurs after skin infections (e.g., impetigo).

• #6

  https://journal.uokufa.edu.iq/index.php/ajb/article/view/11796

  Streptococcus pyogenes is a Gram-positive beta-hemolytic bacteria, also known as group A streptococci, that causes a range of infections. The most common presentation is acute pharyngitis. GAS can be subdivided into 100 serotypes by the M-protein antigen that is located on the cell surface and by fimbriae (hairlike fuzz) that project from the outer edge of the cell. […] GAS produce and release into the surrounding medium a large number of biologically active extracellular products. Some of these are toxic for human and other mammalian cells. Streptolysin S (SLS) is a small oxygen-stabile toxin responsible for -hemolysis of GAS on blood agar, while streptolysin O (SLO) is an oxygen-labile, cholesterol-dependent toxin. Both SLS and SLO injure cell membranes, not only lysing red blood cells, but also damaging other eukaryotic cells and membranous subcellular organelles. […] Streptococcal pyrogenic exotoxins (SPEs) are secreted factors with the capacity to act as superantigens and trigger T-cell proliferation and cytokine release.

• #7 Bacterial Pharyngitis: Background, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/225243-overview

  Adhesins enable GABHS attachment at sites such as the pharynx. This attachment allows for colonization and competition with normal host flora. […] Some strains produce erythrogenic toxins, which cause the rash of scarlet fever in susceptible hosts. […] GABHS is spread from person to person through large droplet nuclei. […] Consequently, close quarters (eg, barracks, daycares, dormitories) facilitate transmission. […] The risk of acquiring GABHS from an infected family member is 40%, and nearly 1 in 4 infected individuals eventually exhibit symptoms. […] GABHS pharyngitis may also cause suppurative and nonsuppurative complications. Invasion of nearby structures may cause suppurative complications such as otitis media, sinusitis, peritonsillar abscess, retropharyngeal abscess, and cervical adenitis. Nonsuppurative complications of bacterial pharyngitis include rheumatic heart disease and poststreptococcal glomerulonephritis.

• #7 Bacterial Pharyngitis: Background, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/225243-overview

  Beta-hemolytic streptococci have the ability to cause large zones of hemolysis on blood agar, aiding in microbiological identification. […] Perhaps the most important virulence factor of GABHS is the M protein. This protein, located peripherally on the cell wall, is required for invasive infection. T cells exposed to this M protein are postulated to cross-react with similar epitopes on human cardiac myosin and laminin, contributing to the pathogenesis of rheumatic heart disease. […] GABHS contains a hyaluronic acid capsule, which also plays an important role in infection. […] Certain GABHS exotoxins act as superantigens by up-regulating T cells. […] These superantigens can prompt a release of proinflammatory cytokines and may synergize with lipopolysaccharide. It has been speculated that these superantigens evade the pharyngeal immune response, resulting in proliferation of GABHS while permitting immune-mediated elimination of commensal organisms.

• #8 Pathogenesis, epidemiology and control of Group A Streptococcus infection

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9998027/

  The hyaluronic acid capsule of GAS is composed of repeating disaccharide units of glucuronic acid and N-acetylglucosamine and confers the characteristic wet mucoid colony morphology. The GAS capsule is structurally identical to human hyaluronic acid, a major component of extracellular matrices found in many body tissues including connective and epithelial tissues. The GAS capsule therefore acts to camouflage the pathogen from the host immune system. […] GAS has evolved many ingenious strategies to avoid immune clearance. A new form of molecular mimicry has recently been described, in which a highly conserved surface-associated protein (S protein) was shown to selectively bind red blood cell membranes. S protein-dependent membrane coating of the GAS cell surface protects against phagocytic killing, providing a critical link between the characteristic haemolytic activity of this pathogen and an immune camouflage strategy that might help facilitate blood survival and dissemination.

• #8 Pathogenesis, epidemiology and control of Group A Streptococcus infection

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9998027/

  Almost all clinical isolates of GAS secrete two potent cytolytic toxins, streptolysin S (SLS) and streptolysin O (SLO), that cause pore formation in eukaryotic cell membranes. Both cytolysins are cytotoxic against a wide range of host cells, including epithelial and immune cells. Various functions have been assigned to SLS and SLO, ranging from soft-tissue damage, tissue invasion and innate immune evasion to the activation of pro-inflammatory responses. […] The broad substrate specificity of SpeB leads to cleavage of a wide range of host and bacterial proteins, including intercellular barrier proteins at epithelial junctions, host extracellular matrix proteins, complement factors, the cathelicidin-derived antimicrobial peptide LL-37, autophagy components and chemokines. SpeB also displays pro-inflammatory properties by directly cleaving and activating the precursors of IL-1 and epithelial IL-36, two potent pro-inflammatory cytokines that are critical for host defence responses to infection and injury. Another recently discovered pro-inflammatory mechanism involves the cleavage and activation of pore-forming GSDMA in skin epithelial cells which triggers pyroptosis, a lytic form of inflammatory cell death. […] The coordinated activities of SLO and NADase further prevent maturation of phagolysosomes, inhibit IL-8 secretion and promote GAS survival in macrophages, where streptolysins SLO and SLS and M protein activate the inflammasome pathway to induce IL-1 production and pyroptosis.

• #9 Group A Strep | Caparon Lab | Washington University in St. Louis

  https://caparonlab.wustl.edu/group-a-strep/

  The capsule of S. pyogenes is non-antigenic since it is composed of hyaluronic acid, which is chemically similar to that of host connective tissue. This allows the bacterium to hide its own antigens and to go unrecognized as antigenic by its host. The Hyaluronic acid capsule also prevents opsonized phagocytosis by neutrophils or macrophages. […] Colonization of tissues by S. pyogenes is thought to result from a failure in the constitutive defenses (normal flora and other nonspecific defense mechanisms) which allows establishment of the bacterium at a portal of entry (often the upper respiratory tract or the skin) where the organism multiplies and causes an inflammatory purulent lesion. […] The streptococcal invasins act in a variety of ways summarized in Table 1 at the end of this article. Streptococcal invasins lyse eukaryotic cells, including red blood cells and phagocytes; they lyse other host macromolecules, including enzymes and informational molecules; they allow the bacteria to spread among tissues by dissolving host fibrin and intercellular ground substances.

• #9 Group A Strep | Caparon Lab | Washington University in St. Louis

  https://caparonlab.wustl.edu/group-a-strep/

  Streptococcus pyogenes owes its major success as a pathogen to its ability to colonize and rapidly multiply and spread in its host while evading phagocytosis and confusing the immune system. […] Acute diseases associated with Streptococcus pyogenes occur chiefly in the respiratory tract, bloodstream, or the skin. Streptococcal disease is most often a respiratory infection (pharyngitis or tonsillitis) or a skin infection (pyoderma). Some strains of streptococci show a predilection for the respiratory tract; others, for the skin. Generally, streptococcal isolates from the pharynx and respiratory tract do not cause skin infections. […] S. pyogenes is the leading cause of uncomplicated bacterial pharyngitis and tonsillitis commonly referred to as strep throat. Other respiratory infections include sinusitis, otitis, and pneumonia. Infections of the skin can be superficial (impetigo) or deep (cellulitis). Invasive streptococci cause joint or bone infections, destructive wound infections (necrotizing fasciitis) and myositis, meningitis and endocarditis.

• #9 Group A Strep | Caparon Lab | Washington University in St. Louis

  https://caparonlab.wustl.edu/group-a-strep/

  Three streptococcal pyrogenic exotoxins (SPE), formerly known as Erythrogenic toxin, are recognized: types A, B, C. These toxins act as superantigens by a mechanism similar to those described for staphylococci. […] The occurrence of cross-reactive antigens in S. pyogenes and heart tissues possibly explains the autoimmune responses that develop following some infections. The antibody mediated immune (AMI) response (i.e., level of serum antibody) is higher in patients with rheumatic fever than in patients with uncomplicated pharyngitis.

• #9 Group A Strep | Caparon Lab | Washington University in St. Louis

  https://caparonlab.wustl.edu/group-a-strep/

  Two post streptococcal sequelae, rheumatic fever and glomerulonephritis, may follow streptococcal disease, and occur in 1-3% of untreated infections. These conditions and their pathology are not attributable to dissemination of bacteria, but to aberrant immunological reactions to Group A streptococcal antigens. Scarlet fever and streptococcal toxic shock syndrome are systemic responses to circulating bacterial toxins. […] The cell surface of Streptococcus pyogenes accounts for many of the bacterium’s determinants of virulence, especially those concerned with colonization and evasion of phagocytosis and the host immune responses. […] The M proteins are clearly virulence factors associated with both colonization and resistance to phagocytosis. More than 50 types of S. pyogenes M proteins have been identified on the basis of antigenic specificity, and it is the M protein that is the major cause of antigenic shift and antigenic drift in the Group A streptococci.

• #10 How the strep bacterium hides from the immune system | ScienceDaily

  https://www.sciencedaily.com/releases/2019/12/191203114506.htm

  A bacterial pathogen that causes strep throat and other illnesses cloaks itself in fragments of red blood cells to evade detection by the host immune system, according to a new study. The researchers found that Group A Streptococcus (GAS) produces a previously uncharacterized protein, named S protein, which binds to the red blood cell membrane to avoid being engulfed and destroyed by phagocytic immune cells. […] By arming GAS with this form of immune camouflage, S protein enhances bacterial virulence and decreases survival in infected mice. […] „Our study describes a completely novel mechanism for immune evasion,” says corresponding author David Gonzalez of the University of California, San Diego. […] „These findings suggest that S protein co-opts red blood cell membranes for molecular mimicry, or imitation of host molecules, to evade the immune response,” Gonzalez says.

• #11 Group A Streptococcus – National Collaborating Centre for Infectious Diseases

  https://nccid.ca/debrief/group-a-streptococcus/

  Group A streptococcal disease (GAS) is caused by the bacteria Streptococcus pyogenes (S. pyogenes) gram positive, beta-hemolytic bacteria that can be found on the skin or in the throat. […] Several virulence factors contribute to human infection by GAS via the secretion or release of a variety of extracellular products. The main virulence factors include, but are not limited to, the presence of M protein fragments assisting with GAS colonization, invasions by the toxins streptolysin S and O, bacterial dissemination by streptokinase, and more. […] The vast majority of GAS diseases are mild and non-invasive, such as strep throat (acute pharyngitis), skin and soft tissue infections (e.g., impetigo and cellulitis), and fevers and rashes (e.g., scarlet fever). […] In rare cases, S. pyogenes enter parts of the body where bacteria are not normally found, such as in the blood, deep tissue, or lungs. These infections are called invasive GAS (iGAS) and can lead to severe diseases such as necrotizing fasciitis (flesh eating disease), toxic shock syndrome (TSS), and lung infections (e.g., pneumonia).

• #11 Group A Streptococcus – National Collaborating Centre for Infectious Diseases

  https://nccid.ca/debrief/group-a-streptococcus/

  Strep throat symptoms usually occur within two to five days after being exposed to GAS and can resolve within one week without treatment. However, antibiotic treatment is encouraged to prevent severe manifestations and spreading the bacteria to others. […] In rare cases, strep throat can lead to rheumatic fever, kidney disease, ear and sinus infections, and abscesses around the tonsils or in the neck. […] The incubation period for GAS is not clearly defined and depends on the clinical syndrome. Non-invasive GAS, such as strep throat and scarlet fever, generally have incubation periods of 2 to 5 days, with the exception of impetigo, which has an incubation period of approximately 10 days. […] GAS is generally spread person-to-person by fluid secretions from the nose and throat of an infected person (via coughing or sneezing) or by direct contact with infected wounds on the skin.

• #11 Group A Streptococcus – National Collaborating Centre for Infectious Diseases

  https://nccid.ca/debrief/group-a-streptococcus/

  Diagnoses for GAS are generally made by isolating GAS from a normally sterile site (e.g., blood, tissue from deep inside a wound, cerebrospinal fluid). However, diagnoses vary depending on the clinical syndrome. […] Treatment will vary depending on the type of GAS disease. In the absence of a GAS vaccine, antibiotics (e.g., penicillin, macrolide, or cephalosprin) are used to treat most GAS diseases.

• #12 Strep throat pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Strep_throat_pathophysiology

  Group A strep pharyngitis is most commonly spread through direct person-to-person transmission, typically through saliva or nasal secretions from an infected person. Rarely, contaminated food, especially milk and milk products, can result in outbreaks. The pathogenesis of GAS throat involves adhesion of bacteria to pharyngeal mucosa with the help of adhesins on the surface of organism. It then invades the mucosal tissue by producing various proteases and cytolysins causing inflammation, which manifests as the signs and symptoms of pharyngitis. […] The pathogenesis of GAS in the throat involves adhesion of bacteria to pharyngeal mucosa with the help of adhesins on the surface of organism. […] It then invades the mucosal tissue by producing various proteases and cytolysins causing inflammation manifesting as signs and symptoms of pharyngitis. […] M protein on the surface of group A streptococcal infection plays important role in the pathogenesis of rheumatic fever.

• #13 Pharyngitis | AAFP

  https://www.aafp.org/pubs/afp/issues/2004/0315/p1465.html

  The incidence of complications with GABHS infection, such as rheumatic fever and peritonsillar abscess, is much lower than generally perceived.17 Peritonsillar abscess occurs in fewer than 1 percent of patients treated with antibiotics.1 Patients with peritonsillar abscess typically have a toxic appearance and may present with a hot potato voice, fluctuant peritonsillar mass, and asymmetric deviation of the uvula. However, clinical impression is only moderately accurate in diagnosing peritonsillar abscess (78 percent sensitivity and 50 percent specificity in one series of 14 patients).20 Intraoral ultrasound examination is an accurate diagnostic test if abscess is suspected. […] Rheumatic fever is exceedingly rare in the United States and other developed countries (annual incidence less than one case per 100,000).21 This illness should be suspected in any patient with joint swelling and pain, subcutaneous nodules, erythema marginatum or heart murmur, and a confirmed streptococcal infection during the preceding month. Patients will have an elevated antistreptolysin-O titer and erythrocyte sedimentation rate.

• #13 Pharyngitis | AAFP

  https://www.aafp.org/pubs/afp/issues/2004/0315/p1465.html

  Poststreptococcal glomerulonephritis is another rare complication of GABHS pharyngitis, although treatment with antibiotics does not prevent it. Patients present with hematuria and, frequently, edema in the setting of a recent streptococcal infection with an elevated antistreptolysin-O titer. […] Scarlet fever is associated with GABHS pharyngitis and usually presents as a punctate, erythematous, blanchable, sandpaper-like exanthem. The rash is found in the neck, groin, and axillae, and is accentuated in body folds and creases (Pastias lines).1,4,19 The pharynx and tonsils are erythematous and covered with exudates. The tongue may be bright red with a white coating (strawberry tongue).4

• #13 Pharyngitis | AAFP

  https://www.aafp.org/pubs/afp/issues/2004/0315/p1465.html

  The 2000 National Ambulatory Medical Care Survey found that acute pharyngitis accounts for 1.1 percent of visits in the primary care setting and is ranked in the top 20 reported primary diagnoses resulting in office visits.3 Peak seasons for sore throat include late winter and early spring.4 Transmission of typical viral and GABHS pharyngitis occurs mostly by hand contact with nasal discharge, rather than by oral contact.7,8 Symptoms develop after a short incubation period of 24 to 72 hours. […] GABHS is the most common bacterial cause of pharyngitis.1618 […] Symptoms of strep throat may include pharyngeal erythema and swelling, tonsillar exudate, edematous uvula, palatine petechiae, and anterior cervical lymphadenopathy. Untreated, GABHS infection lasts seven to 10 days.4,13,19 Patients with untreated streptococcal pharyngitis are infectious during the acute phase of the illness and for one additional week.1 Effective antibiotic therapy shortens the infectious period to 24 hours, reduces the duration of symptoms by about one day, and prevents most complications.

• #14 Strep Throat – lji.org

  https://www.lji.org/diseases/strep-throat/

  Strep throat is one of a several conditions, among them pneumonia, scarlet fever, impetigo, and flesh-eating necrotizing fasciitis, caused by the bacterium Streptococcus pyogenes, better known as group A Streptococcus (GAS). […] Recurrent strep throat in children is also a problem worldwide. Even after antibiotic treatment, some children who experience recurrent strep will need to have their tonsils removed. […] Work from the lab of LJI vaccinologist Shane Crotty, Ph.D., suggests that recurrent tonsillitis (or strep throat) has a genetic basis. […] Their goal was to identify immune activities potentially unique to either susceptibility group, with a focus on specialized sites called germinal centers, which reside in tonsils and other lymph nodes. […] Interestingly, children with recurrent tonsillitis had consistently smaller germinal center areas than did children with a normal rate of infection.

• #14 Strep Throat – lji.org

  https://www.lji.org/diseases/strep-throat/

  Moreover, evaluation of a large number of children hinted that conditions associated with recurrent strep susceptibility runs in families, suggesting a genetic component. […] Crotty and Dan have since conducted genetic testing and identified two specific genetic variants in the HLA genomic regionone variant that is associated with increased susceptibility to recurrent tonsillitis and another that protects against the disease. […] These LJI-led studies suggest molecular strategies to make a novel vaccine to stimulate a protective immune response and prevent recurring bouts of strep throat.

• #15

  https://healthmatch.io/strep-throat

  Strep throat is caused by an infection with a bacteria called group A Streptococcus pyogenes, or Strep. The infection affects the tonsils and back of the throat, causing an acute sore throat and potentially other symptoms. […] The primary reason for treating strep pharyngitis is to prevent rheumatic heart disease, which can lead to serious problems with the valves in your heart. […] One study showed that children with recurring strep throat produced fewer antibodies to Strep bacterial toxin and may also have been producing cytotoxic T cells that were harming their B immune cells. […] In other words, there is a genetic immune system dysfunction involved. […] The bacteria primarily lives in the throat and can be spread through saliva or nasal secretions. […] Strep throat is highly contagious.

• #15

  https://healthmatch.io/strep-throat

  The incubation period is two to five days before you show symptoms. […] Once you have started antibiotics, you are unlikely to still be contagious after 12 hours. […] In rare cases, the bacteria may move through the bloodstream and lymphatic system to other body parts, causing an invasive strep infection. […] These life-threatening conditions most often occur in people with chronic illnesses such as cancer, diabetes, and kidney failure or in those immunocompromised or on steroids. […] Another sequela of strep infections is post-streptococcal glomerulonephritis (PSGN), although it is uncommon. […] This complication is also caused by a dysfunctional immune system response that damages the kidneys.

• #16 Clinical Guidance for Group A Streptococcal Pharyngitis | Group A Strep | CDC

  https://www.cdc.gov/group-a-strep/hcp/clinical-guidance/strep-throat.html

  Group A streptococcal pharyngitis is an infection of the oropharynx caused by Streptococcus pyogenes (group A strep bacteria). […] The incubation period of group A strep pharyngitis is approximately 2 to 5 days. […] Suppurative complications result from the spread of group A strep bacteria from the pharynx to adjacent structures. […] Nonsuppurative sequelae of group A strep pharyngitis include: Acute rheumatic fever, Post-streptococcal glomerulonephritis. […] These complications occur after the original infection resolves and involve sites distant to the initial group A strep infection site. They’re thought to be the result of the immune response and not of direct group A strep infection.

• #17 Streptococcal pharyngitis – Wikipedia

  https://en.wikipedia.org/wiki/Streptococcal_pharyngitis

  Strep throat is caused by group A -hemolytic Streptococcus (GAS or S. pyogenes). Humans are the primary natural reservoir for group A streptococcus. Other bacteria such as nongroup A -hemolytic streptococci and fusobacterium may also cause pharyngitis. It is spread by direct, close contact with an infected person; thus crowding, as may be found in the military and schools, increases the rate of transmission. Dried bacteria in dust are not infectious, although moist bacteria on toothbrushes or similar items can persist for up to fifteen days. Contaminated food can result in outbreaks, but this is rare. Of children with no signs or symptoms, 12% carry GAS in their pharynx, and, after treatment, approximately 15% of those remain positive, and are true „carriers”. […] The primary reason for treatment with antibiotics is to reduce the risk of complications such as rheumatic fever and retropharyngeal abscesses. Antibiotics prevent acute rheumatic fever if given within 9 days of the onset of symptoms. […] Appropriate antibiotics decrease the average 3-5 day duration of symptoms by about one day, and also reduce contagiousness. They are primarily prescribed to reduce rare complications such as rheumatic fever and peritonsillar abscess.

• #18 Group A Streptococcus Treatment and Management

  https://www.uspharmacist.com/article/group-a-streptococcus-treatment-and-management

  Suppurative infections seen with GAS pharyngitis include tonsillopharyngeal cellulitis or abscess, otitis media, sinusitis, necrotizing fasciitis, bacteremia, meningitis, brain abscess, and jugular vein septic thrombophlebitis. […] Nonsuppurative complications of GAS pharyngitis include acute rheumatic fever, poststreptococcal reactive arthritis, scarlet fever, streptococcal toxic shock syndrome, acute glomerulonephritis, and pediatric autoimmune neuropsychiatric disorder associated with GAS.

• #18 Group A Streptococcus Treatment and Management

  https://www.uspharmacist.com/article/group-a-streptococcus-treatment-and-management

  GAS is the most common bacterial cause of streptococcal pharyngitis in children and young adults and peaks in winter and early to mid spring. […] A recent meta-analysis showed that the prevalence of GAS pharyngitis in children aged younger than 5 years was 24%; in those aged younger than 18 years who presented to an outpatient center for treatment, it was 37%. […] Many regions of the world with low income and poor infrastructure continue to suffer a high burden of S pyogenes diseases, with millions of deaths annually. […] The majority of these deaths follow the development of rheumatic heart disease (RHD), which remains a concern in both developed and developing countries. […] However, the majority of S pyogenes associated deaths are attributed to the clinical manifestations associated with invasive disease.

• #19 Strep throat – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/strep-throat/symptoms-causes/syc-20350338

  Strep throat is caused by infection with a bacterium known as Streptococcus pyogenes, also called group A streptococcus. […] Streptococcal bacteria are contagious. They can spread through droplets when someone with the infection coughs or sneezes, or through shared food or drinks. You can also pick up the bacteria from a doorknob or other surface and transfer them to your nose, mouth or eyes. […] Strep throat can lead to serious complications. Antibiotic treatment reduces the risk. […] Strep bacteria may spread, causing infection in: Tonsils, Sinuses, Skin, Blood, Middle ear. […] Strep infection may lead to inflammatory illnesses, including: Scarlet fever, a streptococcal infection characterized by a prominent rash, Inflammation of the kidney (poststreptococcal glomerulonephritis), Rheumatic fever, a serious inflammatory condition that can affect the heart, joints, nervous system and skin, Poststreptococcal reactive arthritis, a condition that causes inflammation of the joints.

• #19 Strep throat – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/strep-throat/symptoms-causes/syc-20350338

  A possible relationship has been suggested between strep infection and a rare condition called pediatric autoimmune neuropsychiatric disorder associated with group A streptococci (PANDAS). Children with this condition experience worsened symptoms of neuropsychiatric conditions, such as obsessive-compulsive disorder or tic disorders, with strep. This relationship currently remains unproved and controversial.

• #20 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-is-Strep-Throat.aspx

  Streptococcus pyogenes is an extracellular Gram-positive pathogen of major clinical importance, as it can trigger postinfectious syndromes such as acute rheumatic fever and post-streptococcal glomerulonephritis approximately one to three weeks after the infection of the pharynx. […] The nonsuppurative sequelae such as acute rheumatic fever, acute post-streptococcal glomerulonephritis, and reactive arthritis are well-recognized complications of strep throat, albeit the underlying pathogenic mechanisms are still poorly understood. […] Molecular mimicry is thought to play a significant role in these processes.

• #21 Rheumatic fever – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/rheumatic-fever/symptoms-causes/syc-20354588

  Rheumatic fever can happen after a throat infection from group A streptococcus bacteria, also called strep bacteria. The bacteria cause strep throat and scarlet fever. Improperly treated strep throat or scarlet fever infections cause rheumatic fever. […] How a strep infection causes rheumatic fever isn’t clear. It may be that the bacteria trick the body’s immune system into attacking healthy tissue. This usually happens in the heart, joints, skin and central nervous system. The incorrect immune system reaction causes swelling of joints and tissues. This swelling is called inflammation.

• #22 PANDAS (Pediatric autoimmune neuropsychiatric disorders associated with streptococcus infections) – Autoimmune Association

  https://autoimmune.org/disease-information/pandas-pediatric-autoimmune-neuropsychiatric-disorders-associated-with-streptococcus/

  PANDAS (Pediatric autoimmune neuropsychiatric disorders associated with Streptococcus) is a neurological and psychiatric condition in which symptoms are brought on or worsened by a Streptococcal (strep) infection. […] The underlying cause of PANDAS is unclear, but studies suggest that a strep infection causes an abnormal immune response resulting in neuropsychiatric symptoms.

• #23 Acute rheumatic fever – Health New Zealand | Te Whatu Ora

  https://www.tewhatuora.govt.nz/for-health-professionals/clinical-guidance/communicable-disease-control-manual/acute-rheumatic-fever

  Group A Streptococcus (GAS) infection ranks in the top 10 infectious causes of global mortality and results in at least half a million deaths per year. Along with invasive GAS infections, acute rheumatic fever (ARF) and subsequent rheumatic heart disease (RHD) in low- and middle-income countries account for most of the burden of disease. In high-income countries rates of ARF and RHD are lower overall, but in Indigenous communities and those experiencing socioeconomic deprivation, higher rates persist. […] Infection with GAS bacteria precedes the development of acute rheumatic fever (ARF) in susceptible people. […] Acute rheumatic fever is a multi-organ inflammatory condition that can follow a GAS infection in susceptible people. In susceptible people, a GAS infection leads to an immune response which becomes dysregulated and self-reactive. During this unbalanced reaction, the immune system makes antibodies against GAS bacteria which may be damaging to parts of the body.

• #23 Acute rheumatic fever – Health New Zealand | Te Whatu Ora

  https://www.tewhatuora.govt.nz/for-health-professionals/clinical-guidance/communicable-disease-control-manual/acute-rheumatic-fever

  Exactly why this immune system response occurs is unknown, but possible reasons are: parts of the GAS bacteria cell wall look similar to antigens in normal heart tissue – as the immune system cannot tell the difference, it creates autoantibodies that damage the heart while mounting an immune response to the bacteria; the GAS bacteria interact with collagen in the heart and other body tissue, altering its shape and inducing an autoimmune response. […] A strong association exists between GAS throat infections (pharyngitis or sore throat) and ARF. However, the pathogenesis of ARF is not completely understood. There is also an association between GAS skin infections and an increased risk of ARF in Aotearoa New Zealand and Australia, but the role of skin infections in ARF has not yet been established. The contributions of asymptomatic GAS throat infections and infections with other Streptococci (groups C and G) to the development of ARF is uncertain.

• #24 Strep A Test: MedlinePlus Medical TestLock

  https://medlineplus.gov/lab-tests/strep-a-test/

  Group A Streptococcus, also known as group A strep, is a type of bacteria that often lives in the nose and throat. It causes strep throat and other infections. Strep throat is an infection that affects the throat and tonsils. […] The infection can spread from person to person through the air, for example from being close to someone who is coughing or sneezing. It can also spread when you touch something that has the bacteria on it and then touch your eyes, mouth, or nose. Another way you can get it is if you share a glass, straw, or utensils with someone who has the infection. […] Once you have been exposed to the group A strep bacteria, it usually takes two to five days before you start to feel sick. […] Strep throat can be easily treated with antibiotics. But if it’s not treated, strep throat can lead to serious health problems (complications). These include rheumatic fever, a disease that can damage the heart and joints, and glomerulonephritis, a type of kidney disease.

• #25 Strep throat > Fact Sheets > Yale Medicine

  https://www.yalemedicine.org/conditions/strep-throat

  Highly contagious, strep throat is spread through airborne droplets (sneezing, coughing, sharing food, drink or utensils). […] If your child’s test comes back positive for strep, antibiotic treatment is required. The medication helps prevent rare but serious complications, including rheumatic fever. […] Penicillin or amoxicillin are typically the first antibiotics a doctor will try, usually for a course of ten days. […] Although rare, complications of strep throat may include inflammation of the kidneys, scarlet fever, rheumatic fever, and abscesses near the tonsils.

• #26 Strep Throat: Symptoms, Causes, Diagnosis & Treatment

  https://my.clevelandclinic.org/health/diseases/4602-strep-throat

  Strep throat is an infection in your throat and tonsils caused by a type of bacteria called group A Streptococcus (group A strep). Strep throat causes severe inflammation and a sore throat. Strep throat gets its name from the type of bacteria that causes it group A Streptococcus. There are more than 120 strains of group A Streptococcus bacteria. Strep throat is a type of group A streptococcal (GAS) infection. Strep throat is very contagious. Some people with the infection don’t have symptoms or look sick. But even if you don’t have symptoms, you can still easily spread the infection to others. However, people who exhibit symptoms or appear sick are more contagious than people who don’t have symptoms. Strep throat spreads from person to person very easily, especially among members of the same household. You can spread the bacteria that causes strep throat to other people through respiratory droplets and direct contact. The bacteria that cause strep throat often live in your nose and throat. When you sneeze, cough or talk, you can spread the infection through respiratory droplets. The incubation period for strep throat is two to five days. An incubation period is the time between when you get infected and when symptoms develop. You can spread the infection to others during this time. If you’re taking antibiotics, you won’t be contagious after the first 24 to 48 hours of treatment. Strep throat treatment includes antibiotics. An antibiotic is a type of medicine that kills the bacteria that cause an infection. Penicillin and amoxicillin are common antibiotics healthcare providers use to treat strep throat. If you’re allergic to penicillin, the provider can prescribe another antibiotic. Strep throat won’t go away on its own. A type of bacteria causes strep throat, and antibiotics treat infections caused by bacteria. Strep throat can lead to more serious illnesses if not treated, so it’s important to start on antibiotics immediately. Left untreated, the bacteria that cause strep throat can spread to other parts of your body. This can cause serious complications, including ear or sinus infections, abscesses, guttate psoriasis, scarlet fever, rheumatic fever, post-streptococcal glomerulonephritis, and invasive streptococcal infection. Only group A Streptococcus bacteria can cause strep throat. It’s never viral.

• #27 Single Cell Bottlenecks in the Pathogenesis of Streptococcus pneumoniae | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1005887

  Herein, we studied a virulent isolate of the leading bacterial pathogen Streptococcus pneumoniae in an infant mouse model of colonization, disease and transmission, both with and without influenza A (IAV) co-infection. […] Our findings reveal that in the setting of IAV co-infection the organism must pass through single cell bottlenecks during bloodstream invasion from the nasopharynx within the host and in transmission between hosts. […] The bottleneck in transmission occurred between bacterial exit from one host and establishment in another explaining why the number of shed organisms in secretions is critical to overcoming it. […] These observations demonstrate how viral infection, and TLR-dependent innate immune responses it stimulates and that are required to control it, drive bacterial contagion.

• #27 Single Cell Bottlenecks in the Pathogenesis of Streptococcus pneumoniae | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1005887

  Many discrete steps are involved in the progression of infectious diseases. Bottlenecks represent key points where the population size/genetic diversity is at a minimum and the pathogen is most vulnerable to intervention strategies. […] The main findings reveal i) a single cell bottleneck during host-to-host transmission and ii) the bottleneck in transmission occurs during events between bacterial exit from one host and establishment in another host. […] Thus, our study identifies key vulnerable stages during S. pneumoniae infection and provides mechanistic understanding for how viral infection promotes bacterial contagion. […] In order to better understand the mechanisms responsible for protection, we sought to identify the steps during infection where pneumococci must pass through a population bottleneck(s)a sharp reduction in the size of the population due to environmental constraints.

• #27 Single Cell Bottlenecks in the Pathogenesis of Streptococcus pneumoniae | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1005887

  A bottleneck would occur, for instance, if only a fraction of infecting organisms are able to pass through a host barrier or evade a local host defense. […] Tight bottlenecks would be attractive weak points for intervention strategies since there would be relatively few organisms to target. […] Our study employed an infant mouse model that recapitulates many of the key features of pneumococcal pathogenesis. […] The tight population bottleneck in the setting of IAV could be due to the selection of a subpopulation of pneumococci because of a requirement for de novo genetic adaptation. […] The tight bottleneck we observed following invasion from the mucosal surface, where pneumococcal bacteremia originates, suggests that a large bolus of pneumococci may not access the bloodstream in this manner. […] The demonstration of a single cell bottleneck in transmission provides context for understanding some its requirements.

• #28

  https://www.cbc.ca/news/health/why-deadly-invasive-strep-a-infections-are-surging-in-canada-and-beyond-1.7095026

  One piece of the puzzle may be the fact that run-of-the-mill strep infections can damage the cells of the upper respiratory tract, noted McGeer. […] Another may lie in changes to the immune system during an acute viral infection. […] „There is no question that having increases in viral infections are associated with increases in complicated bacterial infections, to some degree,” she added. „Any two infections tend to be worse than any one infection.” […] On top of that, the arrival of strep A bacteria can sometimes spark a faulty immune response where the body produces antibodies that, instead of targeting the bacteria, attack the body’s own tissues. That inflammatory reaction leads to autoimmune conditions such as rheumatic fever, which can cause joint pain, swelling and damage to the heart valves.

• #29 Streptococcal Infections (invasive group A strep, GAS)

  https://www.health.ny.gov/diseases/communicable/streptococcal/group_a/fact_sheet.htm

  Group A streptococci are bacteria commonly found in the throat and on the skin. […] Occasionally, however, these bacteria can cause much more severe and even life threatening diseases such as necrotizing fasciitis (occasionally described as „the flesh-eating bacteria”) and streptococcal toxic shock syndrome (STSS). […] Invasive group A streptococcal infections occur when the bacteria gets past the defenses of the person who is infected. This may occur when a person has sores or other breaks in the skin that allow the bacteria to get into the tissue. Health conditions that decrease a person’s immunity to infection also make invasive disease more likely. In addition, there are certain strains of GAS that are more likely to cause severe disease than others. The reason why some strains will cause more severe illness is not totally clear but may involve the production of substances (toxins) that cause shock and organ damage and of enzymes that cause tissue destruction. […] Group A streptococcus bacteria can be treated with common, inexpensive antibiotics. Penicillin is the drug of choice for both mild and severe disease. […] Early treatment may reduce the risk of death although, unfortunately, even appropriate therapy does not prevent death in every case.

• #30 New form of antimicrobial resistance discovered in Group A Streptococcus

  https://frontlinegenomics.com/new-form-of-antimicrobial-resistance-discovered-in-group-a-streptococcus/

  Researchers have identified a new form of antimicrobial resistance (AMR) in Group A Streptococcus (GAS). […] The study, led by Dr Timothy Barnett, Head of the Strep A Pathogenesis and Diagnostics team at the Wesfarmers Centre of Vaccines and Infectious Diseases in Western Australia, uncovered a new AMR mechanism in Group A Streptococcus (GAS). […] Dr Barnett said, “When looking at an antibiotic commonly prescribed to treat Group A Strep skin infections, we found a mechanism of resistance where, for the first time ever, the bacteria demonstrated the ability to take folates directly from its human host when blocked from producing their own. This makes the antibiotic ineffective and the infection would likely worsen when the patient should be getting better.” […] The SMX resistance protein, encoded by thfT, is a folate transporter. The researchers showed that the transporter allowed GAS to bypass the inhibitory effects of SMX.

• #30 New form of antimicrobial resistance discovered in Group A Streptococcus

  https://frontlinegenomics.com/new-form-of-antimicrobial-resistance-discovered-in-group-a-streptococcus/

  The study highlighted the importance of monitoring emerging SMX resistance and the need to change the therapeutic approach. […] “Unfortunately, we suspect this is just the tip of the iceberg – we have identified this mechanism in Group A Strep, but it’s likely that it will be a broader issue across other bacterial pathogens,” said Dr Barnett. […] Since this is a new form of AMR, the researchers investigated detection methods. […] Dr Barnett said, “This new form of resistance is undetectable under conditions routinely used in pathology laboratories, making it very hard for clinicians to prescribe antibiotics that will effectively treat the infection, potentially leading to very poor outcomes and even premature death.” […] The study shows that new diagnostic tools are required to detect SMX resistance to inform effective treatment.

• #31 Pharyngitis – sore throat Information | Mount Sinai – New York

  https://www.mountsinai.org/health-library/diseases-conditions/pharyngitis-sore-throat

  Strep throat is caused by group A streptococcus. […] A strep test or culture is positive. Your provider cannot diagnose strep throat by symptoms or a physical exam alone.

• #32 Integrated analysis of population genomics, transcriptomics and virulence provides novel insights into Streptococcus pyogenes pathogenesis | Nature Genetics

  https://www.nature.com/articles/s41588-018-0343-1

  Streptococcus pyogenes causes 700 million human infections annually worldwide, yet, despite a century of intensive effort, there is no licensed vaccine against this bacterium. […] Data integration provided a novel understanding of the virulence mechanisms of this model organism. Genome-wide association study, expression quantitative trait loci analysis, machine learning, and isogenic mutant strains identified and confirmed a one-nucleotide indel in an intergenic region that significantly alters global transcript profiles and ultimately virulence. […] The integrative strategy that we used is generally applicable to any microbe and may lead to new therapeutics for many human pathogens. […] Contribution of secreted NADase and streptolysin O to the pathogenesis of epidemic serotype M1 Streptococcus pyogenes infections.

• #33 Group A streptococcus: Virulence factors and pathogenic mechanisms – UpToDate

  https://www.uptodate.com/contents/group-a-streptococcus-virulence-factors-and-pathogenic-mechanisms

  Group A streptococcus: Virulence factors and pathogenic mechanisms […] The pathogenic mechanisms underlying these infections are poorly understood, largely because each is the culmination of highly complex interactions between the human host defense mechanisms and specific virulence factors of the organism. […] A number of different cell-surface molecules and secreted products of GAS have been identified as virulence factors. […] Anti-phagocytic properties […] Mechanisms of fever induction […] Cytokine induction […] Role in innate immunity.

• #34 Biology and Pathogenesis of Group A Streptococcus (GAS) | Frontiers Research Topic

  https://www.frontiersin.org/research-topics/1448/biology-and-pathogenesis-of-group-a-streptococcus-gas/articles

  Group A streptococci (GAS) are one of the most frequent human pathogens. […] Despite decades of research, many aspects of the pathogenesis of GAS infection remain unclear. […] The aim of this Research Topic is to provide an overview of the latest research on Group A Streptococcus (GAS) including the area of epidemiology of GAS infections, clinical aspects, pathogenic mechanisms, virulence factors and their regulation, horizontal gene transfer in GAS and its regulation, post-genomics and -proteomics, innate and adaptive immune responses to GAS infection, host auto-immune response and rheumatic fever/heart disease and therapeutic strategies to prevent GAS infections.

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