Materiały źródłowe

• #1 Scarlet Fever – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK507889/

  Scarlet fever is caused by streptococcal pyrogenic exotoxins, a type of superantigen produced by GAS. […] GAS produces streptococcal pyrogenic exotoxins (SPEs), which act as superantigens released during infection. These exotoxins are the primary cause of the erythematous rash associated with scarlet fever. […] GAS superantigens, also referred to as erythrogenic or scarlet fever toxins, are responsible for the characteristic erythematous, sandpaper-like rash and strawberry tongue seen in scarlet fever. […] Many GAS virulence determinants facilitate key processes, including adhesion, colonization, evasion of the innate immune system, invasion, and dissemination within the host. […] Notable toxins include the pyrogenic toxins (also called scarlatina or erythrogenic toxins), which are responsible for the rash seen in scarlet fever. […] The scarlet fever rash was once believed to result from primary toxicity caused by GAS. However, it is now understood to stem from a delayed host-acquired hypersensitivity reaction to streptococcal superantigens.

• #2 Scarlet Fever: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1053253-overview

  Scarlet fever (known as scarlatina in older literature references) is a syndrome characterized by exudative pharyngitis, fever, and bright-red exanthem. It is caused by streptococcal pyrogenic exotoxins (SPEs) types A, B, and C produced by group A beta-hemolytic streptococci (GABHS) found in secretions and discharge from the nose, ears, throat, and skin. Scarlet fever may follow streptococcal wound infections or burns, as well as upper respiratory tract infections. Food-borne outbreaks have been reported. […] Reemergence of the condition is being recognized, perhaps because of newer virulence of the streptococcal bacteria. […] The circulating toxin, produced by GABHS and often referred to as erythemogenic or erythrogenic toxin, causes the pathognomonic rash as a consequence of local production of inflammatory mediators and alteration of the cutaneous cytokine milieu. This results in a sparse inflammatory response and dilatation of blood vessels, leading to the characteristic scarlet color of the rash.

• #3 Scarlet Fever | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/28741

  Many virulence determinants have been identified in GAS, enabling it to perform key processes such as adhesion, colonization, immune evasion, invasion, and dissemination within the host. Key virulence factors include the M-protein, hyaluronic acid, streptokinase, and DNase B. Notable toxins, such as pyrogenic toxins (also known as scarlatina toxins or erythrogenic toxins), are responsible for the rash in scarlet fever. These toxins also induce mononuclear cells to produce tumor necrosis factor- (TNF-), interleukin (IL)-1, and IL-6, which may contribute to fever and shock in patients with streptococcal toxic shock syndrome (STSS). […] GAS is one of the few bacteria that produce superantigen exotoxins, which are among the most potent activators of T cells. These superantigens, also referred to as erythrogenic or scarlet fever toxins, are responsible for the erythematous sandpaper-like rash and strawberry tongue characteristic of scarlet fever. In conditions such as STSS, certain superantigenic exotoxins trigger atypical polyclonal activation of lymphocytes, leading to a rapid onset of shock and multiorgan failure with high mortality rates. Key identified superantigenic exotoxins include toxic shock syndrome toxin-1 (TSST-1) and enterotoxins.

• #4 Streptococcus pyogenes Pharyngitis and Scarlet Fever – Streptococcus pyogenes: Basic Biology to Clinical Manifestations – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK587104/

  Todd and Lancefield observed that S. pyogenes freshly isolated from patients with tonsillitis or scarlet fever grew as matt colonies (those that are large, with an irregular surface), a characteristic that was associated with production of M substance, that is, the M protein. […] The matt (or matte) colony type was subsequently shown to be a later stage of the mucoid colony morphology, which occurs due to abundant production of the hyaluronic acid capsular polysaccharide. […] In vitro passage of matte isolates often resulted in their conversion to the glossy morphology, with the latter colony type being deficient in both the M protein and capsule. […] These observations suggested that expression of the M protein and capsule were associated with symptomatic S. pyogenes pharyngitis, although not necessarily with asymptomatic pharyngeal carriage. […] More recent studies on clinical isolates and in experimental infection in non-human primates have supported these early insights.

• #5 WHO EMRO | Retrospective analysis of an outbreak of scarlet fever in United Arab Emirates | Volume 30 issue 5 | EMHJ volume 30 2024

  https://www.emro.who.int/emhj-volume-30-2024/volume-30-issue-5/retrospective-analysis-of-an-outbreak-of-scarlet-fever-in-united-arab-emirates.html

  Scarlet fever is an infectious disease caused by Streptococcus pyogenes. […] The virulence of S. pyogenes is influenced by the sub-type of Streptococcal M protein, which exhibits high genetic variability. The M protein envelops group A Streptococci and serves as the principal antigen, playing a crucial role in type-specific immunity. The M protein is vital for group A Streptococcus virulence, offering antiphagocytic functions crucial for survival in human tissues and body fluids. […] S. pyogenes secretes infectious erythrogenic toxins, resulting in characteristic red coloured skin rashes caused by increased cytokine production during the early stages of the fever. […] We suggest that clinical resistance to -lactams and the need for hospitalisation are both factors which are more likely to be associated with the organism’s virulence than age or gender. […] Emerging resistance may be due to the high genetic variation of the M pathogen genome, among other factors.

• #6 Streptococcus pyogenes Pharyngitis and Scarlet Fever – Streptococcus pyogenes: Basic Biology to Clinical Manifestations – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK587104/

  The global two-component regulatory system CsrRS (or CovRS) appears to play a critical role in the adaptation of S. pyogenes for survival and persistence in the pharynx. […] Inactivating mutations are present in csrS or, less often, in csrR in approximately 40% of clinical isolates from patients with necrotizing fasciitis or streptococcal toxic shock. […] By contrast, such mutations are rarely observed among pharyngitis isolates—an observation that suggests CsrRS contributes to the survival of S. pyogenes in this host environment. […] Further support for this view comes from studies that show a competitive advantage of wild-type S. pyogenes, as compared to CsrRS mutants during growth in human saliva. […] Along with several other virulence factors, synthesis of the hyaluronic acid capsule is regulated by CsrRS.

• #7 Streptococcal Infections – Infectious Diseases – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/infectious-diseases/gram-positive-cocci/streptococcal-infections

  Scarlet fever, a predominantly childhood disease, usually follows a pharyngeal streptococcal infection; less commonly, it follows streptococcal infections at other sites (eg, the skin). Scarlet fever is caused by group A streptococcal strains that produce an erythrogenic toxin, leading to a diffuse pink-red cutaneous flush that blanches with pressure. […] Many streptococci elaborate virulence factors, including streptolysins, DNAases, and hyaluronidase, which contribute to tissue destruction and spread of infection. A few strains release exotoxins that activate certain T cells, triggering release of cytokines, including tumor necrosis factor-alpha, interleukins, and other immunomodulators. These cytokines activate the complement, coagulation, and fibrinolytic systems, leading to shock, organ failure, and death. […] The mechanism by which certain strains of GABHS cause delayed complications is unclear but may involve cross-reactivity of streptococcal antibodies against host tissue.

• #8 Scarlet Fever: A Deadly History and How it Prevails

  https://asm.org/articles/2023/january/scarlet-fever-a-deadly-history-and-how-it-prevails

  The superantigens SpeA, SpeC and SSA have been directly associated with scarlet fever. The development of scarlet fever depends on both the strain of Group A Strep a patient gets, and how their body responds to the infection. […] Importantly, while the scarlet fever rash itself is not harmful, it is an indicator of Group A Strep disease, which can progress to invasive disease (i.e., necrotizing fasciitis or toxic shock syndrome) and be fatal, if left untreated. […] Expanded surveillance and research are needed to understand these outbreaks, but the pathogenesis and epidemiology of the disease provide additional context clues.

• #9 Streptococcal superantigens and the return of scarlet fever | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1010097

  Streptococcus pyogenes (group A Streptococcus) is a globally disseminated and human-adapted bacterial pathogen that causes a wide range of infections, including scarlet fever. Scarlet fever is a toxin-mediated disease characterized by the formation of an erythematous, sandpaper-like rash that typically occurs in children aged 5 to 15. This infectious disease is caused by toxins called superantigens, a family of highly potent immunomodulators. […] Mechanistically, superantigens function to force the broad activation of a large number of T cells by bridging the V region of TCR -chains with MHC class II molecules. This unusual V-specific activation of T cells differs from classical T cell activation because superantigens bypass prior processing and presentation, and such, the peptide specificity of the T cell becomes irrelevant.

• #10 Streptococcal superantigens and the return of scarlet fever | PLOS Pathogens

  https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1010097

  Genomic analyses have revealed that the speA gene had almost disappeared from M1 isolates obtained in the mid-20th century, which coincided with a sharp decline in severe invasive GAS infections during that time. We can only speculate that this event may have also played a role in the fall of scarlet fever incidence. However, the speA2 allele was introduced in the globally disseminated M1T1 clone in the 1980s, well before the resurgence of scarlet fever (approximately 30 years). Nonetheless, there is increasing evidence that acquisition of prophage carrying genes encoding virulence factors (SpeA, SSA, SpeC, and Spd1) and antibiotic resistance contributes to the increased fitness and virulence of contemporary GAS strains causing scarlet fever and invasive disease. […] By targeting T cells, superantigens stimulate uncontrolled cytokine responses that simultaneously recruit and then subvert the activity of effector cells, impeding the hosts ability to combat infections. Human tonsils exposed to superantigen, including S. pyogenes supernatants, demonstrate B cell apoptosis with a marked reduction in immunoglobulin synthesis.

• #11 Scarlet fever – Wikipedia

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

  Scarlet fever, also known as scarlatina, is an infectious disease caused by Streptococcus pyogenes, a Group A streptococcus (GAS). The rash occurs as a result of capillary damage by exotoxins produced by S.pyogenes. […] The rash of scarlet fever, which is what differentiates this disease from an isolated group A strep pharyngitis (or strep throat), is caused by specific strains of group A streptococcus that produce a streptococcal pyrogenic exotoxin, which is mainly responsible for the skin manifestation of the infection. […] Streptococcal pyrogenic exotoxins SPEs A, B, C. and F have been identified. The pyrogenic exotoxins, also called erythrogenic toxins, cause the erythematous rash of scarlet fever. […] The strains of group A streptococcus that cause scarlet fever need specific bacteriophages for there to be pyrogenic exotoxin production. Specifically, bacteriophage T12 is responsible for the production of speA.

• #12 1.1: Scarlet Fever – Biology LibreTexts

  https://bio.libretexts.org/Bookshelves/Microbiology/Microbiology_(Boundless)/15%3A_Diseases/15.03%3A_Bacterial_Diseases_of_the_Respiratory_System/15.3A%3A_Pharyngitis/1.01%3A_Scarlet_Fever

  Scarlet fever is caused by an erythrogenic toxin, a substance produced by the bacterium Streptococcus pyogenes (group A strep.) when it is infected by a certain bacteriophage. […] Scarlet fever is caused by secretion of pyrogenic (fever inducing) exotoxins by the infected Streptococcus. Exotoxin A (speA) is probably the best studied of these toxins. It is carried by the bacteriophage T12, which integrates into the Streptococcal genome, from where the toxin is transcribed. […] While antibiotics are effective against scarlet fever, the illness is actually caused by a bacteriophage infecting Streptococcus that has infected a person. […] The bacteriophage T12 inserts into the genome of Streptococcus. This leads to the expression of an exotoxin, which causes scarlet fever.

• #13 Scarlet Fever | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/28741

  The scarlet fever rash was once believed to result from primary toxicity caused by GAS. However, it is now understood to stem from a delayed host-acquired hypersensitivity reaction to streptococcal superantigens. Furthermore, the rash typically appears in individuals who have been previously exposed to GAS and is thus pre-sensitized, while it is absent in those with no prior GAS infection. The skin reactivity is likely due to rapid cytokine release and leukocyte presence, triggered by the amplified response to GAS superantigens during secondary antigen exposure.

• #14

  https://step2.medbullets.com/pediatrics/120586/scarlet-fever

  acute bacterial infection with diffuse erythematous eruption associated with pharyngitis […] delayed-type hypersensitivity to S. pyogenes exotoxin A

• #15 Scarlet Fever (Scarlatina) – Dermatology Advisor

  https://www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/scarlet-fever-scarlatina/

  The mechanism of SPEA is not fully understand as of yet, but it is significant in that quantities of this exotoxin produced by GAS strains are known to vary tremendously from decade to decade. […] The toxins elicit a delayed-type hypersensitivity, thus requiring prior antigenic exposure for the disease to occur. This explains why scarlet fever rarely affects infants since they have not yet been exposed to the exotoxins necessary to produce anti-toxin antibodies. […] Scarlet fever most commonly occurs following streptococcal pharyngitis or tonsillitis although other infectious foci such as the skin, soft tissue, surgical wounds (ie, surgical scarlet fever), burns, pelvic organs (ie, puerperal scarlet fever), and food-borne illness are also potential sources.

• #16 Scarlet Fever: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1053253-overview

  The erythrogenic toxins produced by GABHS are the cause of the rash of scarlet fever. […] The organism is able to survive extremes of temperature and humidity, which allows spread by fomites. […] The incubation period for scarlet fever ranges from 12 hours to 7 days. Patients are contagious during the acute illness and during the subclinical phase. […] Known complications, such as septicemia, vasculitis, hepatitis, or rheumatic fever, should be considered on a case-by-case basis as determined by the presence of clinical history and examination findings suggestive of those diseases. […] Very rare complications, such as septic shock with multisystem organ failure, have been reported.

• #17 Scarlet fever – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/scarlet-fever/symptoms-causes/syc-20377406

  Scarlet fever is caused by the same type of bacteria that causes strep throat group A streptococcus (strep-toe-KOK-us), also called group A strep. In scarlet fever, the bacteria release a toxin that produces the rash and red tongue. […] The infection spreads from person to person by droplets released when an infected person coughs or sneezes. The incubation period the time between exposure and illness is usually 2 to 4 days.

• #18 Scarlet Fever – Streptococcal Infections – Bacterial Diseases – Infectious Diseases – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.18.76.

  Scarlet fever, also known as scarlatina, presents as diffuse erythematous rash occurring in the setting of streptococcal infection, usually pharyngitis. […] Pathogenesis: The site of bacterial entry is the oral cavity for classic scarlet fever, and damaged skin for surgical scarlet fever. Clinical manifestations (fever, rash, vomiting) are caused by pyrogenic exotoxins produced by some streptococcal strains. Skin involvement is due to erythrogenic toxin (types A, B, and C). The streptococcal superantigen that causes the streptococcal toxic shock syndrome is also a pyrogenic toxin.

• #19 Scarlet Fever | Concise Medical Knowledge

  https://www.lecturio.com/concepts/scarlet-fever/

  Scarlet fever is caused by -hemolytic, pyrogenic toxin-producing strains of Streptococcus. Key mediator of the characteristic rash: streptococcal pyrogenic exotoxins A, B, and C. Transmission of S. pyogenes is primarily via respiratory secretions. Local infection occurs: Bacteria adhere to the pharyngeal epithelium, causing pharyngitis, purulent tonsillar exudate, cervical lymphadenopathy, and fever. Some strains of S. pyogenes produce pyrogenic exotoxins, which act as superantigens. Antigens stimulate T cells, which release cytokines, leading to an inflammatory cutaneous reaction and blood vessel dilatation. Produces the characteristic rash of scarlet fever. While the pharynx is the most common site of replication, scarlet fever may follow streptococcal skin and soft tissue infection.

• #20 Azthena logo with the word Azthena

  https://www.news-medical.net/news/20201006/Supercharged-clones-trigger-the-re-emergence-of-scarlet-fever.aspx

  A University of Queensland-led team of international researchers says supercharged „clones” of the bacteria Streptococcus pyogenes are to blame for the resurgence of the disease, which has caused high death rates for centuries. […] Co-author Professor Mark Walker and the team found a variety of Streptococcus pyogenes bacteria that had acquired „superantigen” toxins, forming new clones. […] We’ve shown that these acquired toxins allow Streptococcus pyogenes to better colonise its host, which likely allows it to out-compete other strains. […] These supercharged bacterial clones have been causing our modern scarlet fever outbreaks. […] The research team then removed the toxin genes from the clones causing scarlet fever, and these modified 'knock-out’ clones were found to be less able to colonise in an animal model of infection.

• #21 Prophage exotoxins enhance colonization fitness in epidemic scarlet fever-causing Streptococcus pyogenes | Nature Communications

  https://www.nature.com/articles/s41467-020-18700-5

  The capacity of North-East Asian serotype M12 (emm12) Streptococcus pyogenes (group A Streptococcus, GAS) to cause scarlet fever has been linked epidemiologically to the presence of novel prophages, including prophage HKU.vir encoding the secreted superantigens SSA and SpeC and the DNase Spd1. […] We demonstrate that streptolysin O (SLO)-induced glutathione efflux from host cellular stores is a previously unappreciated GAS virulence mechanism that promotes SSA release and activity, representing the first description of a thiol-activated bacterial superantigen. […] Investigating single, double and triple isogenic knockout mutants of the HKU.vir-encoded exotoxins, we find that SpeC and Spd1 act synergistically to facilitate nasopharyngeal colonization in a mouse model. […] These results offer insight into the pathogenesis of scarlet fever-causing GAS mediated by prophage HKU.vir exotoxins.

• #22

  https://link.springer.com/article/10.1007/BF02868209

  The intravenous injection of scarlet fever toxin leads to acute changes in the white blood picture. The changes are correlated to the dose; a small dose causes lymphopenia and granulocytosis, while higher doses are followed by initial granulocytopenia. […] Tolerant rabbits do not have granulocytopenia, but lymphopenia persists. Tolerance to the leucopenic effect of the toxin probably develops somewhat sooner and lasts longer than tolerance to its pyrogenic effect. […] The blood picture of a cortisone-treated rabbit after the intravenous injection of scarlet fever toxin resembles the blood picture of a tolerant rabbit. The significance and associations of these observations are briefly discussed.

• #23

  https://link.springer.com/article/10.1007/BF02878839

  Scarlet fever toxin was found to liberate leukocytic pyrogen from granulocytes in vitro. […] In comparative experiments with Salmonella paratyphi B endotoxin and scarlet fever toxin it was tested whether leukocytes from rabbits tolerant to one of these toxins are able to synthetize and liberate endogenous pyrogen. […] Leukocytes from rabbits tolerant to endotoxin liberated leukocytic pyrogen following challenge with endotoxin or with scarlet fever toxin. […] Leukocytes from animals tolerant to scarlet fever toxin liberated leukocytic pyrogen in the presence of endotoxin, but were insensitive to homologous, i.e. scarlet fever toxin. […] Similarly, leukocytes from cortisone-treated animals did not liberate leukocytic pyrogen if they were incubated with scarlet fever toxin, but liberation of leukocytic pyrogen did take place under challenge with endotoxin. […] Leukocytes from normal animals incubated in Hanks solution without toxin did not synthetize endogenous pyrogen.

• #24 Content – Health Encyclopedia – University of Rochester Medical Center

  https://www.urmc.rochester.edu/encyclopedia/content?contenttypeid=90&contentid=p02544

  Scarlet fever is caused by bacteria called group A beta-hemolytic streptococcus (GABHS). These bacteria release a poison (toxin) that travels through your child’s bloodstream and causes a rash. […] If not treated, scarlet fever can lead to several serious conditions of the heart, kidneys, and liver. When the bacteria affect the heart or joints, it is often called rheumatic fever.

• #25 Clinical Guidance for Scarlet Fever | Group A Strep | CDC

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

  Scarlet fever, also called scarlatina, is caused by pyrogenic exotoxin-producing Streptococcus pyogenes (group A strep bacteria). […] The rash usually persists for about one week and desquamation may follow. […] 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.

• #26 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). […] Patients with group A strep pharyngitis may also present with a scarlatiniform rash. The resulting syndrome is scarlet fever. […] 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.

• #27 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. […] 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. […] 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.

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

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

  Scarlet fever is most common among children aged 5 to 18 years. Individuals with scarlet fever may have red, blanching rashes with tiny bumps that feel like sandpaper. The rash may first appear as small, flat blotches on the torso, neck, under arm, and groin before spreading to other parts of the body. […] In rare cases, scarlet fever can lead to post-streptococcal glomerulonephritis (PSGN) and rheumatic fever. […] 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.

• #29 Scarlet fever | NHS inform

  https://www.nhsinform.scot/illnesses-and-conditions/infections-and-poisoning/scarlet-fever/

  Scarlet fever is a bacterial illness that mainly affects children. It is caused by Streptococcus pyogenes bacteria, also known as Group A Streptococcus, which are found on the skin and in the throat. […] The symptoms of scarlet fever will only develop in people susceptible to toxins produced by the Streptococcus bacteria. Most children over 10 years of age will have developed immunity to these toxins. […] Scarlet fever is usually treated with a 10-day course of antibiotics. This is often in the form of penicillin or amoxicillin tablets, although liquid may be used for young children. […] Most cases of scarlet fever don’t cause complications, particularly if the condition is properly treated. However, there’s a small risk of the infection spreading to other parts of the body and causing more serious infections, like pneumonia (inflammation of the lungs).

• #30 Mechanism of recurrent outbreak of the scarlet fever epidemics in mainland China | medRxiv

  https://www.medrxiv.org/content/10.1101/2024.08.09.24311775v1

  In mainland China, most infectious diseases occur once a year, except for scarlet fever, which has been steadily breaking out twice a year in recent years. […] However, the oscillatory mechanism of scarlet fever remains unclear. This study aimed to uncover how meteorological factors contribute to the recrudescence of scarlet fever in mainland China. […] We found that the scarlet fever epidemics generally occur twice a year in various provinces of China, and the timing of these outbreaks peaks progressively from southern to northern regions. Furthermore, we established an atlas that shows the relationship between scarlet fever oscillation and meteorological factors. Our findings indicated a significant correlation between the oscillation characteristics of scarlet fever in 50% of provinces and each natural meteorological factor.

• #31 Measles and Scarlet Fever Epidemic Synergy and Evolving Pathogenic Virulence in Victoria, Australia, 1853–1916 | Social Science History | Cambridge Core

  https://www.cambridge.org/core/journals/social-science-history/article/measles-and-scarlet-fever-epidemic-synergy-and-evolving-pathogenic-virulence-in-victoria-australia-18531916/7915365660DAE8493050AB68B9393E43

  Four synchronous epidemics of measles and scarlet fever are observed in the historical data collected by colonial authorities in Victoria, Australia from 1853 to 1876, suggesting some sort of synergistic relationship between the two diseases. […] We conclude that the most likely explanation for the observed pattern is an epidemic synergy that ended after the 1876 epidemic. […] We hypothesize that this synergistic relationship between measles and scarlet fever in mid-nineteenth-century Victoria ended due to a shift in the dominant group A streptococci (GAS) M-type or the loss of a GAS bacteriophage. […] Support for this hypothesis comes from observations that other diagnoses associated with group A strep infections also changed their mortality profiles during the 1870s, particularly Brights disease, a possible descriptor of post-streptococcal glomerulonephritis.

• #32 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 a dominant new emm1 GAS lineage (M1UK) that is characterized by increased SpeA production, which may be contributing to the upsurge of scarlet fever and invasive infections in England.

• #33 Prophage exotoxins enhance colonization fitness in epidemic scarlet fever-causing Streptococcus pyogenes | Nature Communications

  https://www.nature.com/articles/s41467-020-18700-5

  Exotoxin-driven enhanced colonization provides an evidence-based hypothesis for the reemergence of scarlet fever globally. […] The phage-encoded DNase Spd1 is linked with the expansion of scarlet fever GAS in North-East Asia. […] These findings demonstrate that Spd1 promotes growth of HKU16 in whole blood, reduces susceptibility to neutrophil mediated killing and facilitates NET degradation. […] Our data demonstrate that SLO is highly effective at triggering the release of significant amounts of GSH from host cells, which is utilized for extracellular growth of GAS and likely provides a reducing extracellular microenvironment required for efficient SSA activation in vivo. […] We hypothesize that prophage-encoded exotoxin acquisition has enhanced colonization fitness of scarlet fever-causing GAS emm12 clones in North-East Asia.

• #34 Mechanism of recurrent outbreak of the scarlet fever epidemics in mainland China | medRxiv

  https://www.medrxiv.org/content/10.1101/2024.08.09.24311775v1

  Our study presents a detailed description of the temporal and spatial changes in the oscillatory characteristics of scarlet fever for the first time and explores the oscillatory characteristics of natural meteorological conditions and their correlation with the number of scarlet fever infections. These findings could serve as a valuable guide for government prevention and control measures for the scarlet fever epidemic.

• #35 Measles and Scarlet Fever Epidemic Synergy and Evolving Pathogenic Virulence in Victoria, Australia, 1853–1916 | Social Science History | Cambridge Core

  https://www.cambridge.org/core/journals/social-science-history/article/measles-and-scarlet-fever-epidemic-synergy-and-evolving-pathogenic-virulence-in-victoria-australia-18531916/7915365660DAE8493050AB68B9393E43

  We situate the emergence and end of this pattern within the demographic and socioeconomic conditions of the Victorian gold-mining boom in the 1850s to 1870s and postboom changes in fertility, mortality, and housing infrastructure, highlighting the importance of social conditions in disease evolution.

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