Scarlet fever

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Scarlet fever
Other namesScarlatina, [1] scarletina [2]
Strawberry tongue seen in scarlet fever
Specialty Infectious disease
Symptoms Sore throat, fever, headaches, swollen lymph nodes, characteristic rash [1]
Complications Glomerulonephritis, rheumatic heart disease, arthritis [1]
Usual onset5–15 years old [1]
Causes Strep throat, streptococcal skin infections [1]
Diagnostic method Throat culture [1]
Prevention Handwashing, not sharing personal items, staying away from sick people [1]
Treatment Antibiotics [1]
PrognosisTypically good [3]

Scarlet fever is a disease which can occur as a result of a group A streptococcus (group A strep) infection, also known as Streptococcus pyogenes. [1] The signs and symptoms include a sore throat, fever, headaches, swollen lymph nodes, and a characteristic rash. [1] The rash is red and feels like sandpaper and the tongue may be red and bumpy. [1] It most commonly affects children between five and 15 years of age. [1]


Scarlet fever affects a small number of people who have strep throat or streptococcal skin infections. [1] The bacteria are usually spread by people coughing or sneezing. [1] It can also be spread when a person touches an object that has the bacteria on it and then touches their mouth or nose. [1] The characteristic rash is due to the erythrogenic toxin, a substance produced by some types of the bacterium. [1] [4] The diagnosis is typically confirmed by culturing the throat. [1]

There is no vaccine. [1] Prevention is by frequent handwashing, not sharing personal items, and staying away from other people when sick. [1] The disease is treatable with antibiotics, which prevent most complications. [1] Outcomes with scarlet fever are typically good if treated. [3] Long-term complications as a result of scarlet fever include kidney disease, rheumatic heart disease, and arthritis. [1] It was a leading cause of death in children in the early 20th century. [5] [6]

Signs and symptoms

Strawberry tongue is a characteristic of scarlet fever Skarlatina.jpg
Strawberry tongue is a characteristic of scarlet fever
The rash of scarlet fever Scarlet fever 2.jpg
The rash of scarlet fever
Red cheeks and pale area around the mouth in scarlet fever Scarlet fever 1.1.JPG
Red cheeks and pale area around the mouth in scarlet fever
Characteristic red cheeks and rash of scarlet fever Scarlet Fever.jpg
Characteristic red cheeks and rash of scarlet fever

Rash which has a characteristic appearance, spreading pattern, and desquamating process "Strawberry tongue"

Strep throat

Typical symptoms of streptococcal pharyngitis (also known as strep throat): [10]

The following symptoms will usually be absent: cough, hoarseness, runny nose, diarrhea, and conjunctivitis. [10] Their presence indicates it is more likely a viral infection.


The rash begins 12 days following the onset of symptoms caused by the strep pharyngitis (sore throat, fever, fatigue). [13] This characteristic rash has been denoted as "scarlatiniform" and it appears as a diffuse redness of the skin with small papules, or bumps, which resemble goose pimples. [7] [14] These bumps are what give the characteristic sandpaper texture to the rash. The reddened skin will blanch when you apply pressure to it. It is possible for the skin to be itchy, but it will not be painful. [7] The rash generally starts at the flexion of the elbow and other surfaces. [15] It than appears on the trunk and then gradually spreads out to the arms and legs. [14] The palms, soles and face are usually left uninvolved by the rash. The face, however, is usually flushed, most prominently in the cheeks, with a ring of paleness around the mouth. [16] After the rash spreads, it becomes more pronounced in creases in the skin, such as the skin folds in the inguinal and axillary regions of the body. [9] Also in those areas it is possible for there to be Pastia's Lines which are petechiae arranged in a linear pattern. [9] Within 1 week of onset the rash begins to fade followed by a longer process of desquamation, or shedding of the outer layer of skin, which lasts several weeks. [12] The desquamation process usually begins on the face and progresses downward on the body. [7] After the desquamation the skin will be left with a sunburned appearance. [13]


Throat of a child with a positive throat culture for streptococcal pharyngitis Pos strep.JPG
Throat of a child with a positive throat culture for streptococcal pharyngitis

The streptococcal pharyngitis which is the usual presentation of scarlet fever in combination with the characteristic rash commonly involves the tonsils. The tonsils will appear swollen and reddened. The palate and uvula are also commonly affected by the infection. The involvement of the soft palate can be seen as tiny red and round spots known as Forchheimer spots. [11]

Variable presentations

The features of scarlet fever can differ depending on the age and race of the person. Children less than 5 years old can have atypical presentations. Children less than 3 years old can present with nasal congestion and a lower grade fever. [17] Infants can potentially only present with increased irritability and decreased appetite. [17]

Children who have darker skin can have a different presentation in that the redness of the skin involved in the rash and the ring of paleness around the mouth can be less obvious. [7] Suspicion based on accompanying symptoms and diagnostic studies are important in these cases.


Following exposure to streptococcus, it takes 12 hours to 7 days for the onset of the symptoms. This may include fever, fatigue, and sore throat. The characteristic scarlatiniform rash then comes 12–48 hours later. During the first few days of the rash development and rapid generalization, the Pastia's Lines and strawberry tongue are also present. [7] The rash starts fading within 3–4 days, followed by the desquamation of the rash, which lasts several weeks to a month. [13] [11] If the case of scarlet fever is uncomplicated, recovery from the fever and clinical symptoms other than the process of desquamation occurs in 5–10 days. [18]


The complications which can arise from scarlet fever when left untreated or inadequately treated can be divided into two categories: suppurative and nonsuppurative.

Suppurative complications: These are rare complications which either arise from direct spread to structures which are close to the primary site of infection, which in most cases of Scarlet Fever is the pharynx. Possible problems from this method of spread include peritonsillar or retropharyngeal abscesses, cellulitis, mastoiditis or sinusitis. It is also possible for the streptococcal infection to spread through the lymphatic system or the blood to areas of the body further away from the pharynx. A few examples of the many complications which can arise from those methods of spread include endocarditis, pneumonia, or meningitis. [16]

Nonsuppurative complications: These complications arise from certain subtypes of group A streptococci which cause an autoimmune response in the body through what has been termed molecular mimicry. The antibodies which the person's immune system developed to attack the group A streptococci are in these cases also able to attack the person's own tissues. The following complications result depending on which tissues in the person's body are targeted by those antibodies. [14]


Spread of strep throat occurs by close contact, via respiratory droplets (for example, saliva or nasal discharge). [13] A person in close contact with another person infected with group A streptococcal pharyngitis has a 35% chance of becoming infected. [17] One in ten children who are infected with group A streptococcal pharyngitis will develop scarlet fever. [12]


Streptococcus pyogenes (pictured) Streptococcus pyogenes.jpg
Streptococcus pyogenes (pictured)

The rash of scarlet fever, which is what differentiates this disease from an isolated group A step pharyngitis (or strep throat), is caused by specific strains of group A streptococcus which produce a pyrogenic exotoxin. [13] These toxin producing strains cause scarlet fever in people who do not already have antitoxin antibodies. Streptococcal pyrogenic exotoxins A, B, and C (speA, speB, and speC) have been identified. The pyrogenic exotoxins are also called erythrogenic toxins and cause the erythematous rash of scarlet fever. [13] The strains of group A streptococcus which cause scarlet fever need specific bacteriophages in order for there to be pyrogenic exotoxin production. Specifically, bacteriophage T12 is responsible for the production of speA. [20] Streptococcal Pyrogenic Exotoxin A, speA, is the one which is most commonly associated with cases of scarlet fever which are complicated by the immune mediated sequelae acute rheumatic fever and poststreptococcal glomerulonephritis. [11]

These toxins are also known as “superantigens” because they are able to cause an extensive immune response within the body through activation of some of the main cells responsible for the persons immune system. [18] The body responds to these toxins by making antibodies to those specific toxins. However, those antibodies do not completely protect the person from future group A streptococcal infections since there are 12 different pyrogenic exotoxins possible. [13]


The disease is caused by secretion of pyrogenic exotoxins by the infecting Streptococcus bacteria. [21] [22] Streptococcal pyrogenic 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. The phage itself integrates into a serine tRNA gene on the chromosome. [23]

The T12 virus itself has not been placed into a taxon by the International Committee on Taxonomy of Viruses. It has a double-stranded DNA genome and on morphological grounds appears to be a member of the Siphoviridae.

The speA gene was cloned and sequenced in 1986. [24] It is 753 base pairs in length and encodes a 29.244 kiloDalton (kDa) protein. The protein contains a putative 30- amino-acid signal peptide; removal of the signal sequence gives a predicted molecular weight of 25.787 kDa for the secreted protein. Both a promoter and a ribosome binding site (Shine-Dalgarno sequence) are present upstream of the gene. A transcriptional terminator is located 69 bases downstream from the translational termination codon. The carboxy terminal portion of the protein exhibits extensive homology with the carboxy terminus of Staphylococcus aureus enterotoxins B and C1.

Streptococcal phages other than T12 may also carry the speA gene. [25]


Although the presentation of scarlet fever can be clinically diagnosed, further testing may be required to distinguish it from other illnesses. [7] Also, history of a recent exposure to someone with strep throat can be useful. [13] There are two methods used to confirm suspicion of scarlet fever; rapid antigen detection test and throat culture. [17]

The rapid antigen detection test is a very specific test but not very sensitive. This means that if the result is positive (indicating that the group A strep antigen was detected and therefore confirming that the person has a group A strep pharyngitis) then it is appropriate to treat them with antibiotics. However, if the rapid antigen detection test is negative (indicating that they do not have group A strep pharyngitis), then a throat culture is required to confirm since it could be a false negative result. [26] The throat culture is the current gold standard for diagnosis. [17]

Serologic testing looks for the antibodies that the body produces against the streptococcal infection including antistreptolysin-O and antideoxyribonuclease B. It takes the body 2–3 weeks to make these antibodies so this type of testing is not useful for diagnosing a current infection. However, it is useful when assessing a person who may have one of the complications from a previous streptococcal infection. [12] [17]

Throat cultures done after antibiotic therapy can show if the infection has been removed. These throat swabs, however, are not indicated because up to 25% of properly treated individuals can continue to carry the streptococcal infection while asymptomatic. [19]

Differential diagnosis


One method is long-term use of antibiotics to prevent future group A streptococcal infections. This method is only indicated for people who have had complications like recurrent attacks of acute rheumatic fever or rheumatic heart disease. Antibiotics are limited in their ability to prevent these infections since there are a variety of subtypes of group A streptococci that can cause the infection. [13]

The vaccine approach has a greater likelihood of effectively preventing group A streptococcal infections because vaccine formulations can target multiple subtypes of the bacteria. [13] A vaccine developed by George and Gladys Dick in 1924 was discontinued due to poor efficacy and the introduction of antibiotics. Difficulties in vaccine development include the considerable strain variety of group A streptococci present in the environment and the amount of time and number of people needed for appropriate trials for safety and efficacy of any potential vaccine. [31] There have been several attempts to create a vaccine in the past few decades. These vaccines, which are still in the development phase, expose to the person to proteins present on the surface of the group A streptococci to activate an immune response that will prepare the person to fight and prevent future infections. [32]

There used to be a diphtheria scarlet fever vaccine. [33] It was, however, found not to be effective. [34] This product was discontinued by the end of World War II.


Antibiotics to combat the streptococcal infection are the mainstay of treatment for scarlet fever. Prompt administration of appropriate antibiotics decreases the length of illness. Peeling of the outer layer of skin, however, will happen despite treatment. [7] One of the main goals of treatment is to prevent the child from developing one of the suppurative or nonsuppurative complications, especially acute rheumatic fever. [17] As long as antibiotics are started within 9 days, it is very unlikely for the child to develop acute rheumatic fever. [13] Antibiotic therapy has not been shown to prevent the development of poststreptococcal glomerulonephritis. [14] [7] Another important reason for prompt treatment with antibiotics is the ability to prevent transmission of the infection between children. An infected individual is most likely to pass on the infection to another person during the first 2 weeks. [19] A child is no longer contagious (able to pass the infection to another child) after 24 hours of antibiotics. [13]

The antibiotic of choice is penicillin V which is taken by mouth in pill form. Children who are not able to take pills can be given amoxicillin which comes in a liquid form and is equally effective. Duration of treatment is 10 days. [17] Benzathine Penicillin G can be given as a one time intramuscular injection as another alternative if swallowing pills is not possible. [35] If the person is allergic to the family of antibiotics which both penicillin and amoxicillin are a part of (beta-lactam antibiotics), a first generation cephalosporin is used. [26] Cephalosporin antibiotics, however, can still cause adverse reactions in people whose allergic reaction to penicillin is a Type 1 Hypersensitivity reaction. In those cases it is appropriate to choose clindamycin or erythromycin instead. [26]

Tonsillectomy, although once a reasonable treatment for recurrent streptococcal pharyngitis, is not indicated. This is due to the fact that a person can still be infected with group A streptococcus without their tonsils. [19]

Antibiotic resistance

A drug-resistant strain of scarlet fever, resistant to macrolide antibiotics such as erythromycin, but retaining drug-sensitivity to beta-lactam antibiotics such as penicillin, emerged in Hong Kong in 2011, accounting for at least two deaths in that city—the first such in over a decade. [36] About 60% of circulating strains of the group A streptococcus that cause scarlet fever in Hong Kong are resistant to macrolide antibiotics, says Professor Kwok-yung Yuen, head of Hong Kong University's microbiology department. Previously, observed resistance rates had been 10–30%; the increase is likely the result of overuse of macrolide antibiotics in recent years.


Scarlet fever occurs equally in both males and females. [12] Children are most commonly infected, typically between 5–15 years old. Although streptococcal infections can happen at any time of year, infection rates peak in the winter and spring months, typically in colder climates. [13]

The morbidity and mortality of scarlet fever has declined since the 18th and 19th century when there were epidemics caused by this disease. [37] Around 1900 the mortality rate in multiple places reached 25%. [38] The improvement in prognosis can be attributed to the use of penicillin in the treatment of this disease. [10] The frequency of scarlet fever cases has also been declining over the past century. There have been several reported outbreaks of the disease in various countries in the past decade. [39] The reason for these recent increases remains unclear in the medical community. Between 2013 and 2016 population rates of scarlet fever in England increased from 8.2 to 33.2 per 100,000 and hospital admissions for scarlet fever increased by 97%. [40]


It is unclear when a description of this disease was first recorded. [41] Hippocrates, writing around 400 BC, described the condition of a person with a reddened skin and fever. [42]

The first description of the disease in the medical literature appeared in the 1553 book De Tumoribus praeter Naturam by the Sicilian anatomist and physician Giovanni Filippo Ingrassia, where he referred to it as rossalia. He also made a point to distinguish that this presentation had different characteristics to measles. [42] It was redescribed by Johann Weyer during an epidemic in lower Germany between 1564 and 1565; he referred to it as scalatina anginosa. The first unequivocal description of scarlet fever appeared in a book by Joannes Coyttarus of Poitiers, De febre purpura epidemiale et contagiosa libri duo, which was published in 1578 in Paris. Daniel Sennert of Wittenberg described the classical 'scarlatinal desquamation' in 1572 and was also the first to describe the early arthritis, scarlatinal dropsy, and ascites associated with the disease.

In 1675 the term that has been commonly used to refer to scarlet fever, "scarlatina", was written by Thomas Sydenham, an English physician. [42]

In 1827, Richard Bright was the first to recognize the involvement of the renal system in scarlet fever.

The association between streptococci and disease was first described in 1874 by Theodor Billroth, discussing people with skin infections. [42] Billroth also coined the genus name Streptococcus. In 1884 Friedrich Julius Rosenbach edited the name to its current one, Streptococcus pyogenes, after further looking at the bacteria in the skin lesions. [42] The organism was first cultured in 1883 by the German surgeon Friedrich Fehleisen from erysipelas lesions.

Also in 1884, the German physician Friedrich Loeffler was the first to show the presence of streptococci in the throats of people with scarlet fever. Because not all people with pharyngeal streptococci developed scarlet fever, these findings remained controversial for some time. The association between streptococci and scarlet fever was confirmed by Alphonse Dochez and George and Gladys Dick in the early 1900s. [43]

Nil Filatov (in 1895) and Clement Dukes (in 1894) described an exanthematous disease which they thought was a form of rubella, but in 1900, Dukes described it as a separate illness which came to be known as Dukes' disease, [44] Filatov's disease, or fourth disease. However, in 1979, Keith Powell identified it as in fact the same illness as the form of scarlet fever which is caused by staphylococcal exotoxin and is known as staphylococcal scalded skin syndrome. [45] [46] [47] [48]

Scarlet fever serum from horses was used in the treatment of children beginning in 1900 and reduced mortality rates significantly.

In 1906, the Austrian pediatrician Clemens von Pirquet postulated that disease-causing immune complexes were responsible for the nephritis that followed scarlet fever. [49]

Bacteriophages were discovered in 1915 by Frederick Twort. His work was overlooked and bacteriophages were later rediscovered by Felix d'Herelle in 1917. The specific association of scarlet fever with the group A streptococci had to await the development of Lancefield's streptococcal grouping scheme in the 1920s. George and Gladys Dick showed that cell-free filtrates could induce the erythematous reaction characteristic of scarlet fever, proving that this reaction was due to a toxin. Karelitz and Stempien discovered that extracts from human serum globulin and placental globulin can be used as lightening agents for scarlet fever and this was used later as the basis for the Dick test. The association of scarlet fever and bacteriophages was described in 1926 by Cantucuzene and Boncieu. [50]

An antitoxin for scarlet fever was developed in 1924.

The first toxin which causes this disease was cloned and sequenced in 1986 by Weeks and Ferretti. [24] The discovery of penicillin and its subsequent widespread use has significantly reduced the mortality of this once feared disease. Reports of cases of scarlet fever have been on the rise in countries including England, Wales, South Korea, Vietnam, China, and Hong Kong in recent years. Researchers are unsure as to what has caused the spike in cases of the disease. [51] [52]

The Dick test

The Dick test was invented in 1924 and was used to identify those susceptible to scarlet fever. [53] The Dick test consisted of injecting a diluted strain of the streptococci known to cause scarlet fever into a person's skin. A local reaction in the skin at the site of injection appeared in people who were susceptible to developing scarlet fever. This reaction was most notable around 24 hours after the injection but could be seen as early as 4–6 hours. If there is no reaction seen in the skin, then that person was assumed to have already developed immunity to the disease and was not at risk of developing it. [54]

Related Research Articles

<i>Streptococcus</i> genus of bacteria

Streptococcus is a genus of gram-positive coccus or spherical bacteria that belongs to the family Streptococcaceae, within the order Lactobacillales, in the phylum Firmicutes. Cell division in streptococci occurs along a single axis, so as they grow, they tend to form pairs or chains that may appear bent or twisted.

Erysipelas human disease

Erysipelas is a bacterial infection of the upper dermis extending to the subcutaneous lymphatic vessels which causes a rash characterized by a well-defined area or areas of bright red, inflamed and rough or leathery skin. It usually affects skin on the face, arms, legs, hands and feet. It is caused by beta-hemolytic group A Streptococcus bacteria on scratches or otherwise infected areas. Erysipelas is more superficial than cellulitis, and is typically more raised and demarcated. The term is from Greek ἐρυσίπελας, meaning "red skin".

Group A streptococcal infection human disease

A group A streptococcal infection is an infection with group A streptococcus (GAS). Streptococcus pyogenes comprises the vast majority of the Lancefield group A streptococci, and is often used as a synonym for GAS. However, S. dysgalactiae can also be group A. S. pyogenes is a beta-hemolytic species of Gram positive bacteria that is responsible for a wide range of both invasive and noninvasive infections.

<i>Streptococcus pyogenes</i> Species of bacterium

Streptococcus pyogenes is a species of Gram-positive, aerotolerant bacterium in the genus Streptococcus. These bacteria are extracellular, and made up of non-motile and non-sporing cocci. It is clinically important for humans. It is an infrequent, but usually pathogenic, part of the skin microbiota. It is the predominant species harboring the Lancefield group A antigen, and is often called group A Streptococcus (GAS). However, both Streptococcus dysgalactiae and the Streptococcus anginosus group can possess group A antigen. Group A streptococci when grown on blood agar typically produces small zones of beta-hemolysis, a complete destruction of red blood cells. It is thus also called group A (beta-hemolytic) Streptococcus (GABHS), and it can make colonies greater than 5 mm in size.

Streptococcal pharyngitis infection of the back of the throat including the tonsils caused by group A streptococcus (GAS)

Streptococcal pharyngitis, also known as strep throat, is an infection of the back of the throat including the tonsils caused by group A streptococcus (GAS). Common symptoms include fever, sore throat, red tonsils, and enlarged lymph nodes in the neck. A headache, and nausea or vomiting may also occur. Some develop a sandpaper-like rash which is known as scarlet fever. Symptoms typically begin one to three days after exposure and last seven to ten days.

Pharyngitis type of upper respiratory tract infection

Pharyngitis is inflammation of the back of the throat, known as the pharynx. It typically results in a sore throat and fever. Other symptoms may include a runny nose, cough, headache, and a hoarse voice. Symptoms usually last 3–5 days. Complications can include sinusitis and acute otitis media. Pharyngitis is a type of upper respiratory tract infection.

Rheumatic fever Post-streptococcal inflammatory disease

Rheumatic fever (RF) is an inflammatory disease that can involve the heart, joints, skin, and brain. The disease typically develops two to four weeks after a streptococcal throat infection. Signs and symptoms include fever, multiple painful joints, involuntary muscle movements, and occasionally a characteristic non-itchy rash known as erythema marginatum. The heart is involved in about half of the cases. Damage to the heart valves, known as rheumatic heart disease (RHD), usually occurs after repeated attacks but can sometimes occur after one. The damaged valves may result in heart failure, atrial fibrillation and infection of the valves.

Tonsillitis Inflammation of the tonsils

Tonsillitis is inflammation of the tonsils, typically of rapid onset. It is a type of pharyngitis. Symptoms may include sore throat, fever, enlargement of the tonsils, trouble swallowing, and large lymph nodes around the neck. Complications include peritonsillar abscess.

A complication in medicine, or medical complication, is an unfavorable result of a disease, health condition, or treatment. Complications may adversely affect the prognosis, or outcome, of a disease. Complications generally involve a worsening in severity of disease or the development of new signs, symptoms, or pathological changes which may become widespread throughout the body and affect other organ systems. Thus, complications may lead to the development of new diseases resulting from a previously existing disease. Complications may also arise as a result of various treatments.

<i>Streptococcus agalactiae</i> species of bacterium

Streptococcus agalactiae is a gram-positive coccus with a tendency to form chains. It is a beta-hemolytic, catalase-negative, and facultative anaerobe.

Group B streptococcal infection

Group B streptococcal infection, also known as Group B streptococcal disease or just Group B strep, is the infection caused by the bacterium Streptococcus agalactiae. Group B streptococcal infection can cause serious illness and sometimes death, especially in newborns, the elderly, and people with compromised immune systems.

Anti-streptolysin O is the antibody made against streptolysin O, an immunogenic, oxygen-labile streptococcal hemolytic exotoxin produced by most strains of group A and many strains of groups C and G Streptococcus bacteria. The "O" in the name stands for oxygen-labile; the other related toxin being oxygen-stable streptolysin-S. The main function of streptolysin O is to cause hemolysis — in particular, beta-hemolysis.

Rapid strep test test for strep throat

The rapid strep test (RST) is a rapid antigen detection test (RADT) that is widely used in clinics to assist in the diagnosis of bacterial pharyngitis caused by group A streptococci (GAS), sometimes termed strep throat. There are currently several types of rapid strep test in use, each employing a distinct technology. However, they all work by detecting the presence of GAS in the throat of a person by responding to GAS-specific antigens on a throat swab.

Centor criteria set of criteria which may be used to identify the likelihood of a bacterial infection in adult patients complaining of a sore throat

The Centor criteria are a set of criteria which may be used to identify the likelihood of a bacterial infection in adult patients complaining of a sore throat. They were developed as a method to quickly diagnose the presence of Group A streptococcal infection or diagnosis of streptococcal pharyngitis in "adult patients who presented to an urban emergency room complaining of a sore throat."

A throat culture is a laboratory diagnostic test that evaluates for the presence of a bacterial or fungal infection in the throat. A sample from the throat is collected by swabbing the throat and placing the sample into a special cup (culture) that allows infections to grow. If an organism grows, the culture is positive and the presence of an infection is confirmed. The type of infection is found using a microscope, chemical tests, or both. If no infection grows, the culture is negative. Common infectious organisms tested for by a throat culture include Candida albicans known for causing thrush and Group A streptococcus known for causing strep throat, scarlet fever, and rheumatic fever. Throat cultures are more sensitive than the rapid strep test (70%) for diagnosing strep throat, but are nearly equal in terms of specificity.

<i>Streptococcus canis</i> species of bacterium

Streptococcus canis is a group G beta-hemolytic species of Streptococcus. It was first isolated in dogs, giving the bacterium its name. These bacteria are characteristically different from Streptococcus dysgalactiae, which is a human-specific group G species that has a different phenotypic chemical composition. S. canis is important to the skin and mucosal health of cats and dogs, but under certain circumstances, these bacteria can cause opportunistic infections. These infections were known to afflict dogs and cats prior to the formal description of the species in Devriese et al., 1986. However, additional studies revealed cases of infection in other mammal species, including cattle and even humans. Instances of mortality from S. canis in humans are very low with only a few reported cases, while actual instances of infection may be underreported due to mischaracterizations of the bacteria as S. dysgalactiae. This species, in general, is highly susceptible to antibiotics, and plans to develop a vaccine to prevent human infections are currently being considered.

Streptococcus dysgalactiae is a gram positive, beta-haemolytic, coccal bacterium belonging to the family Streptococcaceae. It is capable of infecting both humans and animals, but is most frequently encountered as a commensal of the alimentary tract, genital tract, or less commonly, as a part of the skin flora. The clinical manifestations in human disease range from superficial skin-infections and tonsillitis, to severe necrotising fasciitis and bacteraemia. The incidence of invasive disease has been reported to be rising. Several different animal species are susceptible to infection by S.dysgalactiae, but bovine mastitis and infectious arthritis in lambs have been most frequently reported.

Erythrogenic toxin

Erythrogenic toxins, also referred to as streptococcal pyrogenic exotoxins, are secreted by strains of the bacterium Streptococcus pyogenes. SpeA and SpeC are superantigens, which induce inflammation by nonspecifically activating T cells and stimulating the production of inflammatory cytokines. SpeB, the most abundant streptococcal extracellular protein, is a cysteine protease. Pyrogenic exotoxins are implicated as the causative agent of scarlet fever and streptococcal toxic shock syndrome. There is no consensus on the exact number of pyrogenic exotoxins. Serotypes A-C are the most extensively studied and recognized by all sources, but others note up to thirteen distinct types, categorizing SpeF-M as additional superantigens.

Bacteriophage T12 is a bacteriophage that infects the bacterial species Streptococcus pyogenes, and converts a harmless strain of bacteria into a virulent strain. It carries the speA gene which codes for erythrogenic toxin A. speA is also known as streptococcal pyogenic exotoxin A, scarlet fever toxin A, or even scarlatinal toxin. Note that when the term 'spe'A is italicized, the reference is to the gene. In contrast, when the term 'spe'A is not italicized, the toxin itself is being referred to. Erythrogenic toxin A converts a harmless, nonvirulent strain of Streptococcus pyogenes to a virulent strain through lysogeny, a life cycle which is characterized by the ability of the genome to become a part of and be stably maintained in the host cell for generations. Phages with a lysogenic life cycle are also called temperate phages. A virulent strain of bacteria is one that is "extremely infective" and causes medical, clinical symptoms. Bacteriophage T12, a member of a family of related speA-carrying bacteriophages, is also a prototypic phage for all the speA-containing phages of Streptococcus pyogenes, meaning that its genome is the prototype for the genomes of all such phages of S.pyogenes. It is the main suspect as the cause of scarlet fever, an infectious disease that affects small children.

Anti-Deoxyribonuclease B titres are a quantitative measure of the presence of serologic antibodies obtained from patients suspected of having a recent group A (Beta-hemolytic) streptococcus bacteria infection, from Streptococcus pyogenes.


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